Mechanisms and consequences of gut commensal translocation in chronic diseases

Fine, Rebecca; Vieira, Sílvio M.; Gilmore, Michael S.; Kriegel, Martin

doi:10.1080/19490976.2019.1629236

Cited by 83 publications

(69 citation statements)

References 83 publications

(146 reference statements)

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“…Although gut barrier disruption has not been reported to be a pre requisite for nonalcoholic steatohepatitis (NASH) development and belongs to the 'multiple hit' pathogenesis of disease progression [60], more recent observations in preclinical models have shown that disruption of epithelial and vascular barriers in the intestine were early events reported in NASH [61]. Gut-liver axis deterioration has also been described in patients with chronic liver diseases who develop sepsis and multiorgan failure [62,63]. Zhou et al in their recent retrospective cohort study of 191 patients reported that more than half of hospitalized patients developed sepsis as a common complication of SARS-CoV-2 infection [18].…”

Section: Discussionmentioning

confidence: 99%

COVID-19, MERS and SARS with Concomitant Liver Injury—Systematic Review of the Existing Literature

Kukla

Skonieczna-Żydecka

Kotfis

et al. 2020

JCM

100

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The novel coronavirus SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection has been predominantly linked to respiratory distress syndrome, but gastrointestinal symptoms and hepatic injury have also been reported. The mechanism of liver injury is poorly understood and may result as a consequence of viral hepatitis, systemic inflammatory response, gut barrier and microbiome alterations, intensive care treatment or drug toxicity. The incidence of hepatopathy among patients with coronavirus disease 2019 (COVID-19) is unclear, but studies have reported liver injury in patients with SARS and Middle East respiratory syndrome (MERS). We aimed to systematically review data on the prevalence of hepatic impairments and their clinical course in SARS and MERS Coronaviridae infections. A systematic literature search (PubMed/Embase/Cinahl/Web of Science) according to preferred reporting items for systematic review and meta-analysis protocols (PRISMA) was conducted from database inception until 17/03/2020 for studies that evaluated the incidence of hepatic abnormalities in SARS CoV-1, SARS CoV-2 and MERS infected patients with reported liver-related parameters. A total of forty-three studies were included. Liver anomalies were predominantly mild to moderately elevated transaminases, hypoalbuminemia and prolongation of prothrombin time. Histopathology varied between non-specific inflammation, mild steatosis, congestion and massive necrosis. More studies to elucidate the mechanism and importance of liver injury on the clinical course and prognosis in patients with novel SARS-CoV-2 infection are warranted.

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Section: Discussionmentioning

confidence: 99%

COVID-19, MERS and SARS with Concomitant Liver Injury—Systematic Review of the Existing Literature

Kukla

Skonieczna-Żydecka

Kotfis

et al. 2020

JCM

100

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“…In the lamina propria, B cells may also switch into IgA in a T cell-independent way (21). The T cell-independent generation of SIgA by B cells may represent a mechanism to generate IgA expressing a wide repertoire of Ig genes, useful to face the thousands of different bacterial species of the microbiota (23,24,42), and to control host-microbiota mutualism, reducing the risk of bacterial translocation and immune activation (43)(44)(45). IgM memory B cells have been shown to home to the gut and to locally switch to IgA (21,46).…”

Section: Discussionmentioning

confidence: 99%

Lack of Gut Secretory Immunoglobulin A in Memory B-Cell Dysfunction-Associated Disorders: A Possible Gut-Spleen Axis

et al. 2020

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Background: B-1a B cells and gut secretory IgA (SIgA) are absent in asplenic mice. Human immunoglobulin M (IgM) memory B cells, which are functionally equivalent to mouse B-1a B cells, are reduced after splenectomy. Objective: To demonstrate whether IgM memory B cells are necessary for generating IgA-secreting plasma cells in the human gut. Methods: We studied intestinal SIgA in two disorders sharing the IgM memory B cell defect, namely asplenia, and common variable immune deficiency (CVID). Results: Splenectomy was associated with reduced circulating IgM memory B cells and disappearance of intestinal IgA-secreting plasma cells. CVID patients with reduced circulating IgM memory B cells had a reduced frequency of gut IgA + plasma cells and a disrupted film of SIgA on epithelial cells. Toll-like receptor 9 (TLR9) and transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI) induced IgM memory B cell differentiation into IgA + plasma cells in vitro. In the human gut, TACI-expressing IgM memory B cells were localized under the epithelial cell layer where the TACI ligand a proliferation inducing ligand (APRIL) was extremely abundant. Conclusions: Circulating IgM memory B cell depletion was associated with a defect of intestinal IgA-secreting plasma cells in asplenia and CVID. The observation that IgM memory B cells have a distinctive role in mucosal protection suggests the existence of a functional gut-spleen axis.

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“…The role of the gut-liver axis in immune pathologies is highlighted by recent examples of breaches of the gut epithelial barrier leading to liver and systemic immune pathologies (reviewed in ref. 53 ). These include Enterococcus gallinarum translocating from the mouse small intestine to the MLNs, liver and, over time, the spleen, driving both organ-specific and systemic autoimmunity through various mechanisms 11 (fIg.…”

Section: Wwwnaturecom/nrmicromentioning

confidence: 99%

Host–microbiota interactions in immune-mediated diseases

2020

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The immune system evolved not only to fend off pathogens but also to tolerate beneficial microbiota that evolved to live in symbiosis with the host 1. This is perhaps best exemplified from an immunological viewpoint by the paradigm that not only self but also commensal antigens are recognized by regulatory T (T reg) cells that suppress pathological immune responses 2,3. Thus, under immune homeostasis, the immune system tolerates beneficial commensal bacteria but can respond to these same microbiota during tissue disruption or other homeostatic perturbations 4. Self-non-self discrimination of host antigens is a fundamental process that is established and maintained by well-defined central and peripheral tolerance mechanisms (Box 1). How the host immune system develops and responds to the microbiota remains an immunological conundrum of self-non-self discrimination that is poorly understood. Immune-mediated diseases develop in genetically prone individuals when tolerance mechanisms are broken. These diseases are characterized by immunologically mediated tissue damage that is either directed against self-antigens (autoimmunity), transplanted or transfused antigens (alloimmunity), innocuous environmental agents that are inhaled or ingested (allergy) or in the absence of specific antigens (autoinflammation) (Box 2). It is increasingly appreciated that the microbiota directly and indirectly modulates tolerogenic processes that keep inflammatory responses in check. These responses may occur at barrier surfaces

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Mechanisms and consequences of gut commensal translocation in chronic diseases

Cited by 83 publications

References 83 publications

COVID-19, MERS and SARS with Concomitant Liver Injury—Systematic Review of the Existing Literature

COVID-19, MERS and SARS with Concomitant Liver Injury—Systematic Review of the Existing Literature

Lack of Gut Secretory Immunoglobulin A in Memory B-Cell Dysfunction-Associated Disorders: A Possible Gut-Spleen Axis

Host–microbiota interactions in immune-mediated diseases

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