Inflammatory Reaction Research Articles

A case of prolonged corneal sulfur foreign bodies and review of literature

BackgroundThis case mainly describes a relatively rare case of an old mineral-like corneal foreign body that existed for up to 20 years, and did not significantly affect the visual quality of the patient.Case presentationA 56-year-old male miner complained of right eye vision loss for 3 years, swollen and painful for 4 months. Admission examination: Best corrected visual acuity was no light perception in the right eye and 20/20 in the left eye. Anterior segment examination: A large number of spot-like grayish-brown mineral foreign bodies in the conjunctiva of the nasal conjunctiva, emulsified silicone oil floating in the anterior chamber, Corneal foreign bodies in the right eye were widely distributed in the upper cortex and the proelastic layer. There were fewer foreign bodies in the left cornea. Previous medical history, 20 years ago due to forging and burning sulphur mine explosion, resulting in a large number of ore foreign bodies in the conjunctiva of both eyes. As these corneal foreign bodies did not affect the visual quality of the patient, we adopted a conservative treatment plan, did not remove these foreign bodies, and only carried out symptomatic treatment for the patient’s secondary ocular hypertension. The patient was followed up normally in the outpatient department, and no cornea-related complications occurred up to now.ConclusionsFirst of all, it is necessary to understand the source and nature of the foreign body in patients with corneal and conjunctival foreign body injuries. In the second, for the old corneal metal foreign body, when the patient’s visual acuity is stable and there are no symptoms of corneal irritation and inflammatory reaction, it can be Conservative treatment or outpatient follow-up observation. In the end, corneal Optical coherence tomography imaging should not be ignored, which is very important for determining the depth of embedding and the location of the corneal foreign body.

Gut microbiota promotes macrophage M1 polarization in hepatic sinusoidal obstruction syndrome via regulating intestinal barrier function mediated by butyrate

ABSTRACT Background The intestinal-liver axis is associated with various liver diseases. Here, we verified the role of the gut microbiota and macrophage activation in the progression of pyrrolizidine alkaloids-induced hepatic sinusoidal obstruction syndrome (PA-HSOS), and explored the possible mechanisms and new treatment options. Methods The HSOS murine model was induced by gavage of monocrotaline (MCT). An analysis of 16S ribosomal DNA (16S rDNA) of the feces was conducted to determine the composition of the fecal microbiota. Macrophage clearance, fecal microbiota transplantation (FMT), and butyrate supplementation experiments were used to assess the role of intestinal flora, gut barrier, and macrophage activation and to explore the relationships among these three variables. Results Activated macrophages and low microflora diversity were observed in HSOS patients and murine models. Depletion of macrophages attenuated inflammatory reactions and apoptosis in the mouse liver. Moreover, compared with control-FMT mice, the exacerbation of severe liver injury was detected in HSOS-FMT mice. Specifically, butyrate fecal concentrations were significantly reduced in HSOS mice, and administration of butyrate could partially alleviated liver damage and improved the intestinal barrier in vitro and in vivo. Furthermore, elevated lipopolysaccharides in the portal vein and high proportions of M1 macrophages in the liver were also detected in HSOS-FMT mice and mice without butyrate treatment, which resulted in severe inflammatory responses and further accelerated HSOS progression. Conclusions These results suggested that the gut microbiota exacerbated HSOS progression by regulating macrophage M1 polarization via altered intestinal barrier function mediated by butyrate. Our study has identified new strategies for the clinical treatment of HSOS.

Analgesic Effect of Sulforaphane: A New Application for Poloxamer-Hyaluronic Acid Hydrogels

Sulforaphane (SFN) has shown potential as an antioxidant and anti-inflammatory agent. To improve its druggability, we developed new analgesic formulations with sulforaphane-loaded hyaluronic acid (HA)-poloxamer (PL) hydrogel. This study evaluated the pre-clinical safety and effectiveness of these formulations. Effectiveness was tested on Wistar rats divided into groups (n = 15) receiving (IM, 10 mg/kg) SFN formulations or control groups (without SFN). This study used a hind paw incision postoperative pain model to evaluate mechanical hypersensitivity with von Frey filaments. TNF-α, IL-1β, substance P, and CGRP levels verified anti-inflammatory activity in the hind paw tissue. Histopathology of tissues surrounding the injection site was assessed after 2 and 7 days post-treatment. To corroborate drug safety, cell viability of 3T3 and RAW 264.7 cultures was assessed. Additionally, RAW 264.7 cultures primed with carrageenan evaluated nitric oxide (NO) levels. All animals exhibited post-incisional hypersensitivity, and F2 (PL 407/338 (18/2%) + HA 1% + SFN 0.1%) showed a longer analgesic effect (p < 0.05). F2 reduced TNF-α, IL-1β, and CGRP levels (p < 0.05). Histopathological evaluation showed mild to moderate inflammatory reactions after the formulations’ injections. F2 produced no significant difference in cell viability (p > 0.05) but reduced NO production (p < 0.05). Thus, our results highlight the biocompatibility and effectiveness of F2.

