scholarly journals HLA-G Is Widely Expressed by Mast Cells in Regions of Organ Fibrosis in the Liver, Lung and Kidney

2021 ◽  
Vol 22 (22) ◽  
pp. 12490
Author(s):  
Nicolas Mouchet ◽  
Nicolas Vu ◽  
Bruno Turlin ◽  
Nathalie Rioux-Leclercq ◽  
Stéphane Jouneau ◽  
...  
Keyword(s):  
Mast Cells ◽  
B Lymphocytes ◽  
Renal Fibrosis ◽  
Alcoholic Cirrhosis ◽  
Protective Role ◽  
Viral Etiology ◽  
General Process ◽  
G Cells ◽  
Lung And Kidney ◽  
Organ Fibrosis

We previously demonstrated that mast cells expressing HLA-G are associated with regions of hepatitis C virus-induced liver fibrosis. Here, we aimed to determine whether HLA-G expression in mast cells is specific to viral etiology, the liver, or to the general process of fibrosis. We enumerated HLA-G+ cells and mast cells by the immunohistochemistry of (i) liver blocks from 41 cases of alcoholic cirrhosis, (ii) 10 of idiopathic pulmonary fibrosis (IPF), and (iii) 10 of renal fibrosis. The nature of the HLA-G+ cells was specified by multiplex immunofluorescence using software. More than half of all HLA-G+ cells were mast cells in fibrotic areas of alcoholic cirrhosis and IPF. In the kidneys, subjected to fibrosis, the HLA-G+ cells were indeed mast cells but could not be counted. Moreover, in certain cases of the liver and lung, we observed a number of cellular nodes, which were secondary or tertiary follicles, in which HLA-G was highly expressed by B lymphocytes. In conclusion, HLA-G+ mast cells could be observed in the fibrotic regions of all organs studied. Previous studies suggest a protective role for HLA-G+ mast cells against inflammation and fibrosis. The observed follicles with B lymphocytes that express HLA-G may also reinforce their antifibrotic role.

Apigenin Alleviates Renal Fibroblast Activation through AMPK and ERK Signaling Pathways In Vitro

2020 ◽  
Vol 21 (11) ◽  
pp. 1107-1118
Author(s):  
Ningning Li ◽  
Zhan Wang ◽  
Tao Sun ◽  
Yanfei Lei ◽  
Xianghua Liu ◽  
...  
Keyword(s):  
Renal Fibrosis ◽  
Transforming Growth Factor ◽  
Therapeutic Potential ◽  
Protective Role ◽  
Fibroblast Proliferation ◽  
Fibroblast Activation ◽  
And Function ◽  
Activated Fibroblasts ◽  
Tgf Β1

Objective: Renal fibrosis is a common pathway leading to the progression of chronic kidney disease. Activated fibroblasts contribute remarkably to the development of renal fibrosis. Although apigenin has been demonstrated to play a protective role from fibrotic diseases, its pharmacological effect on renal fibroblast activation remains largely unknown. Materials and Methods: Here, we examined the functional role of apigenin in the activation of renal fibroblasts response to transforming growth factor (TGF)-β1 and its potential mechanisms. Cultured renal fibroblasts (NRK-49F) were exposed to apigenin (1, 5, 10 and 20 μM), followed by the stimulation of TGF-β1 (2 ng/mL) for 24 h. The markers of fibroblast activation were determined. In order to confirm the anti-fibrosis effect of apigenin, the expression of fibrosis-associated genes in renal fibroblasts was assessed. As a consequence, apigenin alleviated fibroblast proliferation and fibroblastmyofibroblast differentiation induced by TGF-β1. Result: Notably, apigenin significantly inhibited the fibrosis-associated genes expression in renal fibroblasts. Moreover, apigenin treatment significantly increased the phosphorylation of AMP-activated protein kinase (AMPK). Apigenin treatment also obviously reduced TGF-β1 induced phosphorylation of ERK1/2 but not Smad2/3, p38 and JNK MAPK in renal fibroblasts. Conclusion: In a summary, these results indicate that apigenin inhibits renal fibroblast proliferation, differentiation and function by AMPK activation and reduced ERK1/2 phosphorylation, suggesting it could be an attractive therapeutic potential for the treatment of renal fibrosis.

scholarly journals Alkoholos májbetegség: a genetikai-epigenetikai tényezők szerepe és az absztinencia hatása

2019 ◽  
Vol 160 (14) ◽  
pp. 524-532 ◽  
Author(s):  
Alajos Pár ◽  
Gabriella Pár
Keyword(s):  
Risk Factors ◽  
Liver Disease ◽  
Environmental Factors ◽  
Alcoholic Liver Disease ◽  
Liver Toxicity ◽  
Hepatitis Virus ◽  
Alcoholic Cirrhosis ◽  
Protective Role ◽  
Micro Rna ◽  
Alcoholic Fatty Liver

