Neutrophil Cell Research Articles

EFFECT OF GALAM LEAF EXTRACT AND TRI-CALCIUM SILICATE CEMENT ON NEUTROPHIL CELLS IN WISTAR RAT PULP

Background: Pulp capping is a method of sealing the pulp chamber in teeth with cavities that extend to the pulp. Direct pulp capping involves applying a material directly onto the exposed pulp tissue. Tri-calcium silicate cement (Ca3SiO5) is commonly used due to its nanoparticle mineral composition, but it can cause continued inflammation. Galam leaf (Melaleuca cajuputi) is known for its anti-inflammatory properties, owing to secondary metabolites like alkaloids, flavonoids, polyphenols, and saponins, potentially compensating for the drawbacks of tri-calcium silicate cement. Purpose: To determine the effect of combining Galam leaf extract (Melaleuca cajuputi subsp. Cumingiana (Turz) Barlow) with tri-calcium silicate cement as a direct pulp capping material on neutrophil cell count in the pulp of Wistar rats (Rattus norvegicus). Methods: This pure experimental study used a posttest-only control design. Thirty-six Wistar rats were divided into nine groups: one received a combination of 100% Galam leaf extract and tri-calcium silicate cement; one positive control group received tri-calcium silicate cement alone; and one negative control group received direct placement with glass ionomer cement (GIC). The neutrophil cell count was assessed on days 1, 2, and 3. Results: Two-way ANOVA results indicated a significant effect based on treatment and time (p < 0.05). Further analysis with the Post Hoc Bonferroni test (p < 0.05) revealed differences in neutrophil cell counts across nearly all groups on days 1, 2, and 3. Conclusion: The combination of 100% Galam leaf extract and tri-calcium silicate cement significantly reduced neutrophil cell counts compared to both positive and negative control groups on days 1, 2, and 3, indicating anti-inflammatory effect.

P102 PH-SENSOR GPR68 PLAYS A ROLE IN THE CARDIOPROTECTIVE EFFECTS OF A HIGH FIBRE DIET

Background/Objective: Dietary fibre lowers blood pressure (BP) via short-chain fatty acids, acidic metabolites released from fibre fermentation by the bacteria in the large intestine. This acidic microenvironment may activate pH-sensing receptor GPR68, expressed primarily on immune cells, which play a crucial role in BP regulation. Here, we aimed to investigate whether GPR68 confers the cardioprotective effects of a high-fibre diet in hypertension by regulating inflammatory responses. Methods: 6–8-week-old male wildtype (WT) and GPR68-deficient (Gpr68-/-) fed a control or high-fibre diet underwent subcutaneous implantation of minipumps containing Angiotensin II (0.75 mg/kg body weight/day, 4 weeks, n=8/group). BP was measured weekly by tail-cuff. Morphometric, histological, and flow cytometric analyses were performed following the 4-week protocol. Results: High-fibre-fed WT mice exhibited blunted elevations in systolic BP (week 4; p=0.0508) and lower cardiac interstitial collagen deposition (p=0.0495) compared to WT mice fed a control diet. However, high fibre did not lower BP (week 4; control vs high-fibre, p=0.689) or cardiac collagen deposition (p=0.842) in Gpr68-/- mice. High-fibre-fed WT mice exhibited improved aortic elastin content compared to control-fed WT mice (p=0.0503), whereas this remained negligible in Gpr68-/- mice (p=0.885). Flow cytometric analysis revealed that high fibre decreased aortic macrophage (p=0.0072) and neutrophil cell counts (p=0.0273) in mice, irrespective of genotype. High fibre also decreased overall renal immune cell counts (p=0.0213) and dendritic cells (p=0.0488) in mice, irrespective of genotype. Finally, high fibre-fed mice had overall decreased circulating immune cell counts (p=0.0264), specifically CD8+ T cells (p=0.0235), and γδ T cells (p=0.0264). Conclusions: High fibre intervention on Angiotensin II-treated GPR68-deficient mice did not lower their BP or cardiac fibrosis. All angiotensin II-treated mice fed a high-fibre diet exhibited prominent changes in various immune cell populations, irrespective of genotype. Nonetheless, this study provides novel insight that GPR68 is involved in the cardioprotective effects of a high-fibre diet. This is most likely via in an immune-independent manner, warranting further investigations into its underlying mechanisms of action.