High C-Reactive Protein Serum Levels as a Risk Factor for Preeclampsia

Introduction: Preeclampsia is a hypertensive syndrome in pregnancy characterized by increased blood pressure, proteinuria, and complications such as liver dysfunction and visual impairment. This condition is associated with an inflammatory reaction and failure of trophoblast invasion of maternal arteries, which involves an increase in proinflammatory cytokines that indirectly induce CRP production. However, data showing the value of CRP levels as an indicator of the incidence of preeclampsia in Indonesia is minimal. This study aims to evaluate CRP levels as a predictor of preeclampsia.Methods: This case-control study involved pregnant women with preeclampsia and normal pregnant women who went to the Obstetric Emergency Installation at Prof. Hospital. Dr. I.G.N.G Ngoerah Denpasar. All data were obtained from patient medical records and then analyzed using the SPSS v.22.Results: This study involved 56 pregnant women consisting of 28 normotensive pregnant women (control) and 28 pregnant women with preeclampsia (cases) at Prof. Dr. I.G.N.G. Ngoerah General Hospital Denpasar from January to December 2023. The median age was 27.5 years (control) and 26.0 years (cases), with an age range of 18–40 years. The median BMI WAS 21.65 kg/m2 (controls) and 21.80 kg/m2 (cases). Most patients in both groups were nulliparous (50.0%, controls; 42.9%, cases). Based on ROC analysis, the CRP cut-off value of 7.76 mg/dL has a sensitivity of 76.7%, specificity of 78.6%, and an area under the curve (AUC) of 0.737, where pregnant women with high CRP (≥7.76 mg/dL) had a 12.048-fold higher risk (95%CI 3.496–41.515; p < 0.001) of experiencing preeclampsia compared to pregnant women with low CRP levels.Conclusion: High serum CRP levels are a risk factor for preeclampsia. These findings indicate that measuring CRP levels can be a potential tool for identifying the risk of preeclampsia in the pregnant population.

MCP-1 exerts the inflammatory response via ILK activation during endometriosis pathogenesis

AimsMCP-1 has been shown to be elevated in endometriosis. ILK functions in several cellular events and interacts with MCP-1-signaling. In the current study, we evaluated the role of MCP-1-ILK signaling in human endometriotic cell's (Hs832(C).TCs) potential for colonization, invasion, adhesion, etc. and differentiation of macrophage along with inflammation in an endometriosis mouse model. Materials and methodsA mouse model of endometriosis with elevated levels of MCP-1 was developed by injecting MCP-1. We examined the migration, adhesion, colonization and invasion of Hs832(C).TCs in response to MCP-1-ILK signaling. We also examined the differentiation of THP-1 cells to macrophage in response to MCP-1-ILK signaling. Key findingsWe observed that MCP-1 increased Ser246 phosphorylation of ILK in Hs832(C).TCs and enhanced the migration, adhesion, colonization, and invasion of Hs832(C).TCs. In the mouse model of endometriosis, we found elevated chemokines (CCL-11, CCL-22 and CXCL13) levels. An increased level of MCP-1 mediated ILK activation, leading to increased inflammatory reaction and infiltration of residential and circulatory macrophages, and monocyte differentiation, but suppressed the anti-inflammatory reaction. The inhibitor (CPD22) of ILK reversed the MCP-1-mediated action by restoring Hs832(C).TCs and THP-1 phenotype. ILK inhibition in a mouse model of endometriosis reduced the effects of MCP-1 mediated pro-inflammatory cytokines, but increased anti-inflammatory response along with T-regulatory and T-helper cell restoration. SignificanceTargeting ILK restores MCP-1 milieu in the peritoneal cavity and endometrial tissues, reduces the inflammatory response, improves the T-regulatory and T-helper cells in the endometriosis mouse model and decreases the migration, adhesion, colonization and invasion of endometriotic cells.

