General Inflammation Research Articles

Skin Temperature of Slaughter Pigs With Tail Lesions.

The aim of this study was to assess the effect of tail lesion severity on skin temperature of slaughter pigs measured at the base of the tail and the ear by infrared thermography camera and to evaluate the association between the temperature measurements. Pigs were randomly selected in the lairage, containing ~200 pigs/pen. Tail lesions were scored according to severity, using a 0-4 scale. Tail lesion scores 0 and 1 were summed as it was difficult to distinguish healed lesions from mild lesions due to animal dirtiness. In total, 269 study pigs were imaged at the two locations. The effect of tail lesion score and sex of the pig on the highest temperature of the infrared image areas were analyzed using linear mixed models. Association between the tail base and ear base temperatures was evaluated using Pearson correlation. Skin temperature measured at the base of the tail was significantly lower for tails scored 0–1 than for all other tail lesion scores (P < 0.05). Pigs with tail lesion scored 2 had significantly lower skin temperatures at the base of the tail than pigs with tail lesion scored 3 or 4 (P < 0.05) while there was no difference in skin temperature at the base of the tail between pigs with tail lesion scored 3 and 4 (P > 0.05). Skin temperature measured at the ear base was significantly lower for pigs with tail lesion scored 0–1 than pigs of all other tail lesion scores (P < 0.05) with no difference between the other scores (P > 0.05). Furthermore, there was an association between the two measurements (r = 0.50; P < 0.001). The findings suggest that even pigs with moderate tail lesions (score 2) may have general inflammation and infection, evidenced by the elevated systemic temperature compared to pigs with none or mild tail lesion (score 0–1).

COVID-19 Pandemic Acute Respiratory Distress Syndrome Survivors: Pain After the Storm?

COVID-19 Pandemic Acute Respiratory Distress Syndrome Survivors: Pain After the Storm?

Long non-coding RNA MALAT1/microRNA 125a axis presents excellent value in discriminating sepsis patients and exhibits positive association with general disease severity, organ injury, inflammation level, and mortality in sepsis patients.

ObjectiveThe present study aimed to investigate the potential value of long non‐coding RNA metastasis‐associated lung adenocarcinoma transcript 1 (lnc‐MALAT1)/microRNA (miR)‐125a axis in disease management and prognosis surveillance of sepsis.MethodsTotally, 196 sepsis patients and 196 healthy controls were enrolled. Blood samples were collected within 24 hours after admission in sepsis patients and were collected at enrollment in healthy controls. The relative expression of lnc‐MALAT1 and miR‐125a in all participants was detected by reverse transcription quantitative polymerase chain reaction, and the inflammatory cytokines in plasma of sepsis patients were measured by enzyme‐linked immunosorbent assay.ResultsLnc‐MALAT1/miR‐125a axis was increased in sepsis patients compared with healthy controls (P < .001) and was of excellent value in distinguishing septic patients from healthy controls with the area under the curve (AUC) of 0.931 (95% CI: 0.908‐0.954). In sepsis patients, lnc‐MALAT1 was negatively associated with miR‐125a, and lnc‐MALAT1/miR‐125a axis was positively correlated with acute pathologic and chronic health evaluation II (APACHE II) score, Sequential Organ Failure Assessment (SOFA) score, serum creatinine, C‐reactive protein, tumor necrosis factor‐α, interleukin (IL)‐1β, IL‐6, and IL‐8, while negatively associated with albumin. Furthermore, lnc‐MALAT1/miR‐125a axis was of value in predicting increased 28‐day mortality risk to some extent (AUC: 0.678, 95% CI: 0.603‐0.754).ConclusionLnc‐MALAT1/miR‐125a axis presents excellent value in differentiating sepsis patients from healthy controls and also exhibits positive association with general disease severity, organ injury, inflammation level, and mortality in sepsis patients.

Care of patients with liver disease during the COVID-19 pandemic: EASL-ESCMID position paper.

