MicroRNA-340-5p inhibits endothelial apoptosis, inflammatory response, and pro-coagulation by targeting KDM4C in anti-neutrophil cytoplasmic antibody (ANCA)-mediated glomerulonephritis through activation of B cells

In the present study, two experiments were conducted to investigate the effect of dietary l-arginine (Arg) supplementation on the inflammatory response and innate immunity of broiler chickens. Expt 1 was designed as a 2 × 3 factorial arrangement (n 8 cages/treatment; n 6 birds/cage) with three dietary Arg concentrations (1·05, 1·42 and 1·90 %) and two immune treatments (injection of lipopolysaccharide (LPS) or saline) given at an interval of 48 h between 14 and 21 d of age. In Expt 2, correlation between dietary Arg concentration (0·99, 1·39, 1·76, 2·13 or 2·53 %) and percentage of circulating B cells (percentage of circulating lymphocytes) was determined. In Expt 1, LPS injection decreased body-weight gain and feed intake and increased feed conversion ratio of the challenged broilers (14–21 d; P< 0·05). LPS injection suppressed (P< 0·05) the percentages of splenic CD11+ and B cells (percentages of splenic lymphocytes) and phagocytic activity of splenic heterophils and macrophages; Arg supplementation linearly decreased the percentages of CD11+, CD14+ and B cells in the spleen (P< 0·10). LPS injection increased (P< 0·05) the expression of IL-1β and IL-6 mRNA in the spleen and caecal tonsils. Arginine supplementation decreased (P< 0·05) the expression of IL-1β, Toll-like receptor 4 (TLR4) and PPAR-γ mRNA in the spleen and IL-1β, IL-10, TLR4 and NF-κB mRNA in the caecal tonsils. In Expt 2, increasing dietary Arg concentrations linearly and quadratically reduced the percentage of circulating B cells (P< 0·01). Collectively, Arg supplementation attenuated the overexpression of pro-inflammatory cytokines probably through the suppression of the TLR4 pathway and CD14+ cell percentage. Furthermore, excessive Arg supplementation (1·76 %) suppressed the percentages of circulating and splenic B cells.

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B-Cell-Deficient Mice Show an Exacerbated Inflammatory Response in a Model of Chlamydophila abortus Infection

Infection and Immunity ◽

10.1128/iai.70.12.6911-6918.2002 ◽

2002 ◽

Vol 70 (12) ◽

pp. 6911-6918 ◽

Cited By ~ 24

Author(s):

Antonio J. Buendía ◽

Laura Del Río ◽

Nieves Ortega ◽

Joaquín Sánchez ◽

María C. Gallego ◽

...

Keyword(s):

Immune Response ◽

B Cells ◽

Inflammatory Response ◽

Transforming Growth Factor ◽

Transforming Growth Factor Β ◽

Immunoglobulin M ◽

Chlamydia Psittaci ◽

Chlamydophila Abortus ◽

Serotype 1

ABSTRACT The resolution of Chlamydophila abortus (Chlamydia psittaci serotype 1) infection is dependent on gamma interferon and CD8+ T cells, and classically, B cells have been considered to play a minimal role in host defense. The role of B cells in the immune response was studied by using a model of infection in mice with genetically modified immunoglobulin M transmembrane domains (μMT). In the absence of B cells, infection with C. abortus leads to an acute severe fatal disease that involves a disseminated intravascular coagulation syndrome. μMT mice displayed an increased level of proinflammatory cytokines in serum, and an increased number of neutrophils was observed in the lesions. The possible deleterious role of neutrophils in the pathogenesis of disease in μMT mice was determined by depletion of the neutrophils with the monoclonal antibody RB6-8C5. This led to an enhancement of the bacterial burden and early mortality in both μMT and wild-type mice, while necrotic lesions remained. Analysis of the presence of immunoregulatory cytokines showed significantly lower levels of transforming growth factor β in the sera of μMT mice. However, mice lacking mature B cells were able to establish a specific immune response that protected them from a secondary challenge. Taken together, these data suggest an immunomodulatory role for B cells in the early events of C. abortus primary infection that can protect mice against an exaggerated inflammatory response.