Effects of "brain-gut coherence" method of acupuncture on motor function and intestinal microflora in the patients with cerebral ischemic stroke

To observe the clinical effect of "brain-gut coherence" method of acupuncture on cerebral ischemic stroke (CIS) and explore its action mechanism. A total of 82 patients with CIS were randomly divided into an observation group (41 cases, 3 cases dropped out, 2 cases discontinued) and a control group (41 cases, 4 cases dropped out, 2 cases excluded). The conventional basic treatment was administered in the two groups. Additionally, in the observation group, "brain-gut coherence" method of acupuncture was delivered. The stimulating points included the parietal and temporal anterior oblique line on the affected side, Zhongwan (CV 12), Guanyuan (CV 4), and bilateral Tianshu (ST 25), Zusanli (ST 36), Shangjuxu (ST 37) and Xiajuxu (ST 39). In the control group, the routine acupuncture was operated at Baihui (GV 20), Yintang (GV 24+), bilateral Fengchi (GB 20) and Zusanli (ST 36), and Hegu (LI 4), Jianyu (LI 15), Quchi (LI 11), Waiguan (TE 5), Futu (ST 32), Sanyinjiao (SP 6) and Taichong (LR 3) on the affected side. Acupuncture stimulation lasted 30 min each time, once daily, and for 5 days a week. The intervention for 4 weeks was required. The scores of Fugl-Meyer assessment scale (FMA), Berg balance scale (BBS) and the modified Barthel index (MBI), as well as the score of gastrointestinal symptoms were compared before and after treatment in the two groups. The neutrophil count (NUE) and the content of the serum N-terminal pro-B-type natriuretic peptide (NT-proBNP) were detected before and after treatment in the two groups. Using 16S rRNA gene sequencing, the structure and relative abundance of intestinal microflora was detected before and after treatment; and with the enzyme linked immunosorbent assay (ELISA) adopted, the levels of intestinal fatty acid-binding protein (iFABP), D-lactate (D-LA), lipopolysaccharide (LPS), lipopolysaccharide binding protein (LBP), tumor necrosis factor-α(TNF-α), interleukin (IL)-1β and IL-6 in the serum were detected before and after treatment in the two groups. After treatment, the scores of FMA, BBS and MBI were increased (P<0.05), and the scores of gastrointestinal symptoms were decreased (P<0.05) compared with those before treatment in the two groups. Compared with the control group, the scores of FMA, BBS and MBI were higher (P<0.05) and the score of gastrointestinal symptoms was lower (P<0.05) in the observation group after treatment. NEU and the content of serum NT-proBNP were reduced in the two groups (P<0.05), and the content of serum NT-proBNP in the observation group was lower than that of the control group (P<0.05) after treatment. Chao1, Ace, Sobs and Shannon indexes were increased after treatment compared with those before treatment in the two groups (P<0.05); and these indexes in the observation group were higher when compared with the control group (P<0.05). After treatment, the relative abundance of Bacteroidaceae, Enterobacteriaceae, Oscillospiraceae, Streptococcaceae and Sutterellaceae was reduced in comparison with that before treatment in the two groups (P<0.05); and the relative abundance of these microflora was lower in the observation group when compared with the control group (P<0.05). After treatment, the relative abundance of Lachnospiraceae, Ruminococcaceae, Bifidobacteriaceae and Coriobacteriaceae was increased in comparison with that before treatment in the two groups (P<0.05); and the relative abundance of these microflora was elevated in the observation group when compared with the control group (P<0.05). After treatment, the levels of iFABP, D-LA, LPS, LBP, TNF-α, IL-1β and IL-6 were reduced when compared with those before treatment in the two groups (P<0.05), and these levels of the observation group were lower than those of the control group (P<0.05). "Brain-gut coherence" method of acupuncture can improve the motor function and gastrointestinal function of the patients with cerebral ischemic stroke, which may be related to modulating the structure of intestinal microflora, alleviating inflammatory reactions and accelerating the intestinal barrier repair.

