Immunity, Inflammation and Disease最新文献

Introduction: As the COVID-19 pandemic transitions, understanding the intricate dynamics of the disease becomes paramount. This systematic review explores the role of antiphospholipid antibodies in COVID-19, focusing on their potential clinical implications.

Methods: This systematic review, following PRISMA guidelines, assesses studies exploring the link between antiphospholipid antibodies and COVID-19. PubMed/Medline, Embase, and Scopus were searched for relevant studies published up to December 22, 2024. Inclusion criteria comprised studies involving patients diagnosed with COVID-19 and reporting on the presence of antiphospholipid antibodies. The risk of bias in individual studies was evaluated using the Joanna Briggs Institute appraisal tool.

Results: Our Study includes 59 records involving a total of 28,489 COVID-19 patients. Antiphospholipid antibodies were tested in 14,498 COVID-19 patients. It was observed that 50.84% of patients tested positive for antiphospholipid antibodies. Various types of antiphospholipid antibodies, including Anticardiolipin, Anti beta2 glycoproteins, and Lupus anticoagulant antibody, displayed prevalence rates in the patients with thrombosis. The overall frequency of antiphospholipid antibodies in thrombosis patients was 38.55%.

Conclusion: The presence of antiphospholipid antibodies in a significant proportion of COVID-19 patients underscores the need for a detailed investigation into their role in thrombotic events. Our study highlights potential avenues for targeted interventions. However, the evolving nature of COVID-19 necessitates continued research efforts to clarify clinical implications and optimize management strategies in this complex landscape of thrombosis and immunology. The review reveals some limitations, such as variability in study designs and demographics and inherent differences in methodologies among included studies. Future studies should address these limitations with standardized methodologies for more conclusive findings.

Background: Malaria remains a significant global health challenge, with substantial mortality rates, particularly in tropical and subtropical regions. A notable sexual dimorphism exists in malaria, with males often experiencing higher infection and mortality rates compared to females.

Objective: This review explores the role of estrogen in modulating immune responses to malaria, potentially explaining the observed sex differences. Estrogen, through its receptors, influences immune cell activation and cytokine production, which are critical in the immune response to malaria.

Results: Utilizing data from the Global Burden of Disease (GBD) study, we analyzed sex differences in malaria burden in Central Sub-Saharan Africa from 2000 to 2021, revealing a significantly lower mortality burden for females compared to males. Epidemiological data and animal model results support the notion that estrogen plays a significant role in modulating immune responses to malaria. Estrogen receptors are widely expressed in immune cells, and estrogen can influence the activation, proliferation, and differentiation of these cells, thereby affecting cytokine production and immune response type. Additionally, selective estrogen receptor modulators (SERMs) show potential as therapeutic agents, with some studies demonstrating their efficacy in reducing parasitemia and improving malaria outcomes.

Conclusion: Understanding the sex differences in the pathogenesis of malaria is crucial for its prevention, treatment, and vaccine development. Estrogen's role in immune regulation highlights the need for sex-specific approaches in disease management.

Background: Chronic wounds are a severe complication of diabetes. Dysregulated inflammatory signalling is thought to underly the poor healing outcomes. Yet, there is little information available on the acute response following injury and its impact on healing.

Methods: Using a murine full thickness excisional wound model, the current study therefore assessed the expression of pro-inflammatory and pro-resolving lipid mediators during the early stages post injury in acute and diabetic wounds and compared the timeframe for transitioning through the phases of healing. Tissue eicosanoid (LTB4, PGE2, TxA2, MaR1, RvE1, RvD1, PD) and MMP-9 levels were assessed at 6 h post wounding using ELISAs. Wound closure, healing dynamics (histology), cellular infiltration and MPO, TNF-α expression (IHC) were assessed at 6 h, day2, day7 post wounding.

