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Article ; Online: A long journey to the colon: The role of the small intestine microbiota in intestinal disease.

Shealy, Nicolas G / Baltagulov, Madi / Byndloss, Mariana X

2024

Abstract: The small intestine represents a complex and understudied gut niche with significant implications for human health. Indeed, many infectious and non-infectious diseases center within the small intestine and present similar clinical manifestations to large ...

Abstract	The small intestine represents a complex and understudied gut niche with significant implications for human health. Indeed, many infectious and non-infectious diseases center within the small intestine and present similar clinical manifestations to large intestinal disease, complicating non-invasive diagnosis and treatment. One major neglected aspect of small intestinal diseases is the feedback relationship with the resident collection of commensal organisms, the gut microbiota. Studies focused on microbiota-host interactions in the small intestine in the context of infectious and non-infectious diseases are required to identify potential therapeutic targets dissimilar from those used for large bowel diseases. While sparsely populated, the small intestine represents a stringent commensal bacterial microenvironment the host relies upon for nutrient acquisition and protection against invading pathogens (colonization resistance). Indeed, recent evidence suggests that disruptions to host-microbiota interactions in the small intestine impact enteric bacterial pathogenesis and susceptibility to non-infectious enteric diseases. In this review, we focus on the microbiota's impact on small intestine function and the pathogenesis of infectious and non-infectious diseases of the gastrointestinal (GI) tract. We also discuss gaps in knowledge on the role of commensal microorganisms in proximal GI tract function during health and disease.
Language	English
Publishing date	2024-05-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	619315-8
ISSN	1365-2958 ; 0950-382X
ISSN (online)	1365-2958
ISSN	0950-382X
DOI	10.1111/mmi.15270
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Trick and no treat: Carbohydrate preemption by commensal Enterobacteriaceae.

Shealy, Nicolas G / Byndloss, Mariana X

Cell host & microbe

2021 Volume 29, Issue 11, Page(s) 1606–1608

Abstract: Have you ever caught family members eating the last piece of your Halloween candy? In this issue of Cell Host & Microbe, Osbelt et al. and Eberl et al. demonstrate how commensal Enterobacteriaceae preempt pathogen carbohydrate utilization, dependent upon ...

Abstract	Have you ever caught family members eating the last piece of your Halloween candy? In this issue of Cell Host & Microbe, Osbelt et al. and Eberl et al. demonstrate how commensal Enterobacteriaceae preempt pathogen carbohydrate utilization, dependent upon the composition of the surrounding gut microbial community.
MeSH term(s)	Candy ; Carbohydrates ; Enterobacteriaceae ; Microbiota ; Symbiosis
Chemical Substances	Carbohydrates
Language	English
Publishing date	2021-12-10
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2278004-X
ISSN	1934-6069 ; 1931-3128
ISSN (online)	1934-6069
ISSN	1931-3128
DOI	10.1016/j.chom.2021.10.006
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Article ; Online: Colonization resistance: metabolic warfare as a strategy against pathogenic Enterobacteriaceae.

Shealy, Nicolas G / Yoo, Woongjae / Byndloss, Mariana X

Current opinion in microbiology

2021 Volume 64, Page(s) 82–90

Abstract: The intestine is home to a large and complex bacterial ecosystem (microbiota), which performs multiple beneficial functions for the host, including immune education, nutrition, and protection against invasion by enteric pathogens (colonization resistance) ...

Abstract	The intestine is home to a large and complex bacterial ecosystem (microbiota), which performs multiple beneficial functions for the host, including immune education, nutrition, and protection against invasion by enteric pathogens (colonization resistance). The host and microbiome symbiotic interactions occur in part through metabolic crosstalk. Thus, microbiota members have evolved highly diverse metabolic pathways to inhibit pathogen colonization via activation of protective immune responses and nutrient acquisition and utilization. Conversely, pathogenic Enterobacteriaceae actively induce an inflammation-dependent disruption of the gut microbial ecosystem (dysbiosis) to gain a competitive metabolic advantage against the resident microbiota. This review discusses the recent findings on the crucial role of microbiota metabolites in colonization resistance regulation. Additionally, we summarize metabolic mechanisms used by pathogenic Enterobacteriaceae to outcompete commensal microbes and cause disease.
MeSH term(s)	Dysbiosis ; Ecosystem ; Enterobacteriaceae/genetics ; Enterobacteriaceae Infections ; Gastrointestinal Microbiome ; Humans
Language	English
Publishing date	2021-10-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1418474-6
ISSN	1879-0364 ; 1369-5274
ISSN (online)	1879-0364
ISSN	1369-5274
DOI	10.1016/j.mib.2021.09.014
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Article: Colonization resistance: metabolic warfare as a strategy against pathogenic Enterobacteriaceae

Shealy, Nicolas G. / Yoo, Woongjae / Byndloss, Mariana X.