Mechanism of Lian Hua Qing Wen capsules regulates the inflammatory response caused by M1 macrophage based on cellular experiments and computer simulations

PurposeThe polarization of macrophages with the resulting inflammatory response play a crucial part in tissue and organ damage due to inflammatory. Study has proved Lian Hua Qing Wen capsules (LHQW) can reduce activation of inflammatory response and damage of tissue derived from the inflammatory reactions. However, the mechanism of LHQW regulates the macrophage-induced inflammatory response is unclear. Therefore, we investigated the mechanism of LHQW regulated the inflammatory response of M1 macrophages by cellular experiments and computer simulations. MethodsThis study has analysed the targets and mechanisms of macrophage regulating inflammatory response at gene and protein levels through bioinformatics. The monomeric components of LHQW were analyzed by High Performance Liquid Chromatography (HPLC). We established the in vitro cell model by M1 macrophages (Induction of THP-1 cells into M1 macrophages). RT-qPCR and immunofluorescence were used to detect changes in gene and protein levels of key targets after LHQW treatment. Computer simulations were utilized to verify the binding stability of monomeric components and protein targets. ResultsMacrophages had 140690 gene targets, inflammatory response had 12192 gene targets, intersection gene targets were 11772. Key monomeric components (including: Pinocembrin, Fargesone-A, Nodakenin and Bowdichione) of LHQW were screened by HPLC. The results of cellular experiments indicated that LHQW could significantly reduce the mRNA expression of CCR5, CSF2, IFNG and TNF, thereby alleviating the inflammatory response caused by M1 macrophage. The computer simulations further validated the binding stability and conformation of key monomeric components and key protein targets, and IFNG/Nodakenin was able to form the most stable binding conformation for its action. ConclusionIn this study, the mechanism of LHQW inhibits the polarization of macrophages and the resulting inflammatory response was investigated by computer simulations and cellular experiments. We found that LHQW may not only reduce cell damage and death by acting on TNF and CCR5, but also inhibit the immune recognition process and inflammatory response by regulating CSF2 and IFNG to prevent polarization of macrophages. Therefore, these results suggested that LHQW may act through multiple targets to inhibit the polarization of macrophages and the resulting inflammatory response.

Immunological mechanisms in steatotic liver diseases: An overview and clinical perspectives.

Steatotic liver diseases (SLD) are the principal worldwide cause of cirrhosis and end-stage liver cancer, affecting nearly a quarter of the global population. SLD includes metabolic dysfunction-associated alcoholic liver disease (MetALD) and metabolic dysfunction-associated steatotic liver disease (MASLD), resulting in asymptomatic liver steatosis, fibrosis, cirrhosis and associated complications. The immune processes include gut dysbiosis, adipose-liver organ crosstalk, hepatocyte death and immune cell-mediated inflammatory processes. Notably, various immune cells such as B cells, plasma cells, dendritic cells, conventional CD4+ and CD8+ T cells, innate-like T cells, platelets, neutrophils and macrophages play vital roles in the development of MetALD and MASLD. Immunological modulations targeting hepatocyte death, inflammatory reactions and gut microbiome include N-acetylcysteine, selonsertib, F-652, prednisone, pentoxifylline, anakinra, JKB-121, HA35, obeticholic acid, probiotics, prebiotics, antibiotics and FMT. Understanding the immunological mechanisms underlying in SLD is crucial for advancing clinical therapeutic strategies.

SNP alleviates mitochondrial homeostasis dysregulation-mediated developmental toxicity in diabetic zebrafish larvae

The incidence of diabetes is increasing annually, and the disease is uncurable due to its complex pathogenesis. Therefore, understanding diabetes pathogenesis and developing new treatments are crucial. This study showed that the NO donor SNP (8 µM) significantly alleviated high glucose-induced developmental toxicity in zebrafish larvae. High glucose levels caused hyperglycemia, leading to oxidative stress and mitochondrial damage from excessive ROS accumulation. This promoted mitochondrial-dependent apoptosis and lipid peroxidation (LPO)-induced ferroptosis, along with immune inflammatory reactions that decreased mitochondrial function and altered intracellular grid morphology, causing imbalanced kinetics and autophagy. After SNP treatment, zebrafish larvae showed improved developmental toxicity and glucose utilization, reduced ROS accumulation, and increased antioxidant activity. The NO-sGC-cGMP signaling pathway, inhibited by high glucose, was significantly activated by SNP, improving mitochondrial homeostasis, increasing mitochondrial count, and enhancing mitochondrial function. It's worth noting that apoptosis, ferroptosis and immune inflammation were effectively alleviated. In summary, SNP improved high glucose-induced developmental toxicity by activating the NO-sGC-cGMP signaling pathway to reduce toxic effects such as apoptosis, ferroptosis and inflammation resulting from mitochondrial homeostasis imbalance.