Results: Eicosanoid expression did not differ between groups (LTB4 24-125 pg/mL, PGE2 63-177 pg/mL, TxA2 529-1184 pg/mL, MaR1 365-2052 pg/mL, RvE1 43-1157 pg/mL, RvD1 1.5-69 pg/mL, PD1 11.5-4.9 ng/mL). An inverse relationship (p < 0.05) between MMP-9 and eicosanoids were however only evident in acute and not in diabetic wounds. Diminished cellular infiltration (x5 fold) (p < 0.05) in diabetic wounds coincided with a significant delay in the expression of TNF-α (pro-inflammatory cytokine) and MPO (neutrophil marker). A significant difference in the expression of TNF-α (C 1.8 ± 0.6; DM 0.7 ± 0.1 MFI) and MPO (C 4.9 ± 1.9; DM 0.9 ± 0.4 MFI) (p < 0.05) was observed as early as 6 h post wounding, with histology parameters supporting the notion that the onset of the acute inflammatory response is delayed in diabetic wounds.

Conclusion: These observations imply that the immune cells are unresponsive to the initial eicosanoid expression in the diabetic wound tissue.

Objective: Pneumococcal meningitis is a serious infectious disease with a high mortality rate and a global presence, and survivors have different degrees of neurological sequelae as a consequence of the host response to the infection. Progranulin (PGRN) is a multifunctional autocrine growth factor that is also a major immunoregulator. We want to investigate the role for PGRN in Pneumococcal meningitis in vivo and in vitro.

Method: Mouse and cell models were established to explore the protective effect and mechanism of PGRN against pneumococcal meningitis.

Results: Progranulin plays a protective role in pneumococcal meningitis by inhibiting pyroptosis. Pyroptosis resulted from exposure of BV-2 cells to the bacterium and this was confirmed in the in vivo model. Administration of the NLRP3 inflammasome inhibitor MCC950 to mice prior to infection inhibited pyroptosis and protected PGRN -/- mice and BV-2 cell model from meningitis.

Conclusion: This study implicates a protective role for PGRN in pneumococcal meningitis by inhibiting pyroptosis, indicating that PGRN may have therapeutic potential.

Background: Although the carcinogenic potential of microbes has long been recognized, their significance may have been underestimated. Currently, the connection between microbiota and cancer is under extensive research. The lung microbiota may serve as a proxy for the state of lung health based on its crucial role in preserving lung hemostasis.

Objectives: This review tried to outline the state of our understanding of the contribution of lung microbiome and lung cancer.

Methods: A literature search was performed using PubMed, Google Scholar, and Scopus databases for recent research focusing on the development and possible pathogenesis of lung microbiome and lung cancer.

Results: Early research on lung cancer indicated that dysbiosis significantly impacted the development and spread of the tumor. As a result of these findings, the study of the lung microbiota as a possible therapeutic target and diagnostic marker has accelerated. Early-stage disease diagnostic biomarkers could be represented as microbiota profiles. Additionally, the microbiome is involved in anticancer therapy. There are limited studies on lung microbiota, and most microbiome studies commonly concentrate on the gut microbiota. A proper understanding of lung microbiota can have several potential therapeutic approaches. Therefore, more studies in this field may initiate remarkable advancements in microbiome-dependent treatment.

Conclusion: Convincing data from studies on both humans and animals indicates that the microbiota might play a role in cancer initiation, influenced by internal and environmental factors of the host. Notably, the lung harbors its microbiome, as do lung cancers. In general view, it seems microbiome diversity in lung cancer patients is reduced. Meanwhile, some genera were increased in lung cancer patients in comparison with a noncancerous population (such as Streptococcus genus), and some of them were decreased (Granulicatella adiacens, G. adiacens). Furthermore, research on the microbiome-carcinogenesis relationship is still in its infancy, and much remains to be fully understood.

Background: The objective of this systematic review was to identify genetic variants of the IL-23, IL-17, IL-23R and IL-17R genes and isoforms and its possible association with increased development of periodontitis and peri-implantitis.

Methods: A systematic review was prepared according to the guidelines, registered in the OSF database with the registration number: 10.17605/OSF. IO/X95ZC. The electronic search was performed in four databases: PubMed, Scopus, Web of Science, and Google Scholar from 1984 until March 15th, 2024. The JBI Critical Appraisal Checklist for Case-Control Studies was used to assess the quality of included studies.