Current opinion in microbiology. 2021 Dec., v. 64

2021

Abstract	The intestine is home to a large and complex bacterial ecosystem (microbiota), which performs multiple beneficial functions for the host, including immune education, nutrition, and protection against invasion by enteric pathogens (colonization resistance). The host and microbiome symbiotic interactions occur in part through metabolic crosstalk. Thus, microbiota members have evolved highly diverse metabolic pathways to inhibit pathogen colonization via activation of protective immune responses and nutrient acquisition and utilization. Conversely, pathogenic Enterobacteriaceae actively induce an inflammation-dependent disruption of the gut microbial ecosystem (dysbiosis) to gain a competitive metabolic advantage against the resident microbiota. This review discusses the recent findings on the crucial role of microbiota metabolites in colonization resistance regulation. Additionally, we summarize metabolic mechanisms used by pathogenic Enterobacteriaceae to outcompete commensal microbes and cause disease.
Keywords	Enterobacteriaceae ; dysbiosis ; ecosystems ; education ; intestinal microorganisms ; intestines ; metabolites ; microbial ecology ; microbiome ; nutrition
Language	English
Dates of publication	2021-12
Size	p. 82-90.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	1418474-6
ISSN	1879-0364 ; 1369-5274
ISSN (online)	1879-0364
ISSN	1369-5274
DOI	10.1016/j.mib.2021.09.014
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Cecum axis (CecAx) preservation reveals physiological and pathological gradients in mouse gastrointestinal epithelium.

Lunnemann, Hannah M / Shealy, Nicolas G / Reyzer, Michelle L / Shupe, John A / Green, Emily H / Siddiqi, Uswah / Lacy, D Borden / Byndloss, Mariana X / Markham, Nicholas O

Gut microbes

2023 Volume 15, Issue 1, Page(s) 2185029

Abstract: The mouse cecum has emerged as a model system for studying microbe-host interactions, immunoregulatory functions of the microbiome, and metabolic contributions of gut bacteria. Too often, the cecum is falsely considered as a uniform organ with an evenly ... ...

Abstract	The mouse cecum has emerged as a model system for studying microbe-host interactions, immunoregulatory functions of the microbiome, and metabolic contributions of gut bacteria. Too often, the cecum is falsely considered as a uniform organ with an evenly distributed epithelium. We developed the cecum axis (CecAx) preservation method to show gradients in epithelial tissue architecture and cell types along the cecal ampulla-apex and mesentery-antimesentery axes. We used imaging mass spectrometry of metabolites and lipids to suggest functional differences along these axes. Using a model of
MeSH term(s)	Animals ; Mice ; Gastrointestinal Microbiome ; Cecum ; Epithelium ; Goblet Cells ; Host Microbial Interactions
Language	English
Publishing date	2023-03-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2575755-6
ISSN	1949-0984 ; 1949-0984
ISSN (online)	1949-0984
ISSN	1949-0984
DOI	10.1080/19490976.2023.2185029
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Iron acquisition by a commensal bacterium modifies host nutritional immunity during

Spiga, Luisella / Fansler, Ryan T / Perera, Yasiru R / Shealy, Nicolas G / Munneke, Matthew J / Torres, Teresa P / David, Holly E / Lemoff, Andrew / Ran, Xinchun / Richardson, Katrina L / Pudlo, Nicholas / Martens, Eric C / Yang, Zhongyue J / Skaar, Eric P / Byndloss, Mariana X / Chazin, Walter J / Zhu, Wenhan

bioRxiv : the preprint server for biology

2023

Abstract: During intestinal inflammation, host nutritional immunity starves microbes of essential micronutrients such as iron. Pathogens scavenge iron using siderophores, which is counteracted by the host using lipocalin-2, a protein that sequesters iron-laden ... ...

Abstract	During intestinal inflammation, host nutritional immunity starves microbes of essential micronutrients such as iron. Pathogens scavenge iron using siderophores, which is counteracted by the host using lipocalin-2, a protein that sequesters iron-laden siderophores, including enterobactin. Although the host and pathogens compete for iron in the presence of gut commensal bacteria, the roles of commensals in nutritional immunity involving iron remain unexplored. Here, we report that the gut commensal
Language	English
Publishing date	2023-06-26
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.06.25.546471
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: An early-life microbiota metabolite protects against obesity by regulating intestinal lipid metabolism.

