The alarmin IL-33 drives a ST2+ Treg-mediated anti-inflammatory immune response during immune-mediated hepatitis

ObjectivesRecent studies suggested that upregulation of anti-inflammatory immune response during early syphilis may be associated with persistence of Treponema pallidum infection despite adequate treatment, resulting in a serofast state. The objective of this study was to determine whether enhanced interleukin (IL)-10-related response during early T. pallidum infection increased the risk of serofast syphilis.MethodsTwo IL10 gene promoter polymorphisms affecting IL-10 production (−1082A>G [rs1800896], −592C>A [rs1800872]) and serum levels of IL-10 were measured in 80 patients with early syphilis before and 6 months after penicillin treatment and in 24 healthy volunteers (control group).ResultsAfter 6 months, patients were stratified based on serological response into two groups: (1) serofast state (n = 28) and (2) serologically cured (n = 52). Pretreatment and post-treatment serum IL-10 levels were significantly higher in patients who remained serofast compared with those who had a serological cure (p<0.001). The GG genotype of the −1082A>G (rs1800896) polymorphism and the CC genotype of the −592C>A (rs1800872) polymorphism were significantly correlated with higher serum IL-10 levels. Moreover, the OR for remaining serofast for carriers of these genotypes was 16.2 (95% CI: 4.1 to 65.0, p<0.0001) and 2.9 (95% CI: 1.4 to 5.9, p=0.002), respectively.ConclusionsWe showed that a pronounced anti-inflammatory immune response may be an important predictor for the serofast state. Additionally, host-related factors such as polymorphisms of immune regulatory genes may influence the risk of remaining serofast after syphilis therapy.

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The impact of the pro- and anti-inflammatory immune response on ventilation time after cardiac surgery

Cytometry Part B Clinical Cytometry ◽

10.1002/cyto.b.10027 ◽

2003 ◽

Vol 53B (1) ◽

pp. 70-74 ◽

Cited By ~ 17

Author(s):

Markus Rothenburger ◽

Tonny D.T. Tjan ◽

Michael Schneider ◽

Elmar Berendes ◽

Christof Schmid ◽

...

Keyword(s):

Immune Response ◽

Cardiac Surgery ◽

Ventilation Time ◽

Inflammatory Immune Response ◽

Anti Inflammatory ◽

The Impact

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Devitalized Stem Cell Microsheets for Sustainable Release of Osteogenic and Vasculogenic Growth Factors and Regulation of Anti-Inflammatory Immune Response

Advanced Biosystems ◽

10.1002/adbi.201600011 ◽

2017 ◽

Vol 1 (3) ◽

pp. 1600011 ◽

Cited By ~ 1

Author(s):

Seyedsina Moeinzadeh ◽

Seyed Ramin Pajoum Shariati ◽

Safaa Kader ◽

Juan M. Melero-Martin ◽

Esmaiel Jabbari

Keyword(s):

Immune Response ◽

Stem Cell ◽

Growth Factors ◽

Inflammatory Immune Response ◽

Anti Inflammatory

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Adenine Nucleotide Translocase 1 Expression Modulates the Immune Response in Ischemic Hearts

Cells ◽

10.3390/cells10082130 ◽

2021 ◽

Vol 10 (8) ◽

pp. 2130

Author(s):

Fatih Yergöz ◽

Julian Friebel ◽

Nicolle Kränkel ◽

Ursula Rauch-Kroehnert ◽

Heinz-Peter Schultheiss ◽

...