SummaryThe coronavirus disease 2019 (COVID-19) pandemic poses an enormous challenge to healthcare systems in affected communities. Older patients and those with pre-existing medical conditions have been identified as populations at risk of a severe disease course. It remains unclear at this point to what extent chronic liver diseases should be considered as risk factors, due to a shortage of appropriate studies. However, patients with advanced liver disease and those after liver transplantation represent vulnerable patient cohorts with an increased risk of infection and/or a severe course of COVID-19. In addition, the current pandemic requires unusual allocation of healthcare resources which may negatively impact the care of patients with chronic liver disease that continue to require medical attention. Thus, the challenge hepatologists are facing is to promote telemedicine in the outpatient setting, prioritise outpatient contacts, avoid nosocomial dissemination of the virus to patients and healthcare providers, and at the same time maintain standard care for patients who require immediate medical attention.

The Role of Magnesium Biodegradable Material in Peripheral Nerve Repair

Peripheral nerve injuries can greatly diminish a patient’s quality of life. The use of permanent metallic material implants, including stainless steel, introduce a toxicity risk, due to release of allergenic particles upon chronic use, The significant difference in hardness versus bodily tissues is also unsatisfactory for long‐time placement. Biodegradable biomaterial scaffolds are an innovative alternative therapeutic methodology to enhance tissue repair. Magnesium is a biodegradable metal which has received significant interest recently because it is both closer in hardness to tissues and it biodegrades safely, releasing Mg ions, playing many beneficial roles in the human body. Mg ions regulate ion channel opening, DNA replication, protein synthesis and are a crucial cofactor for &gt;300 enzymes. Serum deficiencies of Mg result in general inflammation and are implicated in disorders such as Parkinson’s and Alzheimer’s diseases. Thus, Mg metal biodegradable implants have great promise as a new generation of tissue repair materials. In vivo studies in the Pixley lab have shown that peripheral nerve axons regenerating across an injury gap, react positively to the presence of the Mg, including giving indications that they may be drawn towards the magnesium wire within the tissue. The long term goal is to understand cellular reactions to magnesium (Mg) metal, which will aid the development of a clinical application in peripheral nerve repair.ObjectivesToward investigating the underlying cellular mechanisms, this study sought to 1) design in vitro cell culture systems to determine the effects of selected types of Mg metal wires being tested for use in clinical practice. Then, 2) we sought to determine the in vitro responses to Mg metal by two cell types that are important in peripheral nerve repair: Schwann cells and the class of immune cells, macrophages, that are the first to attach to any implant material and that also play a large role in nerve repair.Materials and MethodsCellular interactions with the selected Mg wires were studied in vitro using immunostaining and phagocytosis assays. The cells analyzed were mouse Schwannoma cells (RT4‐D6P2T) and a mouse macrophage cell line (RAW264.7).ResultsSchwannoma cells showed aggregates around the edge of the immobilized Mg wires, though, no significant migration towards/away from Mg wires, but macrophages appear to react to the Mg wires. The research is continuing to determine the mechanism of cellular interactions with the Mg metal, and whether these interactions would influence the quality of the peripheral nerve repair.Support or Funding InformationFunding was provided by the NSF ERC RMB EEC‐0812348

Brain Exposure to Piperacillin in Acute Hemorrhagic Stroke Patients Assessed by Cerebral Microdialysis and Population Pharmacokinetics

