Role of secretory IgA in the mucosal sensing of commensal bacteria

Mathias, Amandine; Pais, Bruno; Favre, Laurent; Benyacoub, Jalil; Corthésy, Blaise

doi:10.4161/19490976.2014.983763

Cited by 97 publications

(71 citation statements)

References 65 publications

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“…typhimurium loads . The NLRP3 inflammasome is the key sensor of tissue damage and activates caspase‐1, which in turn activates downstream pathways that promote the expression of inflammatory factors and NF‐κB . We found that consumption of L .…”

Section: Discussionmentioning

confidence: 86%

Lactobacillus johnsonii L531 ameliorates enteritis via elimination of damaged mitochondria and suppression of SQSTM1‐dependent mitophagy in a Salmonella infantis model of piglet diarrhea

Xia

et al. 2019

FASEB j.

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Newly weaned piglets challenged with Salmonella infantis were particularly susceptible, whereas oral preadministration of Lactobacillus johnsonii L531 alleviated enteritis and promoted intestinal secretory IgA production. Salmonella infantisinduced activation of NLRC4 and NLRP3 inflammasomes and (nuclear factor kappa B) NF-κB signaling in the small intestine was also inhibited by L. johnsonii L531 pretreatment, thus limiting inflammation. An IPEC-J2 cell model of S. infantis infection yielded similar results. Salmonella infantis infection also resulted in mitochondrial damage and impaired mitophagy in the ileum and IPEC-J2 cells, as demonstrated by immunofluorescence colocalization of mitochondria with microtubule-binding protein light chain 3 (LC3) and high expression of autophagy-related proteins PTEN-induced putative kinase 1 (PINK1), sequestosome 1 (SQSTM1/p62), optineurin (OPTN), and LC3 by Western blotting analysis. However, L. johnsonii L531 pretreatment reduced both the extent of mitochondrial damage and autophagyrelated protein expression. Our findings suggest that the amelioration of S. infantisassociated enteritis by L. johnsonii L531 is associated with regulation of NLRC4 and NLRP3 inflammasomes and NF-κB signaling pathway activation and suppression of mitochondrial damage. Amelioration of impaired mitophagy by L. johnsonii L531 could involve eliminating damaged mitochondria and regulating S. infantis-induced activation of the NF-κB-SQSTM1mitophagy signaling pathway in host cells to prevent the further mitochondrial damage and S. infantis dissemination. K E Y W O R D S autophagy, inflammasome, IPEC-J2, pig, probiotic 2822 |

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Section: Discussionmentioning

confidence: 86%

Lactobacillus johnsonii L531 ameliorates enteritis via elimination of damaged mitochondria and suppression of SQSTM1‐dependent mitophagy in a Salmonella infantis model of piglet diarrhea

Xia

et al. 2019

FASEB j.

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“…The presence of S-IgA at mucosal surfaces might warrant that inflammatory processes are kept under control. S-IgA prevents penetration of the mucosal wall by pathogenic microorganisms or foreign antigens, serving as an antiseptic barrier [27]. S-IgA can surround microorganisms and be repelled by mucosal surfaces, can agglutinate microbes and interfere with bacterial motility and can interact with and neutralize bacterial products such as enzymes and toxins [28].…”

Section: Physiological Iga Structure and Functionmentioning

confidence: 99%

Immunoglobulin A nephropathy: a pathophysiology view

2016

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“…The effector section of the gut immune system includes dendritic cells, M‐cells, macrophages, intraepithelial T cells and IgA‐producing plasma cells . Immunoglobulin A is an important mediator of gut immune homeostasis . At birth, the components of the gut lymphoid tissues are underdeveloped for an initial period.…”

Section: The Gut Barriermentioning

confidence: 99%

Current understanding of the role of gut dysbiosis in type 1 diabetes

Abdellatif

Sarvetnick

2019

Journal of Diabetes

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Type 1 diabetes (T1D) is a chronic autoimmune disorder that results from destruction of the insulin‐producing pancreatic β‐cells. The disease mainly affects juveniles. Changes in the composition of the gut microbiota (dysbiosis) and changes in the properties of the gut barrier have been documented in T1D subjects. Because these factors affect immune system functions, they are likely to play a role in disease pathogenesis. However, their exact role is currently not fully understood and is under intensive investigation. In this article we discuss recent advancements depicting the role of intestinal dysbiosis on immunity and autoimmunity in T1D. We also discuss therapies aimed at maintaining a healthy gut barrier as prevention strategies for T1D.

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Role of secretory IgA in the mucosal sensing of commensal bacteria

Cited by 97 publications

References 65 publications

Lactobacillus johnsonii L531 ameliorates enteritis via elimination of damaged mitochondria and suppression of SQSTM1‐dependent mitophagy in a Salmonella infantis model of piglet diarrhea

Lactobacillus johnsonii L531 ameliorates enteritis via elimination of damaged mitochondria and suppression of SQSTM1‐dependent mitophagy in a Salmonella infantis model of piglet diarrhea

Immunoglobulin A nephropathy: a pathophysiology view

Current understanding of the role of gut dysbiosis in type 1 diabetes

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