Keyword(s):

Immune Response ◽

Growth Factor ◽

Inflammatory Cytokines ◽

Adenine Nucleotide ◽

Left Ventricular ◽

Macrophage Infiltration ◽

Adenine Nucleotide Translocase ◽

Inflammatory Immune Response ◽

Anti Inflammatory ◽

Pro Inflammatory Cytokines

Adenine nucleotide translocase 1 (ANT1) transfers ATP and ADP over the mitochondrial inner membrane and thus supplies the cell with energy. This study analyzed the role of ANT1 in the immune response of ischemic heart tissue. Ischemic ANT1 overexpressing hearts experienced a shift toward an anti-inflammatory immune response. The shift was characterized by low interleukin (IL)-1β expression and M1 macrophage infiltration, whereas M2 macrophage infiltration and levels of IL-10, IL-4, and transforming growth factor (TGFβ) were increased. The modulated immune response correlated with high mitochondrial integrity, reduced oxidative stress, low left ventricular end-diastolic heart pressure, and a high survival rate. Isolated ANT1-transgenic (ANT1-TG) cardiomyocytes expressed low levels of pro-inflammatory cytokines such as IL-1α, tumor necrosis factor α, and TGFβ. However, they showed increased expression and cellular release of anti-inflammatory immunomodulators such as vascular endothelial growth factor. The secretome from ANT1-TG cardiomyocytes initiated stress resistance when applied to ischemic wild-type cardiomyocytes and endothelial cells. It additionally prevented macrophages from expressing pro-inflammatory cytokines. Additionally, ANT1 expression correlated with genes that are related to cytokine and growth factor pathways in hearts of patients with ischemic cardiomyopathy. In conclusion, ANT1-TG cardiomyocytes secrete soluble factors that influence ischemic cardiac cells and initiate an anti-inflammatory immune response in ischemic hearts.

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A Pro-Inflammatory Gut Microbiome Characterizes SARS-CoV-2 Infected Patients and a Reduction in the Connectivity of an Anti-Inflammatory Bacterial Network Associates With Severe COVID-19

Frontiers in Cellular and Infection Microbiology ◽

10.3389/fcimb.2021.747816 ◽

2021 ◽

Vol 11 ◽

Author(s):

Johanna Reinold ◽

Farnoush Farahpour ◽

Christian Fehring ◽

Sebastian Dolff ◽

Margarethe Konik ◽

...

Keyword(s):

Immune Response ◽

Immune Responses ◽

Gut Microbiome ◽

Tertiary Care Hospital ◽

Tertiary Care ◽

Cell Number ◽

Care Hospital ◽

Microbiome Composition ◽

Inflammatory Immune Response ◽

Anti Inflammatory

The gut microbiota contributes to maintaining human health and regulating immune responses. Severe COVID-19 illness is associated with a dysregulated pro-inflammatory immune response. The effect of SARS-CoV-2 on altering the gut microbiome and the relevance of the gut microbiome on COVID-19 severity needs to be clarified. In this prospective study, we analyzed the gut microbiome of 212 patients of a tertiary care hospital (117 patients infected with SARS-CoV-2 and 95 SARS-CoV-2 negative patients) using 16S rRNA gene sequencing of the V3-V4 region. Inflammatory markers and immune cells were quantified from blood. The gut microbiome in SARS-CoV-2 infected patients was characterized by a lower bacterial richness and distinct differences in the gut microbiome composition, including an enrichment of the phyla Proteobacteria and Bacteroidetes and a decrease of Actinobacteria compared to SARS-CoV-2 negative patients. The relative abundance of several genera including Bifidobacterium, Streptococcus and Collinsella was lower in SARS-CoV-2 positive patients while the abundance of Bacteroides and Enterobacteriaceae was increased. Higher pro-inflammatory blood markers and a lower CD8+ T cell number characterized patients with severe COVID-19 illness. The gut microbiome of patients with severe/critical COVID-19 exhibited a lower abundance of butyrate-producing genera Faecalibacterium and Roseburia and a reduction in the connectivity of a distinct network of anti-inflammatory genera that was observed in patients with mild COVID-19 illness and in SARS-CoV-2 negative patients. Dysbiosis of the gut microbiome associated with a pro-inflammatory signature may contribute to the hyperinflammatory immune response characterizing severe COVID-19 illness.

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