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10.3389/fimmu.2018.00499 http://scihub22266oqcxt.onion/10.3389/fimmu.2018.00499 C5880908!5880908 !29636751     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29636751 &cmd=llinks): Failed to open stream: HTTP request failed! 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Hydrogen Sulfide Reduces Myeloid-Derived Suppressor Cell-Mediated Inflammatory Response in a Model of Helicobacter hepaticus-Induced Colitis |pdf=|usr=}}{{29636751 }} gab.com Text Hydrogen Sulfide Reduces Myeloid-Derived Suppressor Cell-Mediated Inflammatory Response in a Model of Helicobacter hepaticus-Induced Colitis JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=29636751 #FOAvip Chronic inflammation contributes to tumor initiation in colitis-associated colorectal cancer (CRC). Indeed, inflammatory bowel disease (IBD) patients show an increased risk of developing CRC. Cancer immune evasion is a major issue in CRC and preclinical and clinical evidence has defined a critical role for myeloid-derived suppressor cells (MDSCs) that contribute to tumor growth and progression by suppressing T-cells and modulating innate immune responses. MDSCs comprise a heterogeneous population of immature myeloid cells that can be distinct in two subtypes: CD11b(+)Ly6G(+)Ly6C(low) with granulocytic phenotype (G-MDSCs) and CD11b(+)Ly6G(-)Ly6C(high) with monocytic phenotype (M-MDSCs). Hydrogen sulfide (H(2)S) is an endogenous gaseous signaling molecule that regulates various physiological and pathophysiological functions. In particular, several studies support its anti-inflammatory activity in experimental colitis and ulcer. However, the role of the H(2)S pathway in innate immune-mediated IBD has not yet been elucidated. To better define a possible link between MDSCs and H(2)S pathway in colitis-associated CRC development, we used an innate immune-mediated IBD model induced by infection with the bacterium Helicobacter hepaticus (Hh), closely resembling human IBD. Here, we demonstrated an involvement of MDSCs in colitis development. A significant time-dependent increase of both G-MDSCs and M-MDSCs was observed in the colon and in the spleen of Hh-infected mice. Following, we observed that chronic oral administration of the H(2)S donor DATS reduced colon inflammation by limiting the recruitment of G-MDSCs in the colon of Hh-infected mice. Thus, we identify the metabolic pathway l-cysteine/H(2)S as a possible new player in the immunosuppressive mechanism responsible for the MDSCs-promoted colitis-associated cancer development. Twit Text FOAVip Hydrogen Sulfide Reduces Myeloid-Derived Suppressor Cell-Mediated Inflammatory Response in a Model of Helicobacter hepaticus-Induced Colitis ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=29636751 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29636751 #FOAvip English Wikipedia <ref>{{Cite pmid|29636751 }}</ref> Hydrogen Sulfide Reduces Myeloid-Derived Suppressor Cell-Mediated Inflammatory Response in a Model of Helicobacter hepaticus-Induced Colitis #MMPMID29636751 De Cicco P ; Sanders T ; Cirino G ; Maloy KJ ; Ianaro A Front Immunol 2018[]; 9 (ä): 499 PMID29636751 show ga Chronic inflammation contributes to tumor initiation in colitis-associated colorectal cancer (CRC). Indeed, inflammatory bowel disease (IBD) patients show an increased risk of developing CRC. Cancer immune evasion is a major issue in CRC and preclinical and clinical evidence has defined a critical role for myeloid-derived suppressor cells (MDSCs) that contribute to tumor growth and progression by suppressing T-cells and modulating innate immune responses. MDSCs comprise a heterogeneous population of immature myeloid cells that can be distinct in two subtypes: CD11b(+)Ly6G(+)Ly6C(low) with granulocytic phenotype (G-MDSCs) and CD11b(+)Ly6G(-)Ly6C(high) with monocytic phenotype (M-MDSCs). Hydrogen sulfide (H(2)S) is an endogenous gaseous signaling molecule that regulates various physiological and pathophysiological functions. In particular, several studies support its anti-inflammatory activity in experimental colitis and ulcer. However, the role of the H(2)S pathway in innate immune-mediated IBD has not yet been elucidated. To better define a possible link between MDSCs and H(2)S pathway in colitis-associated CRC development, we used an innate immune-mediated IBD model induced by infection with the bacterium Helicobacter hepaticus (Hh), closely resembling human IBD. Here, we demonstrated an involvement of MDSCs in colitis development. A significant time-dependent increase of both G-MDSCs and M-MDSCs was observed in the colon and in the spleen of Hh-infected mice. Following, we observed that chronic oral administration of the H(2)S donor DATS reduced colon inflammation by limiting the recruitment of G-MDSCs in the colon of Hh-infected mice. Thus, we identify the metabolic pathway l-cysteine/H(2)S as a possible new player in the immunosuppressive mechanism responsible for the MDSCs-promoted colitis-associated cancer development. |Animals [MESH] |Colitis/genetics/*immunology/microbiology/pathology [MESH] |Colon/immunology/microbiology/pathology [MESH] |Disease Models, Animal [MESH] |Helicobacter Infections/*immunology/pathology [MESH] |Helicobacter hepaticus/*immunology [MESH] |Hydrogen Sulfide/*pharmacology [MESH] |Immunity, Cellular/*drug effects [MESH] |Inflammation/genetics/immunology/microbiology/pathology [MESH] |Mice [MESH] |Mice, Knockout [MESH]Hydrogen Sulfide Reduces Myeloid-Derived Suppressor Cell-Mediated Infl(epmc).pdf DeepDyve Pubget Overpricing