Cell host & microbe

2023 Volume 31, Issue 10, Page(s) 1604–1619.e10

Abstract: The mechanisms by which the early-life microbiota protects against environmental factors that promote childhood obesity remain largely unknown. Using a mouse model in which young mice are simultaneously exposed to antibiotics and a high-fat (HF) diet, we ...

Abstract	The mechanisms by which the early-life microbiota protects against environmental factors that promote childhood obesity remain largely unknown. Using a mouse model in which young mice are simultaneously exposed to antibiotics and a high-fat (HF) diet, we show that Lactobacillus species, predominant members of the small intestine (SI) microbiota, regulate intestinal epithelial cells (IECs) to limit diet-induced obesity during early life. A Lactobacillus-derived metabolite, phenyllactic acid (PLA), protects against metabolic dysfunction caused by early-life exposure to antibiotics and a HF diet by increasing the abundance of peroxisome proliferator-activated receptor γ (PPAR-γ) in SI IECs. Therefore, PLA is a microbiota-derived metabolite that activates protective pathways in the small intestinal epithelium to regulate intestinal lipid metabolism and prevent antibiotic-associated obesity during early life.
MeSH term(s)	Humans ; Child ; Animals ; Mice ; Lipid Metabolism ; Pediatric Obesity ; Microbiota ; Diet, High-Fat/adverse effects ; Anti-Bacterial Agents ; Polyesters ; Mice, Inbred C57BL
Chemical Substances	Anti-Bacterial Agents ; Polyesters
Language	English
Publishing date	2023-10-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2278004-X
ISSN	1934-6069 ; 1931-3128
ISSN (online)	1934-6069
ISSN	1931-3128
DOI	10.1016/j.chom.2023.09.002
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Article ; Online: Iron acquisition by a commensal bacterium modifies host nutritional immunity during Salmonella infection.

Spiga, Luisella / Fansler, Ryan T / Perera, Yasiru R / Shealy, Nicolas G / Munneke, Matthew J / David, Holly E / Torres, Teresa P / Lemoff, Andrew / Ran, Xinchun / Richardson, Katrina L / Pudlo, Nicholas / Martens, Eric C / Folta-Stogniew, Ewa / Yang, Zhongyue J / Skaar, Eric P / Byndloss, Mariana X / Chazin, Walter J / Zhu, Wenhan

Cell host & microbe

2023 Volume 31, Issue 10, Page(s) 1639–1654.e10

Abstract: During intestinal inflammation, host nutritional immunity starves microbes of essential micronutrients, such as iron. Pathogens scavenge iron using siderophores, including enterobactin; however, this strategy is counteracted by host protein lipocalin-2, ... ...

Abstract	During intestinal inflammation, host nutritional immunity starves microbes of essential micronutrients, such as iron. Pathogens scavenge iron using siderophores, including enterobactin; however, this strategy is counteracted by host protein lipocalin-2, which sequesters iron-laden enterobactin. Although this iron competition occurs in the presence of gut bacteria, the roles of commensals in nutritional immunity involving iron remain unexplored. Here, we report that the gut commensal Bacteroides thetaiotaomicron acquires iron and sustains its resilience in the inflamed gut by utilizing siderophores produced by other bacteria, including Salmonella, via a secreted siderophore-binding lipoprotein XusB. Notably, XusB-bound enterobactin is less accessible to host sequestration by lipocalin-2 but can be "re-acquired" by Salmonella, allowing the pathogen to evade nutritional immunity. Because the host and pathogen have been the focus of studies of nutritional immunity, this work adds commensal iron metabolism as a previously unrecognized mechanism modulating the host-pathogen interactions and nutritional immunity.
MeSH term(s)	Humans ; Lipocalin-2/metabolism ; Siderophores/metabolism ; Enterobactin/metabolism ; Bacteria/metabolism ; Iron/metabolism ; Salmonella Infections
Chemical Substances	Lipocalin-2 ; Siderophores ; Enterobactin (28384-96-5) ; Iron (E1UOL152H7)
Language	English
Publishing date	2023-09-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	2278004-X
ISSN	1934-6069 ; 1931-3128
ISSN (online)	1934-6069
ISSN	1931-3128
DOI	10.1016/j.chom.2023.08.018
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Article ; Online: Salmonella enterica serovar Typhimurium uses anaerobic respiration to overcome propionate-mediated colonization resistance.