The transcriptome of MHV-infected RAW264.7 cells offers an alternative model for macrophage innate immunity research.

Macrophages are the primary innate immune cells encountered by the invading coronaviruses, and their abilities to initiate inflammatory reactions, to maintain the immunity homeostasis by differential polarization, to train the innate immune system by epigenic modification have been reported in laboratory animal research. In the current in vitro research, murine macrophage RAW 264.7 cell were infected by mouse hepatitis virus, a coronavirus existed in mouse. At 3-, 6-, 12-, 24-, and 48-h post infection (hpi.), the attached cells were washed with PBS and harvested in Trizol reagent. Then The harvest is subjected to transcriptome sequencing. The transcriptome analysis showed the immediate (3 hpi.) up regulation of DEGs related to inflammation, like Il1b and Il6. DEGs related to M2 differential polarization, like Irf4 showed up regulation at 24 hpi., the late term after viral infection. In addition, DEGs related to metabolism and histone modification, like Ezh2 were detected, which might correlate with the trained immunity of macrophages. The current in vitro viral infection study showed the key innated immunity character of macrophages, which suggested the replacement value of viral infection cells model, to reduce the animal usage in preclinical research.

Predictive role of platelets to lymphocytes ratio and neutrophil to lymphocytes ratio in COPD exacerbation

BackgroundThe hallmark of COPD is the progressive destruction of the lung parenchyma, which is frequently brought on by the body's inflammatory reaction to external stimuli (such as smoking cigarettes or pollution). According to reports, the peripheral blood's essential immune-related cell populations' absolute counts and ratios can accurately represent chronic inflammatory diseases. Complex interactions between immune-related cells, such as lymphocytes and neutrophils, are involved in inflammation, which can cause irreversible damage and loss of respiratory tissue. The neutrophil-to-lymphocyte ratio (NLR) and the platelet-to-lymphocyte ratio (PLR), two hematological indicators of inflammation, have been studied in a variety of disease states, including solid tumors, systemic lupus erythematosus, coronary artery disease, retinal artery occlusion, chronic kidney disease, and stable COPD.AimCorrelation between NLR and PLR and outcome of COPD exacerbation.Materials and methodsThis cross-sectional study included 80 patients with COPD exacerbation who visited the outpatient clinic or were admitted to the Chest Department. CRP and calculation of NLR and PLR within 24 h from admission and 1 month after discharge were obtained to identify the prognostic value of NLR and PLR for the exacerbation, hospitalization, mechanical ventilation, and mortality in patients with COPD.ResultsDuring COPD exacerbation PLR, NLR showed a statistically significant correlation with the need for hospitalization with a p value < 0.001. As regards correlation with mortality NLR was statistically significant with a p value of 0.006 while PLR showed a non-significant p value of 0.077. PLR and NLR were correlated with CRP as an inflammatory marker and both were statistically significant with p value 0.004 and < 0.001 respectively. During exacerbation, PLR and NLR were correlated with the need for mechanical ventilation and the results were statistically significant with p value < 0.001. PLR and NLR showed a significant increase during exacerbation compared to stable COPD patients 1 month after discharge with p value of < 0.001.ConclusionPLR and NLR are simple tests that could be used to predict the severity of COPD exacerbation and the need for hospitalization, MV, and mortality prediction.

Genotype-specific expression of uncle fester suggests a role in allorecognition education in a basal chordate.