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IL-10–producing B cells are enriched in murine pericardial adipose tissues and ameliorate the outcome of acute myocardial infarction

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1911464116 ◽

2019 ◽

Vol 116 (43) ◽

pp. 21673-21684 ◽

Cited By ~ 9

Author(s):

Lan Wu ◽

Rajeev Dalal ◽

Connie D. Cao ◽

J. Luke Postoak ◽

Guan Yang ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

B Cells ◽

Inflammatory Response ◽

Healing Process ◽

The Body ◽

Adipose Tissues ◽

Acute Mi ◽

Antiinflammatory Cytokine ◽

Specific Deletion

Acute myocardial infarction (MI) provokes an inflammatory response in the heart that removes damaged tissues to facilitate tissue repair/regeneration. However, overactive and prolonged inflammation compromises healing, which may be counteracted by antiinflammatory mechanisms. A key regulatory factor in an inflammatory response is the antiinflammatory cytokine IL-10, which can be produced by a number of immune cells, including subsets of B lymphocytes. Here, we investigated IL-10–producing B cells in pericardial adipose tissues (PATs) and their role in the healing process following acute MI in mice. We found that IL-10–producing B cells were enriched in PATs compared to other adipose depots throughout the body, with the majority of them bearing a surface phenotype consistent with CD5+ B-1a cells (CD5+ B cells). These cells were detected early in life, maintained a steady presence during adulthood, and resided in fat-associated lymphoid clusters. The cytokine IL-33 and the chemokine CXCL13 were preferentially expressed in PATs and contributed to the enrichment of IL-10–producing CD5+ B cells. Following acute MI, the pool of CD5+ B cells was expanded in PATs. These cells accumulated in the infarcted heart during the resolution of MI-induced inflammation. B cell-specific deletion of IL-10 worsened cardiac function, exacerbated myocardial injury, and delayed resolution of inflammation following acute MI. These results revealed enrichment of IL-10–producing B cells in PATs and a significant contribution of these cells to the antiinflammatory processes that terminate MI-induced inflammation. Together, these findings have identified IL-10–producing B cells as therapeutic targets to improve the outcome of MI.

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B Cells Suppress the Inflammatory Response in a Mouse Model of Primary Biliary Cirrhosis

Gastroenterology ◽

10.1053/j.gastro.2008.11.035 ◽

2009 ◽

Vol 136 (3) ◽

pp. 1037-1047 ◽

Cited By ~ 57

Author(s):

Yuki Moritoki ◽

Weici Zhang ◽

Koichi Tsuneyama ◽

Katsunori Yoshida ◽

Kanji Wakabayashi ◽

...

Keyword(s):

B Cells ◽

Primary Biliary Cirrhosis ◽

Inflammatory Response ◽

Mouse Model ◽

Biliary Cirrhosis

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The G-Protein-coupled bile acid receptor, Gpbar1 (TGR5), negatively regulates hepatic inflammatory response through antagonizing nuclear factor kappa light-chain enhancer of activated B cells (NF-κB) in mice

Hepatology ◽

10.1002/hep.24525 ◽

2011 ◽

Vol 54 (4) ◽

pp. 1421-1432 ◽

Cited By ~ 223

Author(s):

Yan-Dong Wang ◽

Wei-Dong Chen ◽

Donna Yu ◽

Barry M. Forman ◽

Wendong Huang

Keyword(s):

Bile Acid ◽

B Cells ◽

Inflammatory Response ◽

G Protein ◽

Light Chain ◽

Nuclear Factor ◽

Kappa Light Chain ◽

Bile Acid Receptor ◽

G Protein Coupled ◽

Light Chain Enhancer

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IL-10-producing B cells are enriched in murine pericardial adipose tissues and ameliorate the outcome of acute myocardial infarction

10.1101/520742 ◽

2019 ◽

Author(s):