BackgroundThe broad antibacterial spectrum of piperacillin/tazobactam makes the combination suitable for the treatment of nosocomial bacterial central nervous system (CNS) infections. As limited data are available regarding piperacillin CNS exposure in patients without or with low-grade inflammation, a clinical study was conducted (1) to quantify CNS exposure of piperacillin by cerebral microdialysis and (2) to evaluate different dosing regimens in order to improve probability of target attainment (PTA) in brain.MethodsTen acute hemorrhagic stroke patients (subarachnoid hemorrhage, n = 6; intracerebral hemorrhage, n = 4) undergoing multimodality neuromonitoring received 4 g piperacillin/0.5 g tazobactam every 8 h by 30-min infusions for the management of healthcare-associated pneumonia. Cerebral microdialysis was performed as part of the clinical neuromonitoring routine, and brain interstitial fluid samples were retrospectively analyzed for piperacillin concentrations after the first and after multiple doses for at least 5 days and quantified by high-performance liquid chromatography. Population pharmacokinetic modeling and Monte Carlo simulations with various doses and types of infusions were performed to predict exposure. A T>MIC of 50% was selected as pharmacokinetic/pharmacodynamic target parameter.ResultsMedian peak concentrations of unbound piperacillin in brain interstitial space fluid were 1.16 (range 0.08–3.59) and 2.78 (range 0.47–7.53) mg/L after the first dose and multiple doses, respectively. A one-compartment model with a transit compartment and a lag time (for the first dose) between systemic and brain exposure was appropriate to describe the brain concentrations. Bootstrap median estimates of the parameters were: transfer rate from plasma to brain (0.32 h−1), transfer rate from brain to plasma (7.31 h−1), and lag time [2.70 h (coefficient of variation 19.7%)]. The simulations suggested that PTA would exceed 90% for minimum inhibitory concentrations (MICs) up to 0.5 mg/L and 1 mg/L at a dose of 12–16 and 24 g/day, respectively, regardless of type of infusion. For higher MICs, PTA dropped significantly.ConclusionLimited CNS exposure of piperacillin might be an obstacle in treating patients without general meningeal inflammation except for infections with highly susceptible pathogens. Brain exposure of piperacillin did not improve significantly with a prolongation of infusions.

Vegetable and fruit consumption and its association with bone turnover biomarkers in older adults

Purpose Fruits and vegetables (FVs) are a good source of substances that contributed to bone health. However, the relation of FVs consumption with inflammation and bone biomarkers is inconsistent. Thus, this paper aims to assess the association of FVs intake with inflammation and bone biomarkers in older adults. Design/methodology/approach This cross-sectional study was performed on 178 older adults in Tehran, with a mean age of 67.04. Biochemical measurements including serum osteocalcin, high sensitivity c-reactive protein, 25-hydroxyvitamin D 25(OH) D, parathormone and urine terminal telopeptide of Type I collagen (u-CTx) was done. The intake of FVs was calculated using a validated quantitative food frequency questionnaire. Findings Pearson correlation coefficients showed a positive relation between serum osteocalcin and total vegetables (r = 0.167, p = 0.026), juices group (r = 0.155, p = 0.035), starchy vegetables (r = 0.205, p = 0.006) and other vegetable group (r = 0.161, p = 0.032) even after controlling of potential confounders. Analysis of covariance showed that total vegetable were significantly associated with serum osteocalcin (p = 0.041) and PTH levels (p = 0.028). Additionally, no evidence of a significant relationship between total fruit intake and test variables was observed. However, subgroup analyses demonstrated a significant association between citrus fruits and serum 25(OH) D (p = 0.017). A significant relation between starchy vegetable and urine CTx-I was reported (p = 0.016). Moreover, other vegetable subgroup was strongly associated with serum osteocalcin (p = 0.003). Originality/value The results of this paper may provide insight for clinical interventions and also important to make policy for prevention or easing bone disorders and general inflammation related to fruit and vegetable intake.

Formaldehyde, Oxidative Stress, and FeNO in Traffic Police Officers Working in Two Cities of Northern Italy.