Histocompatibility is the ability to discriminate between self and non-self tissues, and has been described in species throughout the metazoa. Despite its universal presence, histocompatibility genes utilized by different phyla are unique- those found in sponges, cnidarians, ascidians and vertebrates are not orthologous. Thus, the origins of these sophisticated recognition systems, and any potential functional commonalities between them are not understood. We are studying histocompatibility in the botryllid ascidians, members of the chordate subphylum, Tunicata, which provide a powerful model to understand both the origins and functional aspects of this process. Histocompatibility in the botryllids occurs at the tips of an extracorporeal vasculature that come into contact when two individuals grow into proximity. If compatible, the vessels will fuse, forming a parabiosis between the two individuals. If incompatible, the two vessels will reject- an inflammatory reaction that results in melanin scar formation at the point of contact, blocking anastomosis. Compatibility is determined by a single, highly polymorphic locus called the fuhc with the following rules: individuals that share one or both fuhc alleles will fuse, while those who share neither will reject. The fuhc locus encodes at least six proteins with known roles in allorecognition. One of these genes, called uncle fester, is necessary and sufficient to initiate the rejection response. Here we report the existence of genotype-specific expression levels of uncle fester, differing by up to 8-fold at the mRNA-level, and that these expression levels are constant and maintained for the lifetime of an individual. We also found that these differences had functional consequences: the expression level of uncle fester correlated with the speed and severity of the rejection response. These findings support previous conclusions that uncle fester levels modulate the rejection response, and may be responsible for controlling the variation observed in the timing and intensity of the reaction. The maintenance of genotype specific expression of uncle fester is also evidence of an education process reminiscent of that which occurs in mammalian Natural Killer (NK) cells. In turn, this suggests that while histocompatibility receptors and ligands evolve via convergent evolution, they may utilize conserved intracellular machinery to interpret binding events at the cell surface.

Assessment of the degree of inflammatory reaction in uveitis: diagnostic capabilities of clinical methods

Inflammatory diseases of the uvea demonstrate a high incidence and a significant prevalence among people of working age. Uveitis complications often lead to blindness and low vision in patients of various age groups. Diagnostics and monitoring the efficacy of uveitis therapy requires the use of quantitative criteria to assess the degree of inflammatory reaction. The aim of this review is to analyze the informative value and accuracy of various clinical methods for subjective and objective assessment of the inflammatory reaction in the anterior and posterior segments of the eye in uveitis. To assess the inflammatory reaction in uveitis in everyday clinical practice, biomicroscopy is most often used, which is characterized by subjectivity associated with the level of qualification of the ophthalmologist. Other clinical methods, such as fluorescein angiography, optical coherence tomography-angiography, have high sensitivity and informative value along with independence from the subjective impression of the examiner. However, the first of them is invasive, and the second is still not available to a wide range of practicing ophthalmologists today, especially in the “angio” mode. Laser flare photometry is of special importance in the diagnosis of uveitis. It is both a non-invasive and sensitive method that makes it possible to obtain quantitative indicators characterizing the activity of uveal inflammation. The prospects for the application and development of this method are important both for clinical practice and for research purposes.

Exploring the Role of the Microbiome in Rheumatoid Arthritis—A Critical Review

Rheumatoid arthritis (RA) is a chronic, autoimmune rheumatic disease characterized by synovial joint inflammation with subsequent destruction as well as systemic manifestation, leading to impaired mobility and impaired quality of life. The etiopathogenesis of RA is still unknown, with genetic, epigenetic and environmental factors (incl. tobacco smoking) contributing to disease susceptibility. The link between genetic factors like “shared epitope alleles” and the development of RA is well known. However, why only some carriers have a break in self-tolerance and develop autoimmunity still needs to be clarified. The presence of autoantibodies in patients’ serum months to years prior to the onset of clinical manifestations of RA has moved the focus to possible epigenetic factors, including environmental triggers that could contribute to the initiation and perpetuation of the inflammatory reaction in RA. Over the past several years, the role of microorganisms at mucosal sites (i.e., microbiome) has emerged as an essential mediator of inflammation in RA. An increasing number of studies have revealed the microbial role in the immunopathogenesis of autoimmune rheumatic diseases. Interaction between the host immune system and microbiota initiates loss of immunological tolerance and autoimmunity. The alteration in microbiome composition, the so-called dysbiosis, is associated with an increasing number of diseases. Immune dysfunction caused by dysbiosis triggers and sustains chronic inflammation. This review aims to provide a critical summary of the literature findings related to the hypothesis of a reciprocal relation between the microbiome and the immune system. Available data from studies reveal the pivotal role of the microbiome in RA pathogenesis.