Abstract: The pathogenesis of alcoholic liver disease depends not only on the toxic effects of alcohol, but also on the complex interaction of host’s and environmental factors. Thus, the genetic pre-disposition, co-morbidities and behavioral factors all play a role in the individual variations in the disease outcomes. On the other hand, the essential part of the therapeutic strategy is the complete withdrawal of the harmful etiological agent. The present paper is devoted to overview the genetics, the environmental factors and the effects of abstinence in alcoholic liver disease. Genetic variants in two enzymes involved in the metabolism of ethanol, alcohol-dehydrogenase ADH1B *2 and aldehyde-dehydrogenase ALDH2 *2 through increasing the blood level of acetaldehyde, may play a “protective” role against alcoholism. The P450 CYP2E1 *5 c2, an inducible microsomal oxidase, upregulated by ethanol and by formation of acetaldehyde and reactive oxygen species, increases liver toxicity. Three novel gene polymorphisms – such as the patatin-like phospholipase domain-containing 3 (PNPLA3 I148M C>G), the transmembrane 6 superfamily member 2 (TM6SF2 E167K), and the membrane-bound O-acyltransferase domain-containing 7 (MB0AT7 rs641738 C>T) – have been proven as risk factors of steatosis, fibrosis and even hepatocellular carcinoma in both alcoholic and non-alcoholic fatty liver disease patients. Alcohol-induced epigenetic effects, reversible but inheritable gene expression alterations – as histon modulations, DNA methylation and micro-RNA-s – are of importance in the pathogenesis as well, and in the future, they may serve as diagnostic markers and therapeutic targets. Women are at greater risk of developing alcoholic cirrhosis, furthermore, malnutrition, obesity, diabetes, smoking, and hepatitis virus infections are also risk factors. Alcoholic liver disease should be regarded as a preventable disease. Several clinical studies revealed that abstinence may result in the regression of steatohepatitis and fibrosis, compensation of cirrhosis, improving disease outcome and increasing survival even in patients with advanced stages. Early diagnosis and multidisciplinary interventions are highly required to achieve long-term abstinence and to prevent alcoholic cirrhosis. Orv Hetil. 2019; 160(14): 524–532.

scholarly journals Digital Image Analysis of Picrosirius Red Staining: A Robust Method for Multi-Organ Fibrosis Quantification and Characterization

Biomolecules ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 1585
Author(s):  
Guillaume E. Courtoy ◽  
Isabelle Leclercq ◽  
Antoine Froidure ◽  
Guglielmo Schiano ◽  
Johann Morelle ◽  
...  
Keyword(s):  
Digital Method ◽  
Computer Assisted ◽  
Kidney Fibrosis ◽  
Collagen Accumulation ◽  
Organ Specific ◽  
Picrosirius Red ◽  
Lung And Kidney ◽  
Organ Fibrosis ◽  
Accurate Quantification

Current understanding of fibrosis remains incomplete despite the increasing burden of related diseases. Preclinical models are used to dissect the pathogenesis and dynamics of fibrosis, and to evaluate anti-fibrotic therapies. These studies require objective and accurate measurements of fibrosis. Existing histological quantification methods are operator-dependent, organ-specific, and/or need advanced equipment. Therefore, we developed a robust, minimally operator-dependent, and tissue-transposable digital method for fibrosis quantification. The proposed method involves a novel algorithm for more specific and more sensitive detection of collagen fibers stained by picrosirius red (PSR), a computer-assisted segmentation of histological structures, and a new automated morphological classification of fibers according to their compactness. The new algorithm proved more accurate than classical filtering using principal color component (red-green-blue; RGB) for PSR detection. We applied this new method on established mouse models of liver, lung, and kidney fibrosis and demonstrated its validity by evidencing topological collagen accumulation in relevant histological compartments. Our data also showed an overall accumulation of compact fibers concomitant with worsening fibrosis and evidenced topological changes in fiber compactness proper to each model. In conclusion, we describe here a robust digital method for fibrosis analysis allowing accurate quantification, pattern recognition, and multi-organ comparisons useful to understand fibrosis dynamics.

scholarly journals Adenosine-Activated Mast Cells Induce IgE Synthesis by B Lymphocytes: An A2B-Mediated Process Involving Th2 Cytokines IL-4 and IL-13 with Implications for Asthma

2004 ◽  
Vol 172 (12) ◽  
pp. 7726-7733 ◽  
Author(s):  
Sergey Ryzhov ◽  
Anna E. Goldstein ◽  
Anton Matafonov ◽  
Dewan Zeng ◽  
Italo Biaggioni ◽  
...  
Keyword(s):  
Mast Cells ◽  
B Lymphocytes ◽  
Th2 Cytokines ◽  
Ige Synthesis

Less contribution of mast cells to the progression of renal fibrosis in Rat kidneys with chronic renal failure