Tumor microenvironment biomarkers predicting pathological response to neoadjuvant chemoimmunotherapy in locally advanced esophageal squamous cell carcinoma: post-hoc analysis of a single center, phase 2 study

BackgroundNeoadjuvant chemoimmunotherapy has a promising effect on locally advanced esophageal squamous cell carcinoma (ESCC). However, reliable biomarkers robustly predicting therapeutic response are still lacking.MethodsFormalin-fixed and paraffin-embedded pre-neoadjuvant chemoimmunotherapy biopsy samples...

Time to resolution of airway inflammation caused by bronchoalveolar lavage in healthy horses.

Bronchoalveolar lavage (BAL) is a common procedure for evaluation of the equine lower airways. Time to resolution of post-BAL inflammation has not been clearly defined. Residual inflammation, evident by changes in immune cell populations and inflammatory cytokines, will resolve by 72 hours after BAL. Six adult, healthy, institution-owned horses. Randomized, complete cross-over design. Each horse underwent 3 paired BALs, including a baseline and then 48, 72, and 96 hours later, with a 7-day washout between paired BALs. Each sample underwent cytological evaluation and cytokine concentrations were determined by a commercially available multiplex bead immunoassay. Statistical analysis was performed by multilevel mixed-effects Poisson regression analysis. Data are reported as marginal means and 95% confidence interval (CI). Neutrophil, eosinophil and mast cell percentages were not significantly different at any time points. Macrophage percentages were higher at 72 hours (45.0 [95% CI, 41.6-48.4]%) and 96 hours (45.3 [95% CI, 42.9-47.7]%) vs baseline (37.4 [95% CI, 33.5-41.4]%; P < .001 and P = .01, respectively), and at 72 hours and 96 hours vs 48 hours (31.9 [95% CI, 28.1-35.6]%; P < .001). Neutrophil percentage was not significantly increased at 48 hours (P = .11). Interleukin (IL)-6 concentration was increased at 72 hours (5.22 [95% CI, 3.44-6.99] pg/mL) vs 48 hours (4.38 [95% CI, 2.99-5.78] pg/mL; P < .001). Significant lung inflammation was not detected at 72 and 96 hours, suggesting that repeating BAL at 72 hours or more can be done without concern of residual inflammation.

Changes in respiratory tract and gut microbiota in AR mice and their relationship with Th1/Th2/Treg