Personal air formaldehyde (air-FA) was measured as risk factor of airways inflammation and oxidative stress (SO) induction. Overall, 154 police officers were enrolled from two differently urbanised Italian cities, Turin and Pavia. Urinary F2t-isoprostane (15-F2t-IsoP), a prostaglandin-like compound, was quantified as a biomarker of general OS in vivo and fractional exhaled nitric oxide (FeNO) was measured for monitoring local inflammatory processes. Urinary cotinine was quantified as a biomarker of tobacco smoking exposure. Traffic police officers living in Turin showed an increased level of log air-FA (p < 0.001), equal to +53.6% (p < 0.001). Log air-(FA) mean values were 3.38 (C.I. 95% 3.33–3.43) and 2.84 (C.I. 95% 2.77–2.92) in Turin and Pavia, respectively. Log (air-FA) was higher in “outdoor workers” (3.18, C.I. 95% 3.13–3.24, p = 0.035) compared to “indoor workers”, showing an increase of +9.3%, even controlling for sex and city. The analyses on 15-F2t-IsoP and FeNO, both adjusted for log air-FA, highlighted that OS and inflammation were higher (+66.8%, p < 0.001 and +75%, p < 0.001, respectively) in Turin traffic police officers compared to those from Pavia. Our findings suggest that even low exposures to traffic-related emissions and urbanisation may influence both general oxidative stress levels and local inflammation.

Bronchiolitis obliterans syndrome and restrictive allograft syndrome after lung transplantation: why are there two distinct forms of chronic lung allograft dysfunction?

Bronchiolitis obliterans syndrome (BOS) had been considered to be the representative form of chronic rejection or chronic lung allograft dysfunction (CLAD) after lung transplantation. In BOS, small airways are affected by chronic inflammation and obliterative fibrosis, whereas peripheral lung tissue remains relatively intact. However, recognition of another form of CLAD involving multiple tissue compartments in the lung, termed restrictive allograft syndrome (RAS), raised a fundamental question: why there are two phenotypes of CLAD? Increasing clinical and experimental data suggest that RAS may be a prototype of chronic rejection after lung transplantation involving both cellular and antibody-mediated alloimmune responses. Some cases of RAS are also induced by fulminant general inflammation in lung allografts. However, BOS involves alloimmune responses and the airway-centered disease process can be explained by multiple mechanisms such as external alloimmune-independent stimuli (such as infection, aspiration and air pollution), exposure of airway-specific autoantigens and airway ischemia. Localization of immune responses in different anatomical compartments in different phenotypes of CLAD might be associated with lymphoid neogenesis or the de novo formation of lymphoid tissue in lung allografts. Better understanding of distinct mechanisms of BOS and RAS will facilitate the development of effective preventive and therapeutic strategies of CLAD.

Comparison of subcutaneous inflammatory response to commercial and engineered zinc hydroxyapatite implants in rabbits

ABSTRACT Hydroxyapatite (HA) is widely used as a biomaterial for bone repair and metallic prostheses coating. The main limitations of the current commercial synthetic hydroxyapatite compounds include high cost and decreased availability, especially for veterinary medicine purposes. Additionally, it is thought that HA biocompatibility and bioactivity could be enhanced by the addition of metal compounds. The objective of this work was to compare the subcutaneous tissue response of commercial and engineered hydroxyapatite obtained from the bovine femur diaphysis mixed with different concentrations of hexa-hydrated Zinc Nitrate in rabbits. Twenty-Five New Zealand female rabbits were used. Five treatments were done according to HA composition (commercial HA, no Zn-HA, 0.1M Zn, 0.2M Zn, and 0.3M Zn). Each treatment was evaluated at five time-points (8, 15, 30, 60 and 90 days post-implantation). Histopathologic analysis was performed to assess inflammation by polymorphonuclear cells infiltration, neovascularization, and fibrosis. Results obtained in this work suggest that general inflammation decreased after 60 days of implantation regardless of Zn concentration. Fibrosis score was increased in the commercial HP compared to control and Zn-hydrated HA. This paper shows that bovine hydroxyapatite is a biocompatible material regardless of nitrate Zinc concentration and has the same properties of commercial hydroxyapatite.

Abdominal Fat Is Directly Associated With Inflammation In Persons With Type-2 Diabetes Regardless Of Glycemic Control -A Jordanian Study.