Study of tribological characteristics of micro-arc calcium phosphate coatings on titanium

Tribological characteristics of implants, such as wear resistance and friction coefficient, play a critical role in ensuring their durability and functionality when interacting with surrounding tissues. These parameters influence the implant's ability to withstand mechanical loads and minimize wear throughout its service life. Minimizing friction between the implant and biological tissues not only helps prevent mechanical damage but also reduces the risk of inflammatory reactions, ensuring better biological compatibility. In this study, calcium phosphate coatings were obtained using the micro-arc oxidation method with different duty cycle of current to investigate their tribological characteristics. The coatings deposited on titanium had a structure with volcano-like formations with pores ranging from 66 to 98 micrometers. The thickness of the coatings varied from 74.3 to 100 micrometers depending on the conditions during microarc oxidation. Tribological tests were conducted using a ball-on-flat setup with reciprocating motion. The coatings were subjected to tribological tests against SHX15 steel under normal loads of 5 and 20 N. Depending on the applied load, the friction coefficients of the coatings ranged from 0.029 to 0.034 at 5 N and from 0.9 to 1.26 at 20 N. Analysis of wear parameters and micrographs of worn surfaces indicate that the mode with a pulse current duty cycle of 17.3% during micro-arc oxidation allows for the production of titanium surface coatings with high wear resistance.

Exploring the Role of the Microbiome in Rheumatoid Arthritis—A Critical Review

Rheumatoid arthritis (RA) is a chronic, autoimmune rheumatic disease characterized by synovial joint inflammation with subsequent destruction as well as systemic manifestation, leading to impaired mobility and impaired quality of life. The etiopathogenesis of RA is still unknown, with genetic, epigenetic and environmental factors (incl. tobacco smoking) contributing to disease susceptibility. The link between genetic factors like “shared epitope alleles” and the development of RA is well known. However, why only some carriers have a break in self-tolerance and develop autoimmunity still needs to be clarified. The presence of autoantibodies in patients’ serum months to years prior to the onset of clinical manifestations of RA has moved the focus to possible epigenetic factors, including environmental triggers that could contribute to the initiation and perpetuation of the inflammatory reaction in RA. Over the past several years, the role of microorganisms at mucosal sites (i.e., microbiome) has emerged as an essential mediator of inflammation in RA. An increasing number of studies have revealed the microbial role in the immunopathogenesis of autoimmune rheumatic diseases. Interaction between the host immune system and microbiota initiates loss of immunological tolerance and autoimmunity. The alteration in microbiome composition, the so-called dysbiosis, is associated with an increasing number of diseases. Immune dysfunction caused by dysbiosis triggers and sustains chronic inflammation. This review aims to provide a critical summary of the literature findings related to the hypothesis of a reciprocal relation between the microbiome and the immune system. Available data from studies reveal the pivotal role of the microbiome in RA pathogenesis.

Study of tribological characteristics of micro-arc calcium phosphate coatings on titanium

Tribological characteristics of implants, such as wear resistance and friction coefficient, play a critical role in ensuring their durability and functionality when interacting with surrounding tissues. These parameters influence the implant's ability to withstand mechanical loads and minimize wear throughout its service life. Minimizing friction between the implant and biological tissues not only helps prevent mechanical damage but also reduces the risk of inflammatory reactions, ensuring better biological compatibility. In this study, calcium phosphate coatings were obtained using the micro-arc oxidation method with different duty cycle of current to investigate their tribological characteristics. The coatings deposited on titanium had a structure with volcano-like formations with pores ranging from 66 to 98 micrometers. The thickness of the coatings varied from 74.3 to 100 micrometers depending on the conditions during microarc oxidation. Tribological tests were conducted using a ball-on-flat setup with reciprocating motion. The coatings were subjected to tribological tests against SHX15 steel under normal loads of 5 and 20 N. Depending on the applied load, the friction coefficients of the coatings ranged from 0.029 to 0.034 at 5 N and from 0.9 to 1.26 at 20 N. Analysis of wear parameters and micrographs of worn surfaces indicate that the mode with a pulse current duty cycle of 17.3% during micro-arc oxidation allows for the production of titanium surface coatings with high wear resistance.

Effects of anesthesia with sevoflurane on outcome parameters in murine experimental studies.