BackgroundThe etiology of allergic rhinitis (AR) is not fully understood. Studies have shown that the maturation of children's immune systems is closely related to microecology. However, few studies have focused simultaneously on changes in respiratory and gut microbiota in AR and their correlation between microecological changes and Th1/Th2/Treg. ObjectiveThe aim is to investigate the pathogenesis of AR based on respiratory microecology, gut microecology, and Th1/Th2/Treg levels by applying microbiome techniques and correlation analysis. MethodsStandardized OVA-induced AR mice were established. Serum OVA-sIgE, IL-4, IFN-γ, IL-10 were measured by ELISA, Tregs in lymph nodes were determined by flow cytometry, and the histological characteristics of nasal tissues were evaluated by Hematoxylin & Eosin (H&E). Nasal symptoms were observed to determine the reliability of the AR mouse model. Nasal lavage fluid (NALF) and fecal samples were collected after the last OVA challenge. The composition of respiratory microbiota in NALF and gut microbial in feces samples via 16S rRNA gene sequencing between the two groups, further explored the relationship between microbiota and Th1/Th2/Treg levels. ResultsIn the AR group, the incidence of nose rubbing and sneezing in each mouse was significantly increased compared with the control group (all P < 0.001) and the inflammatory cell infiltration of NALF shows a significant increase in eosinophilic and neutrophilic infiltrates upon the AR group; H&E showed that the nasal mucosa of AR mice infiltration of massive eosinophils cells and neutrophils cells. OVA-sIgE and IL-4 in the AR group were increased (P < 0.01, P < 0.05) and IFN-γ, IL-10 were significantly decreased (P < 0.01, P < 0.05). Tregs showed a downward trend in the AR group, but there was no statistical difference. Compared with the control group, the respiratory microbiota of AR mice did not change significantly, while the gut microbiota changed significantly. In gut microbiota, compared to the control group, Shannon index in the AR group revealed a significant decrease at the genus level (P < 0.01), and Simpson index was significantly increased at all levels (all P < 0.05). PCoA also showed significant differences in beta diversity between the two groups (all P < 0.05). Compared to the control group, Deferribacteres at phylum level, Roseburia, Ruminiclostridium, Anaerotruncus at genus level were significantly decreased in the AR group (all P < 0.05). Spearman's rank correlation showed that OVA-sIgE was positively correlated with Bacteroidetes, Muribaculaceae and Erysipelotrichaceae (all P < 0.05); IL-4 was significantly negatively correlated with Epsilonbacteraeota and Deferribacteres (all P < 0.05). Treg was significantly positively correlated with Patescibacteria, Lachnospiraceae, and Saccharimonadaceae in gut microecology. ConclusionOur results showed that the respiratory microbiota of AR mice was not significantly altered, but the gut microbiota varied significantly and there was a correlation between gut microbiota and Th1/Th2/Treg.

Exploring potential therapeutic strategy for hepatocellular carcinoma and COVID-19 using bioinformatics analysis

BackgroundHepatocellular carcinoma (HCC) constitutes an important contributor to fatalities. Coronavirus disease 2019 (COVID-19) frequently presents with complications such as respiratory distress, systemic inflammatory responses, and damage to various organs. Several studies have investigated the relationship between COVID-19 and mortality in patients with liver cancer, but there are few research on the relationship between them. This study is to explore the correlation between the two diseases and drugs treating them.MethodsThe Gene Expression Omnibus (GEO) database provides gene datasets of COVID-19 patients and HCC patients. Through differential gene analysis and weighted gene co-expression network analysis, we determined 223 genes represented in HCC and COVID-19. We then used functional annotation, protein–protein interaction network construction, predictive model development and verification, prognostic value analysis, and miRNA–gene network construction. Besides, we created a drug–hub–gene network by predicting possible medications that interact with hub genes using the Drug–Gene Interaction Database (DGIdb). Ultimately, we applied immunohistochemistry to ascertain the hub genes expression.ResultsThis study revealed that eight core genes (RRM2, TPX2, DTL, CDT1, TYMS, CDCA5, CDC25C, and HJURP) co-existed in both HCC and COVID-19 and were differentially expressed in both HCC and normal tissues.CDC25C, RRM2, CDCA5, and HJURP had diagnostic value (AUC > 0.8) and prognostic value (adjusted P-value < 0.05). Genome enrichment analysis indicated that eight genes may function in liver cancer through engagement in the cell cycle, DNA replication, etc. In liver cancer samples, these genes were significantly and adversely associated with plasma cells while RRM2 was positively associated with neutrophil and NK cell activation and with dendritic cell resting. Using the miRNAnet database and DGIdb, 9 transcription factors, 7 miRNAs, and 51 drugs or molecular compounds were predicted to interact with the hub genes. Finally, RRM2 expression showed significant variation in clinical specimens, and analysis of the association of RRM2 with immunomodulators indicated that RRM2 was closely connected to MICB and CD276.ConclusionsOur study revealed several metabolic genes related to HCC and COVID-19. Moreover, potential drugs related to central genes were predicted. These findings may provide new ideas for treating COVID-19 and HCC.

Relationship between circulating white blood cell count and inflammatory skin disease: a bidirectional mendelian randomization study.