Lan Wu ◽

Rajeev Dalal ◽

Connie Cao ◽

J. Luke Postoak ◽

Qinkun Zhang ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

B Cells ◽

Inflammatory Response ◽

Cardiac Function ◽

Myocardial Injury ◽

Adipose Tissues ◽

Infarcted Heart ◽

Acute Mi ◽

Novel Therapeutic

AbstractAcute myocardial infarction (MI) provokes an inflammatory response in the heart that removes damaged tissues to facilitate repair. However, exaggerated and/or persistent inflammation compromises healing, which may be counteracted by regulatory immune mechanisms. A key regulatory factor in an inflammatory response is the anti-inflammatory cytokine IL-10, which can be produced by a number of immune cells including subsets of B lymphocytes. Here, we investigated IL-10-producing B cells in pericardial adipose tissues (PATs) and their role in the healing process following acute MI in mice. We found abundant IL-10-producing B cells in PATs under homeostatic conditions, with the majority of them bearing cell surface CD5 (CD5+ B cells). These cells were detected early in life, maintained a steady presence during adulthood, and resided in fat-associated lymphoid clusters (FALCs). The cytokine IL-33 was preferentially expressed in PATs under homeostatic conditions and contributed to enrichment of IL-10-producing CD5+ B cells in PATs. CD5+ B cells expanded in PATs following MI, and accumulated in the infarcted heart during the resolution of MI-induced inflammation. B cell-specific deletion of IL-10 worsened cardiac function after MI, exacerbated myocardial injury, and delayed resolution of inflammation. These findings reveal a significant contribution of IL-10-producing B cells to the anti-inflammatory mechanism that terminates MI-induced inflammation, and identify these cells as novel therapeutic targets to improve the outcome of MI.Significance StatementMyocardial infarction (MI) remains a leading cause of mortality and morbidity worldwide. Although it is now recognized that a balanced and timely terminated pro-inflammatory response following acute MI is essential in promoting tissue repair, the underlying regulatory mechanisms are poorly defined. In this report, we show that IL-10-producing B cells in mice 1) are enriched in pericardial adipose tissues (PATs) and influenced by cytokine IL-33 under homeostatic conditions; 2) expand in PATs following MI and accumulate in the infarcted heart during the resolution of MI-induced inflammation; and 3) facilitate resolution of inflammation and reduce myocardial injury to preserve cardiac function after MI. These findings identify IL-10-producing B cells as novel therapeutic targets to improve the outcome of MI.

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Maturation and function of human dendritic cells are regulated by B lymphocytes

Blood ◽

10.1182/blood-2011-06-360768 ◽

2012 ◽

Vol 119 (1) ◽

pp. 106-114 ◽

Cited By ~ 62

Author(s):

Ahsen Morva ◽

Sébastien Lemoine ◽

Achouak Achour ◽

Jacques-Olivier Pers ◽

Pierre Youinou ◽

...

Keyword(s):

Dendritic Cells ◽

T Cell ◽

B Cells ◽

Inflammatory Response ◽

Lupus Erythematosus ◽

Tolerance Induction ◽

Cell Immune Response ◽

Human B Cells ◽

And Function

Abstract Mature dendritic cells (DCs) are stimulators of T-cell immune response, whereas immature DCs support T-cell tolerance. Murine B cells can inhibit the production of IL-12 by DCs and thereby hinder the inflammatory response. Notwithstanding the importance of this modulation, only a few studies are available in humans. Here, we have developed an in vitro model of cocultures to assess its significance. We establish that human activated B cells restrained the development of monocytes into immature DCs and their differentiation into mature DCs. In addition, they decreased the density of HLA-DR from mature DCs, the expression of CD80 and CD86 coactivation molecules, the production of IL-12p70 required for antigen presentation and Th1 differentiation, and inhibited the DC-induced T-cell proliferation. These modulations were mediated by CD19+IgDlowCD38+CD24lowCD27− B cells and needed direct cell-to-cell contacts that involved CD62L for the control of CD80 and CD86 expression and a soluble factor for the control of IL-12 production. Moreover, mature DCs from patients with systemic lupus erythematosus displayed insensitivity to the regulation of IL-12. Overall, it appears that human B cells can regulate DC maturation and function and that inefficient B-cell regulation may influence an improper balance between an effector inflammatory response and tolerance induction.

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