The Experts below are selected from a list of 14502 Experts worldwide ranked by ideXlab platform

Susan R Schwab - One of the best experts on this subject based on the ideXlab platform.

  • microbiota restricts trafficking of bacteria to Mesenteric Lymph Nodes by cx 3 cr1 hi cells
    Nature, 2013
    Co-Authors: Gretchen E Diehl, Randy S Longman, Beatrice Breart, Adolfo Cuesta, Carolina Galan, Jingxin Zhang, Susan R Schwab
    Abstract:

    In mice, commensal bacteria are shown to provide critical signals that limit bacterial trafficking to the Mesenteric Lymph Nodes by immune cells, thus preventing the induction of mucosal immune responses.

  • microbiota restricts trafficking of bacteria to Mesenteric Lymph Nodes by cx 3 cr1 hi cells
    Nature, 2013
    Co-Authors: Gretchen E Diehl, Randy S Longman, Beatrice Breart, Adolfo Cuesta, Carolina Galan, Jingxin Zhang, Susan R Schwab
    Abstract:

    The intestinal microbiota has a critical role in immune system and metabolic homeostasis, but it must be tolerated by the host to avoid inflammatory responses that can damage the epithelial barrier separating the host from the luminal contents. Breakdown of this regulation and the resulting inappropriate immune response to commensals are thought to lead to the development of inflammatory bowel diseases such as Crohn's disease and ulcerative colitis. We proposed that the intestinal immune system is instructed by the microbiota to limit responses to luminal antigens. Here we demonstrate in mice that, at steady state, the microbiota inhibits the transport of both commensal and pathogenic bacteria from the lumen to a key immune inductive site, the Mesenteric Lymph Nodes (MLNs). However, in the absence of Myd88 or under conditions of antibiotic-induced dysbiosis, non-invasive bacteria were trafficked to the MLNs in a CCR7-dependent manner, and induced both T-cell responses and IgA production. Trafficking was carried out by CX(3)CR1(hi) mononuclear phagocytes, an intestinal-cell population previously reported to be non-migratory. These findings define a central role for commensals in regulating the migration to the MLNs of CX(3)CR1(hi) mononuclear phagocytes endowed with the ability to capture luminal bacteria, thereby compartmentalizing the intestinal immune response to avoid inflammation.

Randy S Longman - One of the best experts on this subject based on the ideXlab platform.

  • microbiota restricts trafficking of bacteria to Mesenteric Lymph Nodes by cx 3 cr1 hi cells
    Nature, 2013
    Co-Authors: Gretchen E Diehl, Randy S Longman, Beatrice Breart, Adolfo Cuesta, Carolina Galan, Jingxin Zhang, Susan R Schwab
    Abstract:

    In mice, commensal bacteria are shown to provide critical signals that limit bacterial trafficking to the Mesenteric Lymph Nodes by immune cells, thus preventing the induction of mucosal immune responses.

  • microbiota restricts trafficking of bacteria to Mesenteric Lymph Nodes by cx 3 cr1 hi cells
    Nature, 2013
    Co-Authors: Gretchen E Diehl, Randy S Longman, Beatrice Breart, Adolfo Cuesta, Carolina Galan, Jingxin Zhang, Susan R Schwab
    Abstract:

    The intestinal microbiota has a critical role in immune system and metabolic homeostasis, but it must be tolerated by the host to avoid inflammatory responses that can damage the epithelial barrier separating the host from the luminal contents. Breakdown of this regulation and the resulting inappropriate immune response to commensals are thought to lead to the development of inflammatory bowel diseases such as Crohn's disease and ulcerative colitis. We proposed that the intestinal immune system is instructed by the microbiota to limit responses to luminal antigens. Here we demonstrate in mice that, at steady state, the microbiota inhibits the transport of both commensal and pathogenic bacteria from the lumen to a key immune inductive site, the Mesenteric Lymph Nodes (MLNs). However, in the absence of Myd88 or under conditions of antibiotic-induced dysbiosis, non-invasive bacteria were trafficked to the MLNs in a CCR7-dependent manner, and induced both T-cell responses and IgA production. Trafficking was carried out by CX(3)CR1(hi) mononuclear phagocytes, an intestinal-cell population previously reported to be non-migratory. These findings define a central role for commensals in regulating the migration to the MLNs of CX(3)CR1(hi) mononuclear phagocytes endowed with the ability to capture luminal bacteria, thereby compartmentalizing the intestinal immune response to avoid inflammation.

Beatrice Breart - One of the best experts on this subject based on the ideXlab platform.

  • microbiota restricts trafficking of bacteria to Mesenteric Lymph Nodes by cx 3 cr1 hi cells
    Nature, 2013
    Co-Authors: Gretchen E Diehl, Randy S Longman, Beatrice Breart, Adolfo Cuesta, Carolina Galan, Jingxin Zhang, Susan R Schwab
    Abstract:

    In mice, commensal bacteria are shown to provide critical signals that limit bacterial trafficking to the Mesenteric Lymph Nodes by immune cells, thus preventing the induction of mucosal immune responses.