Observational studies have shown a strong association between circulating white blood cell counts (WBC) and inflammatory skin diseases such as acne and psoriasis. However, the causal nature of this relationship is unclear. We performed a two-way two-sample Mendelian randomization (MR) analysis to investigate potential causal relationships between leukocytes and inflammatory skin diseases. The circulating white blood cell count, basophil cell count, leukocyte cell count, lymphocyte cell count, eosinophil cell count, and neutrophil cell count data were obtained from the Blood Cell Consortium (BCX). The data for inflammatory skin disorders, including acne, atopic dermatitis (AD), hidradenitis suppurativa (HS), psoriasis, and seborrheic dermatitis (SD), were obtained from the FinnGen Consortium R10. The primary analysis utilized inverse variance weighting (IVW) along with additional methods such as MR-Egger, weighted mode, and weighted median estimator. To assess heterogeneity among instrument variables, Cochran's Q test was employed, while MR-Egger intercept and MR-PRESSO were used to test for horizontal pleiotropy. IVW demonstrated that an elevated monocyte count was significantly associated with a decreased risk of psoriasis (OR = 0.897, 95% CI: 0.841-0.957, P = 0.001, FDR = 0.016). Additionally, an increased eosinophil count was causally associated with a higher risk of AD (OR = 1.188, 95% CI: 1.093-1.293, P = 0.000, FDR = 0.002). No inverse causal relationship between inflammatory skin disease and circulating white blood cell count was found. In conclusion, this study provides evidence that increased monocyte count is associated with a reduced risk of psoriasis and that there is a causal relationship between increased eosinophil counts and an increased risk of AD. These findings help us understand the potential causal role of specific white blood cell counts in the development of inflammatory skin diseases.

Ação Imunomoduladora da Estimulação Parassimpática promovida pelo Exercício Físico

Introduction: Physical exercise promotes the stimulation of the vagal nerve and different neural networks, contributing to a more effective anti-inflammatory response in order to contribute to cardiovascular, metabolic and immunological benefits. Objective: To associate the role of physical exercise with parasympathetic stimulation and its possible implications in immunomodulation Methods: This is a qualitative, explanatory and descriptive study on the immunomodulatory action of parasympathetic activation through physical exercise through a bibliographic review. The databases used were: PubMed, Scopus, Scielo and Web of Science involving all original articles from January 2015 and June 2024. Results: The main findings are related to differences in physical exercise intensity, which can contribute to the modulation of the innate immune system and the expression of neutrophil and lymphocyte cell populations, which can contribute to a more specific immune response. Aerobic training and strength training had similar responses in reducing BMI and glycated hemoglobin, reducing sympathetic tone, increasing parasympathetic tone, and improving the sympatho/vagal balance for controlling heart rate variability. There was a negative association between vagal neuroimmunomodulation (NIM) and mortality, since the lower the NIM index, the shorter the survival time in the population sample. Conclusion: Aerobic physical exercise and strength training can contribute to the activation of the parasympathetic system and immune system and provide better adjustments in the innate and adaptive immune response dependent on the intensity and volume of training.

The effect of curcumin 1% methanolic extract on the expression of Matrix Metalloproteinase-1, Matrix Metalloproteinase-8, Matrix Metalloproteinase-13, neutrophil, macrophage, lymphocyte counts in Porphyromonas gingivalis induced periodontitis: a randomized controlled trial