Nephrology ◽  
2017 ◽  
Vol 22 (2) ◽  
pp. 159-167 ◽  
Author(s):  
Asuka Baba ◽  
Masahiro Tachi ◽  
Yutaka Ejima ◽  
Yasuhiro Endo ◽  
Hiroaki Toyama ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Mast Cells ◽  
Renal Fibrosis ◽  
Rat Kidneys

scholarly journals Role of mast cells in the development of renal fibrosis: Use of mast cell–deficient rats

2004 ◽  
Vol 65 (6) ◽  
pp. 2228-2237 ◽  
Author(s):  
Shinobu Miyazawa ◽  
Osamu Hotta ◽  
Naoko Doi ◽  
Yumiko Natori ◽  
Kiyotaka Nishikawa ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Renal Fibrosis

scholarly journals Mast cells enhance proliferation of B lymphocytes and drive their differentiation toward IgA-secreting plasma cells

Blood ◽  
2010 ◽  
Vol 115 (14) ◽  
pp. 2810-2817 ◽  
Author(s):  
Sonia Merluzzi ◽  
Barbara Frossi ◽  
Giorgia Gri ◽  
Serena Parusso ◽  
Claudio Tripodo ◽  
...  
Keyword(s):  
B Cells ◽  
Mast Cells ◽  
B Cell ◽  
B Lymphocytes ◽  
Plasma Cells ◽  
Close Contact ◽  
Spatial Interaction ◽  
Significant Inhibition ◽  
Cell Contact

Abstract The evidence of a tight spatial interaction between mast cells (MCs) and B lymphocytes in secondary lymphoid organs, along with the data regarding the abundance of MCs in several B-cell lymphoproliferative disorders prompted us to investigate whether MCs could affect the proliferation and differentiation of B cells. To this aim, we performed coculture assays using mouse splenic B cells and bone marrow–derived MCs. Both nonsensitized and activated MCs proved able to induce a significant inhibition of cell death and an increase in proliferation of naive B cells. Such proliferation was further enhanced in activated B cells. This effect relied on cell-cell contact and MC-derived interleukin-6 (IL-6). Activated MCs could regulate CD40 surface expression on unstimulated B cells and the interaction between CD40 with CD40 ligand (CD40L) on MCs, together with MC-derived cytokines, was involved in the differentiation of B cells into CD138+ plasma cells and in selective immunoglobulin A (IgA) secretion. These data were corroborated by in vivo evidence of infiltrating MCs in close contact with IgA-expressing plasma cells within inflamed tissues. In conclusion, we reported here a novel role for MCs in sustaining B-cell expansion and driving the development of IgA-oriented humoral immune responses.

scholarly journals Protective Role of Angiotensin II Type 1 Receptor Blocker on Short Time Effect of Oleic Acid Induced Lung and Kidney Injury

2021 ◽  
Vol 12 (1) ◽  
pp. 4
Author(s):  
Mehdi Nematbakhsh ◽  
Ardeshir Talebi ◽  
Fatemeh Emami ◽  
Reza Biranvand ◽  
Zahra Moosavi ◽  
...  
Keyword(s):  
Oleic Acid ◽  
Angiotensin Ii ◽  
Kidney Injury ◽  
Protective Role ◽  
Time Effect ◽  
Receptor Blocker ◽  
Short Time ◽  
Lung And Kidney

Characterization of the Immune Barrier in Human Olfactory Mucosa

1992 ◽  
Vol 106 (2) ◽  
pp. 181-188 ◽  
Author(s):  
Tuesday K. Mellert ◽  
Marilyn L. Getchell ◽  
Larry Sparks ◽  
Thomas V. Getchell
Keyword(s):  
Mast Cells ◽  
B Lymphocytes ◽  
Lamina Propria ◽  
Secretory Component ◽  
Olfactory Mucosa ◽  
Blue Staining ◽  
Humoral Factors ◽  
J Chain ◽  
Human Olfactory Mucosa ◽  
A Site

Immunologic defense factors in the human olfactory mucosa were localized immunohistochemically. Olfactory epithelium was identified with an antiserum to olfactory marker protein, specific for olfactory receptor neurons. Constituents of the secretory immune system, including IgA, IgM, secretory component, and J chain, were localized in the acinar and duct cells of Bowman's glands and in the mucociliary complex. In addition, B lymphocytes in the lamina propria near Bowman's glands displayed immunoreactivity for IgA, IgM, and J chain. Immunostaining also localized other humoral factors. Immunoreactivity for IgG was present throughout the stroma and in B lymphocytes in the lamina propria. Antibody to IgD stained numerous B lymphocytes clustered below the basement membrane. Antibody to IgE stained similarly distributed cells; toluidine blue staining demonstrated that many were mast cells. In addition, antibodies to IgD and IgE stained occasional intraepithelial B lymphocytes or mast cells. Two antimicrobial proteins, lactoferrin and lysozyme, were localized in Bowman's glands and the mucociliary complex. Thus, the human olfactory mucosa, which provides a direct neural route for pathogens to the brain, is a site for synthesis and secretion of immune and other defense factors.

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