  • microbiota restricts trafficking of bacteria to Mesenteric Lymph Nodes by cx 3 cr1 hi cells
    Nature, 2013
    Co-Authors: Gretchen E Diehl, Randy S Longman, Beatrice Breart, Adolfo Cuesta, Carolina Galan, Jingxin Zhang, Susan R Schwab
    Abstract:

    The intestinal microbiota has a critical role in immune system and metabolic homeostasis, but it must be tolerated by the host to avoid inflammatory responses that can damage the epithelial barrier separating the host from the luminal contents. Breakdown of this regulation and the resulting inappropriate immune response to commensals are thought to lead to the development of inflammatory bowel diseases such as Crohn's disease and ulcerative colitis. We proposed that the intestinal immune system is instructed by the microbiota to limit responses to luminal antigens. Here we demonstrate in mice that, at steady state, the microbiota inhibits the transport of both commensal and pathogenic bacteria from the lumen to a key immune inductive site, the Mesenteric Lymph Nodes (MLNs). However, in the absence of Myd88 or under conditions of antibiotic-induced dysbiosis, non-invasive bacteria were trafficked to the MLNs in a CCR7-dependent manner, and induced both T-cell responses and IgA production. Trafficking was carried out by CX(3)CR1(hi) mononuclear phagocytes, an intestinal-cell population previously reported to be non-migratory. These findings define a central role for commensals in regulating the migration to the MLNs of CX(3)CR1(hi) mononuclear phagocytes endowed with the ability to capture luminal bacteria, thereby compartmentalizing the intestinal immune response to avoid inflammation.

Jingxin Zhang - One of the best experts on this subject based on the ideXlab platform.

  • microbiota restricts trafficking of bacteria to Mesenteric Lymph Nodes by cx 3 cr1 hi cells
    Nature, 2013
    Co-Authors: Gretchen E Diehl, Randy S Longman, Beatrice Breart, Adolfo Cuesta, Carolina Galan, Jingxin Zhang, Susan R Schwab
    Abstract:

    In mice, commensal bacteria are shown to provide critical signals that limit bacterial trafficking to the Mesenteric Lymph Nodes by immune cells, thus preventing the induction of mucosal immune responses.

  • microbiota restricts trafficking of bacteria to Mesenteric Lymph Nodes by cx 3 cr1 hi cells
    Nature, 2013
    Co-Authors: Gretchen E Diehl, Randy S Longman, Beatrice Breart, Adolfo Cuesta, Carolina Galan, Jingxin Zhang, Susan R Schwab
    Abstract:

    The intestinal microbiota has a critical role in immune system and metabolic homeostasis, but it must be tolerated by the host to avoid inflammatory responses that can damage the epithelial barrier separating the host from the luminal contents. Breakdown of this regulation and the resulting inappropriate immune response to commensals are thought to lead to the development of inflammatory bowel diseases such as Crohn's disease and ulcerative colitis. We proposed that the intestinal immune system is instructed by the microbiota to limit responses to luminal antigens. Here we demonstrate in mice that, at steady state, the microbiota inhibits the transport of both commensal and pathogenic bacteria from the lumen to a key immune inductive site, the Mesenteric Lymph Nodes (MLNs). However, in the absence of Myd88 or under conditions of antibiotic-induced dysbiosis, non-invasive bacteria were trafficked to the MLNs in a CCR7-dependent manner, and induced both T-cell responses and IgA production. Trafficking was carried out by CX(3)CR1(hi) mononuclear phagocytes, an intestinal-cell population previously reported to be non-migratory. These findings define a central role for commensals in regulating the migration to the MLNs of CX(3)CR1(hi) mononuclear phagocytes endowed with the ability to capture luminal bacteria, thereby compartmentalizing the intestinal immune response to avoid inflammation.

Sander Kersten - One of the best experts on this subject based on the ideXlab platform.

  • feeding angptl4 mice trans fat promotes foam cell formation in Mesenteric Lymph Nodes without leading to ascites
    Journal of Lipid Research, 2017
    Co-Authors: Antwi Boasiako Oteng, Asmita Bhattacharya, Susanne Brodesser, Nguan Soon Tan, Sander Kersten
    Abstract:

    ANGPTL4 regulates plasma triglyceride levels by inhibiting lipoprotein lipase. Inactivation of ANGPTL4 decreases plasma triglycerides and reduces risk of coronary artery disease. Unfortunately, targeting ANGPTL4 for the therapeutic management of dyslipidemia and atherosclerosis is hampered by the observation that mice and monkeys in which ANGPTL4 is inactivated exhibit lipid accumulation in Mesenteric Lymph Nodes. In mice these pathological events exclusively unfold upon feeding a high saturated fatty acid diet and are followed by an ultimately lethal pro-inflammatory response and chylous ascites. Here we show that Angptl4-/- mice fed a diet rich in trans fatty acids develop numerous lipid-filled giant cells in their Mesenteric Lymph Nodes, yet do not have elevated serum amyloid and haptoglobin, do not exhibit ascites, and survive, unlike Angptl4-/- mice fed a saturated fatty acid-rich diet. In RAW264.7 macrophages the saturated fatty acid palmitate markedly increases markers of inflammation and the unfolded protein response, whereas the trans-unsaturated elaidate and the cis-unsaturated oleate have the opposite effect. In conclusion, trans and saturated fatty acids have very distinct biological effects. Furthermore, lipid accumulation in Mesenteric Lymph Nodes is uncoupled from activation of an acute-phase response and chylous ascites, suggesting that ANGPTL4 should not be fully dismissed as target for dyslipidemia.