ObjectiveHailed as one of the most fundamental and important treatment in management of periodontal disease, scalling and root planning has limitations regarding microorganism elimination. Meanwhile, turmeric has been proven to have a therapeutic effect on gingivitis and periodontitis. This study aimed to analyze the impact of curcumin 1% methanolic extract on the expression of Matrix Metalloproteinase-1, Matrix Metalloproteinase-8, Matrix Metalloproteinase -13, neutrophil, macrophage, and lymphocyte number in the gingiva of Wistar rats exposed to Porphyromonas gingivalis bacteria (P. gingivalis). Materials and methodsThe experimental animals used were Wistar rats, arbitrarilly split up into three experimental groups namely: normal, control (induced with periodontitis, received no treatment), and treatment (Periodontitis with 1% curcumin treatment). The samples were taken from the gingival tissue of the mandibular incisors on 1 and 7 days. Immunohistochemical and Hematoxylin Eosin staining were performed to measure the expression of Matrix Metalloproteinase-1, Matrix Metalloproteinase-8, Matrix Metalloproteinase-13, and the number of neutrophils, macrophages, and lymphocytes. Data were analyzed for mean standard deviation. The Oneway ANOVA was then performed to see whether there is a significant difference between experimental groups, the test then commenced with Tukey’s Honestly Significant Difference test with a significance level (α=0.05). ResultsMMP-8, MMP-13, neutrophil, and lymphocyte numbers in the treatment groups were significantly lower with P<0.05 than in the control groups in the 1 and 7 days. Meanwhile, in MMP-1 and macrophage numbers the difference was deemed not significant when control and treatment groups are compared. ConclusionThe administration of 1% curcumin can significantly reduce the expression of MMP-8, MMP-13, neutrophil and lymphocyte cell numbers, but there is no reducing the number of macrophage cells and MMP-1 expression in gingiva of Wistar rats exposed to P. gingivalis bacteria.

Dual protection of aqueous garlic extract biomolecules against hemolysis and its oxidation products in preventing inflammation.

Garlic (Allium sativum) is recognized as functional food, rich in bioactive compounds that can combat diseases associated with oxidative stress. This study aims to investigate the protective potential of aqueous garlic extract against hemolysis and oxidation. Despite being caused by membrane fragility, hemolysis can lead to inflammation through the oxidation of its products, and in some cases, even exacerbate it in certain pathological contexts. Supplementation with antioxidant molecules can improves oxidative status, in this study, we selected garlic, an excellent functional food, and targeted its effects using aqueous extract and pure molecules. The aqueous garlic extract was prepared under safe conditions and subjected to toxicity on human neutrophils and red blood cells before experimentation. The results indicate that aqueous garlic extract significantly reduces hemolysis with a maximum protection of 98. 74 ± 1. 08 % at a concentration of 5μg/ml. Additionally, experiments were conducted with pure compounds found in garlic such as quercetin, gallic acid, and caffeic acid. The outcomes show that quercetin reduces hemolysis of RBC with a maximum protection of 88. 8 ± 2. 89 % at 20 µM followed by caffeic acid and gallic acid. The action mechanism of the extract was tested on human neutrophil cells, the extract significantly reduced luminol-amplified chemiluminescence of PMA-stimulated neutrophils up to 50 % at 10 µg/ml in addition to its ability to directly scavenge hydrogen peroxide. Our results suggest that aqueous garlic extract exerts promising anti-inflammatory activity in vitro. Through its dual protection against hemolysis and Ros production, garlic may indirectly prevent inflammation reducing the oxidation of hemolysis products. These abilities make garlic aqueous extract promising candidate for improving cardiovascular health, reducing oxidative stress and modulating immunity.

Inflammation and Macrophage Loss Mark Increased Susceptibility in a Genetic Model of Acute Viral Infection-Induced Tissue Damage.

M.R2k/b mice are identical to the MA/My parent strain aside from a 5.58-Mb C57L-derived region on chromosome 17 (Cmv5s) that causes increased susceptibility to acute murine CMV (MCMV) infection and the development of significant spleen tissue damage. Spleen pathology begins at the marginal zone (MZ), apparent by 2 d postinfection (dpi), and progresses throughout the red pulp by 4 dpi. To better understand how M.R2k/b mice respond to infection and how Cmv5s contributes to tissue damage in the spleen, we assessed the regulation of myeloid cells and inflammation during acute MCMV infection in MA/My and M.R2k/b mice. We found that Cmv5s drove increased neutrophil accumulation and cell death at the MZ, which corresponded with evidence of localized oxidative stress and increased overall spleen IL-6 and TGF-β1 early during infection. Further assessment of MCMV infection dynamics at the early MZ revealed infected SIGNR1+ MZ macrophages as the first apparent cell type lost during infection in these mice and the likely target of early neutrophil recruitment. Spleen macrophages were also identified as the mediators of differential spleen IL-6 and TGF-β1 between MA/My and M.R2k/b mice. Interrogation of MCMV progression past 2 dpi revealed substantial M.R2k/b F480+ red pulp macrophage loss along with buildup of oxidative stress and MZ macrophage debris that was not neutrophil dependent. Together we identify Cmv5s-driven macrophage loss and inflammation during acute MCMV infection corresponding with the spatial and temporal development of spleen tissue damage.