Background and aimSystemic inflammation is related to the progression of complications associated with diabetes. This study aimed to investigate the association between general and abdominal obesity and inflammation in patients with type-2 diabetes with or without glycemic control.MethodsA total of 198 men (n=73) and women (n=125) diagnosed with type 2 diabetes participated in this study. General obesity markers, body mass index (BMI), and abdominal fat were assessed. Circulating concentrations of glycated hemoglobin (HbA1C), C-reactive protein (CRP), and serum interleukin-6 (IL-6) were determined. Poor glycemic control and good glycemic control were defined as having fasting HbA1C concentrations ≥7% and <7%, respectively. Multivariate adjusted analysis of covariance was used to determine the relation between BMI and abdominal fat and markers of inflammation in patients with good and poor glycemic control.ResultsPatients in <7% HbA1C category, those with high abdominal fat had ≈262% higher CRP and ≈30.6% higher IL-6 compared to those with low abdominal fat (p˂0.05). Patients in ≥7% HbA1C category, those with high abdominal fat had ≈41.4% higher CRP and ≈33.9% higher IL-6 compared to those with low abdominal fat (p˂0.05). Abdominal fat was directly related to CRP (p˂0.023) and IL-6 (p˂0.002) concentrations in both groups of type-2 diabetic patients with <7% and ≥7% HbA1C. In patients with ≥7% HbA1C, BMI was directly related to CRP (p˂0.02) and IL-6 (p˂0.047). Whereas in patients with <7% HbA1C, BMI was not associated with CRP or IL-6 concentrations.ConclusionHigh level of abdominal fat is associated with systemic inflammation in type-2 diabetes regardless of glycemic control. Abdominal fat is a better predictor (determinant) of inflammation than BMI in patients with type-2 diabetes with or without glycemic control.

Deletion of NFKB1 enhances canonical NF-\u03baB signaling and increases macrophage and myofibroblast content during tendon healing

Flexor tendon injuries heal with excessive scar tissue that limits range of motion and increases incidence of re-rupture. The molecular mechanisms that govern tendon healing are not well defined. Both the canonical nuclear factor kappa B (NF-κB) and mitogen activated protein kinase (MAPK) pathways have been implicated in tendon healing. The gene NFKB1 (proteins p105/p50) is involved in both NF-κB and MAPK signaling cascades. In the present study, we tested the hypothesis that global NFKB1 deletion would increase activation of both NF-κB and MAPK through loss of signaling repressors, resulting in increased matrix deposition and altered biomechanical properties. As hypothesized, NFKB1 deletion increased activation of both NF-κB and MAPK signaling. While gliding function was not affected, NFKB1 deletion resulted in tendons that were significantly stiffer and trending towards increased strength by four weeks post-repair. NFKB1 deletion resulted in increased collagen deposition, increase macrophage recruitment, and increased presence of myofibroblasts. Furthermore, NFKB1 deletion increased expression of matrix-related genes (Col1a1, Col3a1), macrophage-associated genes (Adgre1, Ccl2), myofibroblast markers (Acta2), and general inflammation (Tnf). Taken together, these data suggest that increased activation of NF-κB and MAPK via NFKB1 deletion enhance macrophage and myofibroblast content at the repair, driving increased collagen deposition and biomechanical properties.

Abstract 613: Demographic and social patterns of average values of inflammatory markers in U.S. adults: 2010-2017 NHANES analysis