Shelton, Catherine D / Yoo, Woongjae / Shealy, Nicolas G / Torres, Teresa P / Zieba, Jacob K / Calcutt, M Wade / Foegeding, Nora J / Kim, Dajeong / Kim, Jinshil / Ryu, Sangryeol / Byndloss, Mariana X

Cell reports

2021 Volume 38, Issue 1, Page(s) 110180

Abstract: The gut microbiota benefits the host by limiting enteric pathogen expansion (colonization resistance), partially via the production of inhibitory metabolites. Propionate, a short-chain fatty acid produced by microbiota members, is proposed to mediate ... ...

Abstract	The gut microbiota benefits the host by limiting enteric pathogen expansion (colonization resistance), partially via the production of inhibitory metabolites. Propionate, a short-chain fatty acid produced by microbiota members, is proposed to mediate colonization resistance against Salmonella enterica serovar Typhimurium (S. Tm). Here, we show that S. Tm overcomes the inhibitory effects of propionate by using it as a carbon source for anaerobic respiration. We determine that propionate metabolism provides an inflammation-dependent colonization advantage to S. Tm during infection. Such benefit is abolished in the intestinal lumen of Salmonella-infected germ-free mice. Interestingly, S. Tm propionate-mediated intestinal expansion is restored when germ-free mice are monocolonized with Bacteroides thetaiotaomicron (B. theta), a prominent propionate producer in the gut, but not when mice are monocolonized with a propionate-production-deficient B. theta strain. Taken together, our results reveal a strategy used by S. Tm to mitigate colonization resistance by metabolizing microbiota-derived propionate.
MeSH term(s)	Anaerobiosis/physiology ; Animals ; Antibiosis/physiology ; Bacteroides thetaiotaomicron/genetics ; Bacteroides thetaiotaomicron/metabolism ; Female ; Gastrointestinal Microbiome/physiology ; Germ-Free Life ; Intestines/microbiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Knockout ; Nitrates/metabolism ; Propionates/metabolism ; Salmonella Infections, Animal/pathology ; Salmonella typhimurium/growth & development ; Salmonella typhimurium/metabolism
Chemical Substances	Nitrates ; Propionates
Language	English
Publishing date	2021-12-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2021.110180
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: High-fat diet-induced colonocyte dysfunction escalates microbiota-derived trimethylamine

Yoo, Woongjae / Zieba, Jacob K / Foegeding, Nora J / Torres, Teresa P / Shelton, Catherine D / Shealy, Nicolas G / Byndloss, Austin J / Cevallos, Stephanie A / Gertz, Erik / Tiffany, Connor R / Thomas, Julia D / Litvak, Yael / Nguyen, Henry / Olsan, Erin E / Bennett, Brian J / Rathmell, Jeffrey C / Major, Amy S / Bäumler, Andreas J / Byndloss, Mariana X

Science (New York, N.Y.)

2021 Volume 373, Issue 6556, Page(s) 813–818

Abstract: A Western-style, high-fat diet promotes cardiovascular disease, in part because it is rich in choline, which is converted to trimethylamine (TMA) by the gut microbiota. However, whether diet-induced changes in intestinal physiology can alter the ... ...

Abstract	A Western-style, high-fat diet promotes cardiovascular disease, in part because it is rich in choline, which is converted to trimethylamine (TMA) by the gut microbiota. However, whether diet-induced changes in intestinal physiology can alter the metabolic capacity of the microbiota remains unknown. Using a mouse model of diet-induced obesity, we show that chronic exposure to a high-fat diet escalates
MeSH term(s)	Animals ; Cell Hypoxia ; Choline/administration & dosage ; Choline/metabolism ; Colon/cytology ; Colon/physiology ; Diet, High-Fat ; Energy Metabolism ; Epithelial Cells/physiology ; Escherichia coli/genetics ; Escherichia coli/growth & development ; Escherichia coli/metabolism ; Feces/microbiology ; Gastrointestinal Microbiome ; Inflammation ; Intestinal Mucosa/metabolism ; Intestinal Mucosa/physiology ; Male ; Methylamines/blood ; Methylamines/metabolism ; Mice ; Mice, Inbred C57BL ; Mitochondria/metabolism ; Nitrates/metabolism ; Obesity ; Oxygen Consumption
Chemical Substances	Methylamines ; Nitrates ; trimethyloxamine (FLD0K1SJ1A) ; Choline (N91BDP6H0X)
Language	English
Publishing date	2021-08-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.aba3683
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Zs.MG 77: Show issues

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