Results: Eighteen papers with a case-control design were those that ultimately met the eligibility criteria. A total of 3904 individuals (2315 with periodontitis and 90 with peri-implantitis), and 1589 healthy subjects) were studied. The age range of the study population was 14-70 years, with a mean age ± (SD) of 40.43 ± 6.33 years. A total of 28 genetic variants corresponding to the IL-17A (rs 2275913, rs 3819024, rs 10484879) IL-17F (rs 763780), IL-17R (rs 879576) and IL-23R (rs 11209026) genes were analyzed in this study. Six (33.3%) studies found an association between the IL-17A 197 G/A (rs 2275913) genetic variant and peri-implantitis and periodontitis. One study (5.5%) found an association between the IL-17A rs10484879 variant and peri-implantitis and periodontitis.

Conclusion: Six polymorphisms were evaluated, highlighting rs 2275913 of the cytokine IL-17A in patients with periodontitis or peri-implantitis. Only 50% of studies found an association despite having a small sample. This suggests that other factors such as the degree of disease, systemic diseases and ethnic groups studied may play a role.

Introduction: Allergic rhinitis is the specific inflammation against allergen by immune defense cells on the nasal mucosa, which can lead to chronic nasal symptoms such as sneezing, itching, runny nose, and nasal congestion. It is associated with high morbidity including sinusitis, asthma, otitis media, hypertrophied inferior turbinate, and nasal polyps. Despite its complications, it remains poorly recognized and tracked.

Methods: A cross-sectional hospital-based study was done, a total of 221 patients received Ear, Nose And Throat services at Kilimanjaro Christian Medical Center during the study period all patients with a clinical diagnosis of allergic rhinitis were captured; Data was collected using a pre-tested coded questionnaire (Score For Allergic Rhinitis). The data was then analyzed using SPSS version 22.

Results: A total of 221 patients with a clinical diagnosis of allergic rhinitis were approached in a 6 months study period, 111 (50.2%) were females, and 140 (63.4%) were residing in urban areas. The prevalence of allergic rhinitis was 23.9%. Factors such as age OR 0.12, 95% CI (0.03; 0.40), education OR 0.13, 95% CI (0.04; 0.44), occupation OR 3.75, 95% CI (1.36; 10.32), adenotonsillar hypertrophy OR 4.66, 95% CI (2.21; 9.80), and OME OR 4.11, 95% CI (1.32; 12.83) (p = 0.009) were found to be significantly associated with allergic rhinitis. 60.4%, Inferior turbinate hypertrophy is the leading co-morbidity of allergic rhinitis which accounts for 64.7%.

Conclusion: Allergic rhinitis is among the common health problems affecting Tanzanians. It is a commonly seen disorder in younger age ( < 15 years) which is in correlation with other studies done in Africa and worldwide.

Aim: Kikuchi-Fujimoto disease (KFD) rarely affects pediatric patients and is characterized by prolonged fever and cervical lymphadenopathy. The diagnosis of KFD remains challenging and often requires an invasive biopsy. Low serum alkaline phosphatase levels have frequently been observed in patients with KFD; however, the clinical significance of low serum alkaline phosphatase levels remains unclear.

Methods: This retrospective study included pediatric patients aged < 16 years who were pathologically or clinically diagnosed with KFD and infectious mononucleosis between April 2016 and March 2023. Serum alkaline phosphatase levels were analyzed employing age- and sex-specific reference intervals. Clinical and laboratory data were evaluated to determine their association with serum alkaline phosphatase levels.

Results: Thirty patients with KFD and 23 patients with infectious mononucleosis were included in the study. Seventeen patients with KFD (56.7%) had serum alkaline phosphatase levels below the 2.5th percentile of the age- and sex-specific reference intervals. Serum alkaline phosphatase levels were significantly lower in patients with KFD than in those with infectious mononucleosis. Clinical and other laboratory findings were not significantly different between patients with KFD with or without a decline in serum alkaline phosphatase levels.

Conclusion: A decrease in serum alkaline phosphatase levels, particularly when assessed as a percentage of age- and sex-specific reference intervals, may be a valuable and noninvasive supportive feature of KFD in pediatric patients.