Abstract Introduction Inflammation has been found to play a role in disease prognosis and progression of many conditions, such as cancers, thrombolytic, and cardiovascular diseases. However, reference values for inflammatory markers within the U.S. adult population remains an understudied area. As such, this study aims to (1) establish average values of various inflammatory markers within U.S. adults and (2) explore heterogeneity in average values by socio-demographic and behavioral risk factors. Methods Aggregated cross-sectional data from participants ages 20 and older within the 2010-2017 National Health and Nutrition Examination Survey (NHANES) were used. Outcomes included validated measures of general inflammation (lymphocyte count, monocyte count, segmented neutrophil count, eosinophil count, basophil count, platelet count, neutrophil/lymphocyte ratio); risk factors included socio-demographic and behavioral variables such as race, age, sex, nativity, BMI, smoking history and alcohol use. The final sample consisted of 16,849 participants across all of the survey waves. Adjusted linear regression models were used to explore the association between various demographic and behavioral characteristics and inflammatory markers. Results Average lymphocyte count across all participants was 2.17k cells/microliter, neutrophil was 4.23k cells/microliter, and NLR was 2.12. In the fully adjusted linear regression model, average NLR for non-Hispanic Blacks was 0.44 lower than the average NLR for non-Hispanic Whites (95% CI -0.52 to- 0.37). In the fully adjusted model it was found that age, nativity, and smoking status were also statistically significantly associated with NLR. Participants in the 30-59, 60-79, 80+ age categories had 0.09, 0.28. 0.71 higher average NLR values compared to ages 20-29, respectively. Current smokers had a 0.11 average higher than NLR value compared to non-smokers. Former smokers also have an average NLR that is 0.08 higher than non-smokers. Conclusions This study provides population-based average values of inflammatory markers in healthy U.S adults. These values significantly varied by race, age, nativity, and smoking status. Clinical implications indicate the need to consider different cut-off points by race and age for risk assessment as a predictive and prognostic marker for various illnesses. These inflammatory markers can be easily measured in cost-effective simple blood tests, are routinely available in other population-based national surveys, and have the potential to predict the prognosis of cancer treatments, thrombolytic diseases and coronary artery disease. Citation Format: Raisa Haq, Rose Calixte, Marlene Camacho-Rivera. Demographic and social patterns of average values of inflammatory markers in U.S. adults: 2010-2017 NHANES analysis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 613.

Link between Endometriosis, Atherosclerotic Cardiovascular Disease, and the Health of Women Midlife

Endometriosis and atherosclerotic cardiovascular disease (ASCVD) are both essentially diseases of inflammation. It is well established that inflammation is the leading mechanism in the initiation and maintenance of vascular injury and in the development and progression of atherosclerosis. Thus, if women with endometriosis do indeed have increased general inflammation, they are at increased risk of developing microvascular dysfunction and atherosclerosis. Currently available evidence suggests that young female patients with proven endometriosis may be at a higher lifetime risk of developing cardiovascular disease; this may be unrecognized due to the relatively young age of women found to have endometriosis. Other mechanisms proposed to explain the link between endometriosis and ASCVD include similarities in the genetic underpinnings of each condition, including microRNA dysfunction and the association between endometriosis and early menopause, a risk for developing ASCVD. Although physicians today primarily focus on traditional risk factors when evaluating an individual female patient's risk of developing ASCVD, we believe that a history of endometriosis should be included as a possible risk factor and needs further exploration. A better understanding of the mechanisms linking endometriosis with ASCVD will hopefully guide the implementation of new therapies to mitigate the increased cardiovascular disease burden that patients with endometriosis might face.