Tumor necrosis factor regulates leukocyte recruitment but not bacterial persistence during Staphylococcus aureus craniotomy infection

BackgroundCraniotomy is a common neurosurgery used to treat intracranial pathologies. Nearly 5% of the 14 million craniotomies performed worldwide each year become infected, most often with Staphylococcus aureus (S. aureus), which forms a biofilm on the surface of the resected bone segment to establish a chronic infection that is recalcitrant to antibiotics and immune-mediated clearance. Tumor necrosis factor (TNF), a prototypical proinflammatory cytokine, has been implicated in generating protective immunity to various infections. Although TNF is elevated during S. aureus craniotomy infection, its functional importance in regulating disease pathogenesis has not been explored.MethodsA mouse model of S. aureus craniotomy infection was used to investigate the functional importance of TNF signaling using TNF, TNFR1, and TNFR2 knockout (KO) mice by quantifying bacterial burden, immune infiltrates, inflammatory mediators, and transcriptional changes by RNA-seq. Complementary experiments examined neutrophil extracellular trap formation, leukocyte apoptosis, phagocytosis, and bactericidal activity.ResultsTNF transiently regulated neutrophil and granulocytic myeloid-derived suppressor cell recruitment to the brain, subcutaneous galea, and bone flap as evident by significant reductions in both cell types between days 7 to 14 post-infection coinciding with significant decreases in several chemokines, which recovered to wild type levels by day 28. Despite these defects, bacterial burdens were similar in TNF KO and WT mice. RNA-seq revealed enhanced lymphotoxin-α (Lta) expression in TNF KO granulocytes. Since both TNF and LTα signal through TNFR1 and TNFR2, KO mice for each receptor were examined to assess potential redundancy; however, neither strain had any impact on S. aureus burden. In vitro studies revealed that TNF loss selectively altered macrophage responses to S. aureus since TNF KO macrophages displayed significant reductions in phagocytosis, apoptosis, IL-6 production, and bactericidal activity in response to live S. aureus, whereas granulocytes were not affected.ConclusionThese findings implicate TNF in modulating granulocyte recruitment during acute craniotomy infection via secondary effects on chemokine production and identify macrophages as a key cellular target of TNF action. However, the lack of changes in bacterial burden in TNF KO animals suggests the involvement of additional signals that dictate S. aureus pathogenesis during craniotomy infection.

Intracellular signaling involved in the programmed neutrophil cell death leading to the release of extracellular DNA traps in thrombus formation

Intracellular signaling involved in the programmed neutrophil cell death leading to the release of extracellular DNA traps in thrombus formation

Detection of decreased granules in neutrophils by automated hematology analyzers XR-1000 and UniCel DxH 800.

This study aimed to investigate the utility of neutrophil-related cell population data obtained by automated hematology analyzers in assessing myelodysplastic syndrome cases with decreased granules in neutrophils. A total of 108 subjects were classified into normal granule (n = 35), hypogranulation (n = 37), or hypergranulation (n = 36) groups. Neutrophil cell area and granule area were measured by ImageJ. All samples were analyzed on the XR-1000 and UniCel DxH 800, and neutrophil-related parameters were compared among the 3 groups. Neutrophil cell area and the ratio of the granular area showed significant differences among the 3 groups; they were the highest in the hypergranulation group and lowest in the hypogranulation group. XR-1000 data showed significant differences in NE-SFL and NE-FSC among the 3 groups (P < .0001). NE-SFL and NE-FSC discriminated most accurately hypogranulation group against other groups. UniCel DxH 800 data showed significant differences in MN-V-NE, MN-MALS-N, MN-UMALS-NE, SD-UMALS-NE (P <.01), MN-LMALS-NE, and SD-LMALS-NE (P <.05) among the 3 groups. The combination of SD-V-NE and SD-LMALS-NE discriminated most accurately the hypogranulation group against the other groups. NE-SFL and NE-FSC and the combination of SD-V-NE and SD-LMALS-NE are useful in detecting cases with decreased granules in neutrophils.