Background: Post-coronavirus disease 19 lung fibrosis (PCLF) shares common immunological abnormalities with idiopathic pulmonary fibrosis (IPF), characterized by an unbalanced cytokine profile being associated with the development of lung fibrosis. The aim of the present study was to analyze and compare the different subsets of CD4- and CD8-T cells, along with specific cytokine expression patterns, in peripheral blood (PB) from patients affected by PCLF and IPF and healthy controls (HCs).

Methods: One-hundred patients followed at the Rare Lung Disease Center of Siena University Hospital were enrolled. Eight HCs were recruited. PB samples were collected, and CD4- and CD8-T subsets were analyzed through flow cytometry. Multiplex bead-based LEGENDplex™ were used for cytokine quantification.

Results: Higher CD8 percentages were observed in IPF than in HCs and PCLF (p = 0.020 and p = 0.007, respectively). PCLF subgroup showed higher Th-naïve, Th-effector, Tc-naïve, and Tc-reg percentages than IPF (p < 0.001; p = 0.018; p = 0.005; p = 0.017, respectively). Th-naïve and Tc-naïve inversely correlated with Tc-reg (p < 0.0001, r = -0.61 and p = 0.005, r = -0.39, respectively). Tc-naïve-PD1 and Tc-effector-PD1 percentages were higher in PCLF than IPF (p < 0.001), while Tfh-reg and Tfc-reg were significantly higher in IPF than PCLF (p < 0.001). IL-4, IL-2, TNF-α, and IL-17A were more expressed in PCLF than IPF (p < 0.001). IL-8 directly correlated with Tc-naïve percentages in PCLF (p = 0.018, r = 0.35).

Conclusion: A variety of immune cells is involved in the development and progression of pulmonary fibrosis confirming an immunological similarity between IPF and PCLF. T-reg cells play a key role in the worsening of the disease. High cytokine values showed a pro-fibrotic environment in PCLF patients, suggesting dysregulation of the immune system of these patients. Moreover, the immunological similarity between IPF and PCLF patients suggests that SARS-CoV2 infection may trigger the activation of biological pathways common with IPF.

Background: Acute lung injury (ALI), one of the most severe respiratory system diseases, is prevalent worldwide. Annexin A1 (AnxA1) is an important member of the annexin superfamily, known for its wide range of physiological functions. However, its potential protective effect against lipopolysaccharide (LPS)-induced ALI remains unclear.

Materials and methods: Mice were divided into four groups: Sham, LPS + vehicle, LPS + 0.1 μg AnxA1, and LPS + 0.5 μg AnxA1. Lung injury was assessed through histopathology, pulmonary wet-to-dry (W/D) ratio, cell counting of bronchoalveolar lavage fluid (BALF), oxidative stress analysis, and noninvasive pulmonary function testing. Gene and protein expression levels were measured using RT-PCR, ELISA, and western blot analysis.

Results: AnxA1 alleviated LPS-induced ALI by protecting lung tissue from damage, reducing the lung wet/dry (W/D) weight ratio, and improving LPS-induced impaired lung function. Interestingly, administration of AnxA1 was found to repress the infiltration of inflammatory cells by decreasing the total cell count, neutrophils, and protein concentrations in bronchoalveolar lavage fluid (BALF). AnxA1 mitigated the inflammatory response in the pulmonary tissue by lowering the levels of IL-1β, IL-6, and TNF-α in BALF of ALI mice. Additionally, AnxA1 attenuated oxidative stress in lung tissues of ALI mice by restoring the activity of catalase (CAT), SOD, and glutathione (GSH) but reducing the levels of malondialdehyde (MDA). We also found that AnxA1 suppressed activation of the NLRP3 signaling pathway. Mechanistically, AnxA1 activated the Nrf2/HO-1 signaling pathway while preventing the activation of NF-κB.

Conclusion: Collectively, these findings suggest that AnxA1 alleviates LPS-induced ALI and might be a promising novel therapeutic agent against LPS-induced ALI.