Multiple murine studies modelling the immuno-pathophysiological consequences of trauma, shock, burn or sepsis were performed during the last decades. Almost every animal model requires anesthesia for practical and ethical reasons. Furthermore, often, corresponding control groups involve untreated animals without or with a limited exposure to anesthetics. However, the influences of anesthetic drugs on immuno-pathophysiological reactions remain insufficiently investigated. Therefore, we aimed to closer characterize the anesthetic impact exemplified by sevoflurane on the organ performance in mice and thereby investigate the influence of anesthesia itself on major outcome parameters in animal studies. C57/BL6 mice were subjected either to 270min of sevoflurane narcosis or directly euthanized. Plasma, BAL-fluids, lungs, kidneys, liver and intestine were collected and examined for immunological, functional and morphological changes. Systemic levels of the cytokine keratinocyte chemoattractant (KC) were raised in the narcosis group, while concentrations of high mobility group box protein 1 (HMGB-1) as a major inflammatory marker were reduced. In the lungs, levels of HMGB-1 and interleukin 6 (IL-6) were reduced. In contrast, systemic concentrations of intestinal fatty acid binding-protein (i-FABP) as an intestinal damage marker were elevated. Furthermore, liver-type fatty acid binding-protein (L-FABP) levels were lower in the narcosis animals, and inflammatory markers were reduced in liver tissues. Anesthesia also ameliorated the inflammatory reaction in renal tissues, while plasma levels of urea and creatinine were elevated, reflecting either dehydration and/or impaired renal function. As anesthesia with sevoflurane exhibited distinct effects in different organs, it is difficult to predict its specific impact on targets of interest in in vivo studies. Therefore, further studies are required to clarify the effects of different anesthetic drugs. Overall, the inclusion of a control group subjected to the same anesthesia protocol as the experimental groups of interest seems helpful to precisely define the inherent impact of the anesthetic when investigating immuno-pathophysiologic conditions in vivo.

Exploration of leech therapy in treating gouty rats and its uric acid lowering mechanism

BackgroundGout is a hyperuricemia (HUA)-related inflammatory reaction in the joints. Leech therapy has been effective in the gout, but the exact mechanism is unclear. Objectives: In this study, an exploration of the therapeutic mechanism of leech therapy in HUA and gouty arthritis (GA) rats was done. Material and methodsHUA and GA construction utilizing sodium urate crystal, the potassium form of oxygen oxazine acid, and adenine. Serum and tissues were collected to measure uric acid (UA), creatinine (Cr), and urea nitrogen (UN). Enzyme linked immunosorbent assay was executed to evaluate the levels of xanthine oxidase (XOD), interleukin-6 (IL-6)and tumor necrosis factor α (TNF-α). The expression of glucose transporter 9 (GLUT9), organic anion transporter 3 (OAT3), adenosine triphosphate (ATP)-binding cassette efflux transporter G2 (ABCG2) and the nuclear factor kappa B (NF-kB), interleukin-1β (IL-1β), Toll-like Receptor 2 (TLR2) were assessed by Western blot and visualized in immunohistochemistry staining. ResultsLeech therapy reduces the levels of UA, Cr, and UN as well as the liver and serum levels of XOD activity, increasing the expressions of GLUT9, ABCG2, and OAT3 in the kidney. Meanwhile, it reduces joint swelling and lowers the levels of TNF-α, IL-6, IL-1β, TLR2, and NF-kB. ConclusionsLeech therapy regulates the metabolism of uric acid and treats gouty arthritis with an anti-inflammatory effect.

Current Advances in Nanomaterials Affecting Functions and Morphology of Platelets

Nanomaterials have been extensively used in the biomedical field due to their unique physical and chemical properties. They promise wide applications in the diagnosis, prevention, and treatment of diseases. Nanodrugs are generally transported to target tissues or organs by coupling targeting molecules or enhanced permeability and retention effect (EPR) passively. As intravenous injection is the most common means of administration of nanomedicine, the transport process inevitably involves the interactions between nanoparticles (NPs) and blood cells. Platelets are known to not only play a critical role in normal coagulation by performing adhesion, aggregation, release, and contraction functions, but also be associated with pathological thrombosis, tumor metastasis, inflammation, and immune reactions, making it necessary to investigate the effects of NPs on platelet function during transport, particularly the way in which their physical and chemical properties determine their interaction with platelets and the underlying mechanisms by which they activate and induce platelet aggregation. However, such data are lacking. This review is intended to summarize the effects of NPs on platelet activation, aggregation, release, and apoptosis, as well as their effects on membrane proteins and morphology in order to shed light on such key issues as how to reduce their adverse reactions in the blood system, which should be taken into consideration in NP engineering.