Hematological Markers as Predictors of ICU Admission in COVID-19 Patients: A Case-Control Study From a Tertiary Hospital.

COVID-19 illness severity ranges from mild- to life-threatening cases necessitating critical care. Rapid prediction of disease severity and the need for critical care support in COVID-19 patients remain essential, not only for current management but also for preparedness in future pandemics. This study aimed to assess hematological parameters as predictors of intensive care unit (ICU) admission and survival in COVID-19 patients, providing insights applicable to a broad range of infectious diseases. A case-control study was conducted at Hospital Raja Perempuan Zainab II, a tertiary referral hospital in Kelantan, Malaysia, from March 2020 to August 2021. Demographics, clinical, and laboratory data were retrieved from patients' medical records. Statistical analyses, including the Chi-square (χ2) test, independent t-tests, and simple and multiple logistic regressions, were used to analyze the data. A receiver operating characteristic (ROC) curve analysis was conducted to assess the accuracy of the predictors. The median age was 51 years, with females comprising 56.7% (n=148) and males 43.3% (n=113). A total of 88.5% of patients were admitted to non-ICU wards, with a mortality rate of 5.7%. Significant differences were observed in the distribution of hematological parameters between ICU-admitted and non-admitted patients. Neutrophil (OR: 23.96, 95% CI: 7.296-78.675) and white blood cell (WBC) count (OR: 36.677, 95% CI: 2.086-644.889) were the most significant predictors for ICU admission and survival, respectively. WBC and neutrophil counts exhibited high predictive value for ICU admission, while WBC, neutrophil, lymphocyte, and immature granulocyte (IG) counts were significant predictors of survival status among COVID-19 patients. These findings underscore the continued relevance of hematological markers in managing severe respiratory infections and improving critical care triage, with implications for current and future healthcare challenges.

Isolation and characterization of plant-derived exosome-like nanoparticles from Carica papaya L. fruit and their potential as anti-inflammatory agent.

Inflammation is an immune system response that identifies and eliminates foreign material. However, excessive and persistent inflammation could disrupt the healing process. Plant-derived exosome-like nanoparticles (PDENs) are a promising candidate for therapeutic application because they are safe, biodegradable and biocompatible. In this study, papaya PDENs were isolated by a PEG6000-based method and characterized by dynamic light scattering (DLS), transmission Electron Microscopy (TEM), bicinchoninic acid (BCA) assay method, GC-MS analysis, total phenolic content (TPC) analysis, and 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay. For the in vitro test, we conducted internalization analysis, toxicity assessment, determination of nitrite concentration, and assessed the expression of inflammatory cytokine genes using qRT-PCR in RAW 264.7 cells. For the in vivo test, inflammation was induced by caudal fin amputation followed by analysis of macrophage and neutrophil migration in zebrafish (Danio rerio) larvae. The result showed that papaya PDENs can be well isolated using the optimized differential centrifugation method with the addition of 30 ppm pectolyase, 15% PEG, and 0.2 M NaCl, which exhibited cup-shaped and spherical morphological structure with an average diameter of 168.8±9.62 nm. The papaya PDENs storage is stable in aquabidest and 25 mM trehalose solution at -20˚C until the fourth week. TPC estimation of all papaya PDENs ages did not show a significant change, while the DPPH test exhibited a significant change in the second week. The major compounds contained in Papaya PDENs is 2,3-dihydro-3,5-dihydroxy-6-methyl-4H-pyran-4-one (DDMP). Papaya PDENs can be internalized and is non-cytotoxic to RAW 264.7 cells. Moreover, LPS-induced RAW 264.7 cells treated with papaya PDENs showed a decrease in NO production and downregulation mRNA expression of pro-inflammatory cytokine genes (IL-1B and IL-6) and an upregulation in mRNA expression of anti-inflammatory cytokine gene (IL-10). In addition, in vivo tests conducted on zebrafish treated with PDENs papaya showed inhibition of macrophage and neutrophil cell migration. These findings suggest that PDENs papaya possesses anti-inflammatory properties.