Magnetic resonance imaging of noradrenergic neurons

Noradrenaline is a neurotransmitter involved in general arousal, selective attention, memory, inflammation, and neurodegeneration. The purpose of this work was to delineate noradrenergic neurons in vivo by T1-weighted MRI with magnetization transfer (MT). In the brainstem of human and mice, MRI identified the locus coeruleus, dorsal motor vagus nucleus, and nucleus tractus solitarius. Given (1) the long T1 and low magnetization transfer ratio for the noradrenergic cell groups compared to other gray matter, (2) significant correlation between MT MRI signal intensity and proton density, and (3) no correlation between magnetization transfer ratio (or R1) and iron, copper, or manganese in human brain, the high MRI signal of the noradrenergic neurons must be attributed to abundant water protons interacting with any T1-shortening paramagnetic ions in active cells rather than to specific T1-shortening molecules. The absence of a high MRI signal from the locus coeruleus of Ear2(−/−) mice lacking noradrenergic neurons confirms that cell bodies of noradrenergic neurons are the source of the bright MRI appearance. The observation of this high signal in DBH(−/−) mice, in 3-week-old mice, and in mice under hyperoxia/hypercapnia/hypoxia together with the general absence of neuromelanin (NM) in noradrenergic neurons of young rodents further excludes that it is due to NM, dopamine β-hydroxylase, their binding to paramagnetic ions, blood inflow, or hemoglobin. Instead, these findings indicate a high density of water protons whose T1 is shortened by paramagnetic ions as the relevant source of the high MRI signal. In the brain of APP/PS1/Ear2(−/−) mice, a transgenic model of Alzheimer’s disease, MRI detected noradrenergic neuron loss in the locus coeruleus. Proton magnetic resonance spectroscopy revealed that a 60–75% reduction of noradrenaline is responsible for a reduction of N-acetylaspartate and glutamate in the hippocampus as well as for a shortening of the water proton T2 in the frontal cortex. These results suggest that a concurrent shortage of noradrenaline in Alzheimer’s disease accelerates pathologic processes such as inflammation and neuron loss.

The effect of desert dust particles on rheological properties of saliva and mucus

Transported desert dust particles (TDDP) are soil particles suspended in the air. Being spread all over the globe by the winds, TDDP affect animals, including humans, plants and other organisms not only in the areas of their emission. In humans, TDDP are responsible for diseases of the respiratory (e.g. asthma) and circulatory (e.g. heart failure) systems and they also act directly on the epithelium and its mucus layer after deposition in the mouth and respiratory system. The aim of the study was to determine the influence of TDDP on the rheology of mucus and saliva, and thus on their functioning. The artificial mucus and saliva, as well as Arizona TDDP, were used in experiments. The rheological properties of TDDP were determined with the use of an oscillatory rheometer, at various temperatures and in the presence of different amount of TDDP. Moreover, the diffusion time of the marker (rhodamine B) throughout mucus with desert dust particles was examined. The obtained results demonstrate that the presence of TDDP in the saliva and mucus model increases their apparent viscosity. The concentration of particles is positively correlated with the increase of viscosity. However, it has not been demonstrated that the presence of TDDP in mucus significantly influenced the diffusion of a fluorescent marker throughout the mucus. The presence of TDDP in the saliva and mucus may interfere with their moisturising function, and cause difficulties in swallowing by increasing the viscosity of mucus and saliva. Moreover, increased viscosity of mucus may cause problems with its ability to pass to the upper respiratory tracts, which may lead to a general discomfort or local inflammation.

Młodzieńczy toczeń rumieniowaty układowy – opis przypadku

Juvenile systemic lupus erythematosus is an autoimmune, chronic, multisystemic inflammatory disease with an unknown etiology. The average age of juvenile systemic lupus erythematosus (jSLE) diagnosis is 11-14 years old, with a significant female predominance. Clinical manifestations of JSLE are extremely variable, from a relatively mild disease characterised by facial rash, joint pains, fever, fatigue, weight loss, alopecia and arthralgias to a severe life threatening illness.These and other symptoms of diffuse generalized inflammation including lymphadenopathy and hepatosplenomegaly occur both at onset and during disease flares.The authors present the case of a girl hospitalized in the Rheumatology Clinic due to fevers, skin lesions and haematological disorders. The diagnostic difficulty may have been the fact that the symptoms appear also in the course of many pediatric diseases. Finally, based on an in-depth medical history, physical examination and the results of immunological tests, they were recognized at the outset. Juvenile systemic lupus erythematosus is a disease with a diverse clinical picture, therefore, early diagnosis is not easy, but it is necessary to implement effective treatment. Knowledge and experience of the spectrum of paediatric and adolescent disease is important as well as recognition of when features merit further investigation.

Topical application of cashew gum or chlorhexidine gel reduces overexpression of proinflammatory genes in experimental periodontitis.

