Gut microbiota: Role in pathogen colonization, immune responses, and inflammatory disease

Pickard, Joseph M.; Zeng, Melody Y.; Caruso, Roberta; Núñez, Gabriel

doi:10.1111/imr.12567

Cited by 1,108 publications

(847 citation statements)

References 238 publications

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“…In particular, Enterobacteriaceae populations expand during bouts of inflammation (Lupp et al, 2007;Garrett et al, 2010). The outgrowth of these pathobionts in turn exacerbates intestinal inflammation, epithelial cell damage, and wound repair responses (Carvalho et al, 2012;Gronbach et al, 2014;Kang and Martin, 2017;Pickard et al, 2017), thus amplifying known risk factors of CAC development.…”

Section: Introductionmentioning

confidence: 99%

Editing of the gut microbiota reduces carcinogenesis in mouse models of colitis-associated colorectal cancer

Zhu

Miyata

Winter

et al. 2019

Journal of Experimental Medicine

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Chronic inflammation and gut microbiota dysbiosis, in particular the bloom of genotoxin-producing E. coli strains, are risk factors for the development of colorectal cancer. Here, we sought to determine whether precision editing of gut microbiota metabolism and composition could decrease the risk for tumor development in mouse models of colitis-associated colorectal cancer (CAC). Expansion of experimentally introduced E. coli strains in the azoxymethane/dextran sulfate sodium colitis model was driven by molybdoenzyme-dependent metabolic pathways. Oral administration of sodium tungstate inhibited E. coli molybdoenzymes and selectively decreased gut colonization with genotoxin-producing E. coli and other Enterobacteriaceae. Restricting the bloom of Enterobacteriaceae decreased intestinal inflammation and reduced the incidence of colonic tumors in two models of CAC, the azoxymethane/dextran sulfate sodium colitis model and azoxymethane-treated, Il10-deficient mice. We conclude that metabolic targeting of protumoral Enterobacteriaceae during chronic inflammation is a suitable strategy to prevent the development of malignancies arising from gut microbiota dysbiosis.

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Section: Introductionmentioning

confidence: 99%

Editing of the gut microbiota reduces carcinogenesis in mouse models of colitis-associated colorectal cancer

Zhu

Miyata

Winter

et al. 2019

Journal of Experimental Medicine

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“…In Nicaragua, Lactobacillus, Lachnospiraceae, Bifidobacterium, Ruminococcaceae and Veillonella were identified as responsive following rice bran consumption compared to an age and control matched group. These taxa have recognized saccharolytic mechanisms of action 65–67 , are known to produce and promote crossfeeding of short chain fatty acids 68, 69 , as well as provide competitive inhibition of pathogen colonization 70, 71 . The microbial enrichment of these communities as associated with infant growth outcomes has implications for assessing how gut microbes metabolize rice bran components.…”

Section: Discussionmentioning

confidence: 99%

Rice bran supplementation modulates growth, microbiome and metabolome in weaning infants: a clinical trial in Nicaragua and Mali

Zambrana

McKeen

Ibrahim

et al. 2019

Preprint

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Rice bran supplementation provides nutrients, prebiotics and phytochemicals that enhance gut immunity, reduce enteric pathogens in mice and diarrhea in neonatal pigs, and warranted attention for improvement of environmental enteric dysfunction (EED) in children at risk. EED is a condition that drives childhood stunting via intestinal dysbiosis and impaired nutrient metabolism. This study investigated effects of rice bran supplementation on growth, EED biomarkers, gut microbiome and metabolome in weaning infants from 6 to 12 months old in Nicaragua and Mali. Healthy infants were randomized to a control group or rice bran group that received daily supplementation at increasing doses each month. Stool microbiomes were characterized using 16S rDNA amplicon sequencing. Stool metabolomes were analyzed using ultra-high-performance liquid-chromatography tandem mass-spectrometry. Statistical comparisons were completed at 6, 8, and 12 months of age. Daily consumption of rice bran was safe and feasible for infant growth, decreasing alpha-1 antitrypsin levels, and modulating gut microbiome and metabolome when compared to control. Rice bran merits investigation as a practical intervention strategy that could decrease EED prevalence and risk for children from low- and middle-income countries where rice is grown as a staple food, and bran is used as animal feed or wasted.One Sentence SummaryDietary rice bran supplementation during infant weaning from 6-12 months of age improved growth outcomes, modulated environmental enteric dysfunction biomarkers, and supported metabolism by the gut microbiome.The authors declare no competing financial or non financial interests to disclose as defined by Nature Research. There are also no other interests that might be perceived to influence the results and/or discussion reported in this paper.Correspondence and requests for materials should be addressed to Dr. Elizabeth Ryan (e.p.ryan@colostate.edu).

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“…127,128 For example, the glycosylation of intestinal epithelial cells can be regulated by dendritic cells and innate lymphoid cells (ILC3s). With regard to iNKT cells, it was suggested that iNKT cell-derived interleukin-13 (IL-13) regulates goblet cell homeostasis.…”

Section: (3) Mucus Production and Glycosylationmentioning

confidence: 99%

The interaction between invariant Natural Killer T cells and the mucosal microbiota

Hapil¹,

Wingender

2018

Immunology

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SummaryThe surface of mammalian bodies is colonized by a multitude of microbial organisms, which under normal conditions support the host and are considered beneficial commensals. This requires, however, that the composition of the commensal microbiota is tightly controlled and regulated. The host immune system plays an important role in the maintenance of this microbiota composition. Here we focus on the contribution of one particular immune cell type, invariant Natural Killer T (iNKT) cells, in this process. The iNKT cells are a unique subset of T cells characterized by two main features. First, they express an invariant T-cell receptor that recognizes glycolipid antigens presented by CD1d, a non-polymorphic major histocompatibility complex class I-like molecule. Second, iNKT cells develop as effector/memory cells and swiftly exert effector functions, like cytokine production and cytotoxicity, after activation. We outline the influence that the mucosal microbiota can have on iNKT cells, and how iNKT cells contribute to the maintenance of the microbiota composition.

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Gut microbiota: Role in pathogen colonization, immune responses, and inflammatory disease

Cited by 1,108 publications

References 238 publications

Editing of the gut microbiota reduces carcinogenesis in mouse models of colitis-associated colorectal cancer

Editing of the gut microbiota reduces carcinogenesis in mouse models of colitis-associated colorectal cancer

Rice bran supplementation modulates growth, microbiome and metabolome in weaning infants: a clinical trial in Nicaragua and Mali

The interaction between invariant Natural Killer T cells and the mucosal microbiota

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