Neutrophil-derived migrasomes are an essential part of the coagulation system

Migrasomes are organelles that are generated by migrating cells. Here we report the key role of neutrophil-derived migrasomes in haemostasis. We found that a large number of neutrophil-derived migrasomes exist in the blood of mice and humans. Compared with neutrophil cell bodies and platelets, these migrasomes adsorb and enrich coagulation factors on the surface. Moreover, they are highly enriched with adhesion molecules, which enable them to preferentially accumulate at sites of injury, where they trigger platelet activation and clot formation. Depletion of neutrophils, or genetic reduction of the number of these migrasomes, significantly decreases platelet plug formation and impairs coagulation. These defects can be rescued by intravenous injection of purified neutrophil-derived migrasomes. Our study reveals neutrophil-derived migrasomes as a previously unrecognized essential component of the haemostasis system, which may shed light on the cause of various coagulation disorders and open therapeutic possibilities.

Regulation of candidalysin underlies Candida albicans persistence in intravascular catheters by modulating NETosis.

Candida albicans is a leading cause of intravascular catheter-related infections. The capacity for biofilm formation has been proposed to contribute to the persistence of this fungal pathogen on catheter surfaces. While efforts have been devoted to identifying microbial factors that modulate C. albicans biofilm formation in vitro, our understanding of the host factors that may shape C. albicans persistence in intravascular catheters is lacking. Here, we used multiphoton microscopy to characterize biofilms in intravascular catheters removed from candidiasis patients. We demonstrated that, NETosis, a type of neutrophil cell death with antimicrobial activity, was implicated in the interaction of immune cells with C. albicans in the catheters. The catheter isolates exhibited reduced filamentation and candidalysin gene expression, specifically in the total parenteral nutrition culture environment. Furthermore, we showed that the ablation of candidalysin expression in C. albicans reduced NETosis and conferred resistance to neutrophil-mediated fungal biofilm elimination. Our findings illustrate the role of neutrophil NETosis in modulating C. albicans biofilm persistence in an intravascular catheter, highlighting that C. albicans can benefit from reduced virulence expression to promote its persistence in an intravascular catheter.

Bifurcation in an modified model of neutrophil cells with time delay

The hematological stem cells model is introduced with neutrophil dynamics of two department model setting forth. During the cells differentiation and proliferation process, the neutrophils are functioned with negative feedback with delay history, which contains delayed amplification coefficient. In more general view, the new introduction rate is given to replace the familiar Hill function which is helpful to understand the complex dynamics of neutrophils. The double Hopf bifurcation is calculated with the artificial handtools named DDE-Biftool, which is observed as the self-intersection of Hopf lines. The continuation of periodical solutions arising from Hopf points are done and the longer period solutions are manifested with multi-rhythm and bursting oscillation. The near dynamics of double Hopf points is simulated by DDE-Biftool with different route design, the multi-period attractors, quasi-periodical solutions and chaos are observed.

The Impact of Protein Glycosylation on the Identification of Patients with Pediatric Appendicitis.

The identification of pediatric appendicitis is challenging due to the lack of specific markers thereby several factors are included in the diagnostic process such as abdominal pain, ultrasonography and altered laboratory parameters (C reactive protein, absolute neutrophil cell number and white blood cell number). The glycosylation pattern of serum N-glycome was analyzed in this study of 38 controls and 40 patients with pediatric appendicitis. The glycans were released by enzymatic deglycosylation followed by fluorescent labeling and solid-phase extraction. The prepared samples were analyzed by hydrophilic interaction liquid chromatography with fluorescence and mass-spectrometric detection. The generated data were analyzed by multiple statistical tests involving the most important laboratory parameters as well. Significant differences associated with the examined patient groups were revealed suggesting the potential use of glycosylation analysis supporting the detection of pediatric appendicitis.