This study aimed to explore the effect of topically administering an orabase gel containing cashew gum (CG), a complex polysaccharide from Anacardium occidentale L., on the transcription of important proinflammatory (COX-2, NOS-2, INF-γ, OSCAR, and MYD88) and anti-inflammatory genes (IL-10, IL-4, and TGFβ1) in the gingival tissues of rats with ligature-induced periodontitis, compared to the effect observed upon topically applying a well-known antibiofilm agent (chlorhexidine) under the same experimental conditions. The gene expression profile in the gingival tissues of rats with periodontitis treated with CG did not statistically significantly differ from that observed in the group of animals treated with chlorhexidine. Results showed that CG is able to attenuate general inflammation in the periodontium by reducing the transcription of proinflammatory mediators in a MYD88-independent manner, and not by inducing the expression of anti-inflammatory factors. In conclusion, this study demonstrated that CG and chlorhexidine treatment reduced significantly the gene overexpression (COX-2, NOS-2, INF-γ, OSCAR, and TGFβ1) in the model of ligature-induced periodontitis.

Inflammation, infection and depression: an evolutionary perspective.

The evolutionary basis for clinical depression is not well understood. A growing body of literature that is not based on evolutionary logic links inflammation to depression. Integration of these findings with an evolutionary framework for depression, however, needs to address the reasons why the body's inflammatory response would be regulated so poorly that it would result in incapacitating depression. Pathogen induction of inflammation offers an explanation, but the extent to which the association between inflammation and depression can be attributed to general inflammation as opposed to particular effects of pro-inflammatory pathogens remains unclear. This paper reports a study of sexually transmitted pathogens, which addresses this issue. Although several sexually transmitted pathogens were associated with depression according to bivariate tests, only Chlamydia trachomatis and Trichomonas vaginalis were significantly associated with depression by a multivariate analysis that accounted for correlations among the pathogens. This finding is consistent with the hypothesis that infection may contribute to depression through induction of tryptophan restriction, and a consequent depletion of serotonin. It reinforces the idea that some depression may be caused by specific pathogens in specific evolutionary arms races with their human host.

Sorghum Fermented by Aspergillus oryzae NK Enhances Inhibition of Vascular Inflammation in TNF-α-stimulated Human Aortic Smooth Muscle Cells

Sorghum bicolor L. Moench is widely grown all over the world for food and feed. The effects of sorghum extracts on general inflammation have been previously studied, but its anti-vascular inflammatory effects are unknown. Therefore, this study investigated the anti-vascular inflammation effects of sorghum extract (SBE) and fermented extract of sorghum (fSBE) on human aortic smooth muscle cells (HASMCs). After the cytotoxicity test of the sorghum extract, a series of experiments were conducted. The inhibition effects of SBE and fSBE on the inflammatory response and adhesion molecule expression were measured using treatment with tumor necrosis factor-α (TNF-α), a crucial promoter for the development of atherosclerotic lesions, on HASMCs. After TNF-α (10 ng/mL) treatment for 2 h, then SBE and fSBE (100 and 200 μg/mL) were applied for 12h. Western blotting analysis showed that the expression of vascular cell adhesion molecule-1 (VCAM-1) (2.4-fold) and cyclooxygenase-2 (COX-2) (6.7-fold) decreased, and heme oxygenase-1 (HO-1) (3.5-fold) increased compared to the TNF-α control when treated with 200 μg/mL fSBE (P<0.05). In addition, the fSBE significantly increased the expression of HO-1 and significantly decreased the expression of VCAM-1 and COX-2 compared to the TNF-α control in mRNA level (P<0.05). These reasons of results might be due to the increased concentrations of procyanidin B1 (about 6-fold) and C1 (about 30-fold) produced through fermentation with Aspergillus oryzae NK for 48 h, at 37 °C. Overall, the results demonstrated that fSBE enhanced the inhibition of the inflammatory response and adherent molecule expression in HASMCs.