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Cited by 104Gut microbiota and healthClostridium difficile and Clostridium perfringens researchProbiotics and Fermented Foods

Role of the gut microbiota in nutrient competition and protection against intestinal pathogen colonization

Open access
Horrocks, Victoria, King, Olivia G., Yip, Alexander Y. G., Marques, Inês Melo, McDonald, Julie A. K.·2023·Microbiology
DOI 10.1099/mic.0.001377PMC PMC10482380
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Abstract

The human gut microbiota can restrict the growth of pathogens to prevent them from colonizing the intestine (‘colonization resistance’). However, antibiotic treatment can kill members of the gut microbiota (‘gut commensals’) and reduce competition for nutrients, making these nutrients available to support the growth of pathogens. This disturbance can lead to the growth and expansion of pathogens within the intestine (including antibiotic-resistant pathogens), where these pathogens can exploit the absence of competitors and the nutrient-enriched gut environment. In this review, we discuss nutrient competition between the gut microbiota and pathogens. We also provide an overview of how nutrient competition can be harnessed to support the design of next-generation microbiome therapeutics to restrict the growth of pathogens and prevent the development of invasive infections.

AI snapshot

Written from the paper’s full text.

TL;DR

This review argues that gut commensals restrict intestinal pathogen colonization largely through nutrient competition, and that antibiotic-induced microbiota disruption creates nutrient-rich niches exploited by pathogens. It synthesizes evidence on nutrient niches, microbial metabolites, bile acids, and synthetic consortia to propose next-generation microbiome therapeutics.

Key findings

  • Healthy gut microbiota occupies nutrient niches and limits pathogen growth; antibiotic treatment reduces diversity and increases available nutrients. Commensal Enterobacteriaceae are typically 0.1–1 % relative abundance in the healthy gut, but increased from 2–34 % after 4 days of amoxicillin-clavulanic acid in one patient’s faecal microbiota.
  • Nutrient competition can be highly specific: commensal *E. coli* HS and Nissle 1917 together used all five mucus-associated sugars used by *E. coli* O157:H7 and restricted its growth, while individually they could not. *K. oxytoca* utilized 100 carbon sources versus 56 for *K. pneumoniae*, with overlap in 55 carbon sources.
  • Microbial metabolites contribute to colonization resistance: *Bifidobacterium longum* subsp. *infantis* administration reduced intestinal pH from 5.97 to 5.15, and FMT resolved *C. difficile*-associated diarrhoea in 81 % of patients versus 31 % with vancomycin alone. A systematic review found MDR pathogen decolonization ranged from 20–90 % after FMT versus 11–66 % for controls.
  • Synthetic consortia can restrict pathogens: six phylogenetically distinct gut commensal strains eradicated *C. difficile* colonization in mice; a 33-strain human stool consortium prevented systemic *S.* Typhimurium infection in antibiotic-treated mice and eradicated *C. difficile* in two patients. Fructose depletion by *Olsenella* restricted VRE, and depletion of *N*-acetylneuraminic acid and *N*-acetylglucosamine restricted *C. difficile* growth in vitro and in vivo.

Methods

  • Narrative review; no primary experiments or systematic search strategy are reported.
  • Evidence is synthesized from cited human, mouse, ex vivo, and in vitro studies on gut microbiota, nutrient competition, colonization resistance, and microbiome therapeutics.
  • Main analysis is a thematic synthesis of mechanisms and therapeutic strategies, including nutrient niche theory, SCFAs, bile metabolism, FMT, and defined microbial consortia.

Limitations

  • The paper states that greater knowledge is needed on nutrient utilization and preferences by pathogens and gut commensals, cross-feeding relationships, engraftment and persistence of therapeutics, and how different antibiotics affect the intestinal nutrient and metabolite landscape. It also notes that individual variation in baseline microbiota and antibiotic resistance profiles complicates therapeutic development.
  • Evident from the text: as a narrative review, it does not report systematic search criteria, inclusion/exclusion methods, or quantitative synthesis, so conclusions rely on heterogeneous cited studies.
  • The paper notes FMT is not risk-free, including transfer of opportunistic pathogens such as Shiga toxin-producing *E. coli* and enteropathogenic *E. coli*, which increases costs and reduces the donor pool.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1099/mic.0.001377

Cites

137 of 137 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 97 cited sources checked · 0 supported · 0 flagged

  • Premisecitation

    Despite considerable differences in taxonomic composition, there is significant overlap in the microbial functional genes present between individuals.

    “Despite these considerable differences, there is significant overlap in the microbial functional genes present between individuals [10, 11].”
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    The human gut microbiota can restrict the growth of pathogens to prevent them from colonizing the intestine (colonization resistance).

    “The human gut microbiota can restrict the growth of pathogens to prevent them from colonizing the intestine (‘colonization resistance’).”
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  • Premisecitation

    Antibiotic treatment can kill members of the gut microbiota and reduce competition for nutrients, making these nutrients available to support the growth of pathogens.

    “However, antibiotic treatment can kill members of the gut microbiota (‘gut commensals’) and reduce competition for nutrients, making these nutrients available to support the growth of pathogens.”
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  • Premisereasoning

    Antibiotic-induced disturbance can lead to the growth and expansion of pathogens within the intestine, including antibiotic-resistant pathogens.

    “This disturbance can lead to the growth and expansion of pathogens within the intestine (including antibiotic-resistant pathogens), where these pathogens can exploit the absence of competitors and the nutrient-enriched gut environment.”
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  • Premisecitation

    The taxonomic composition of the gut microbiota changes throughout the gastrointestinal tract according to nutrient availability, mucus structure, pH and oxygen availability.

    “The taxonomic composition of the gut microbiota changes throughout the gastrointestinal tract, according to nutrient availability, mucus structure, pH and oxygen availability [1–6].”
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    Premisecitation

    There is high inter-individual variation in the taxonomic composition of the gut microbiota, and no universal species are present in all healthy individuals.

    “There is high inter-individual variation in the taxonomic composition of the gut microbiota, and no universal species are present in all healthy individuals [10].”
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    Premisecitation

    Antibiotic treatment - especially treatment with broad-spectrum antibiotics - kills members of the gut microbiota and disrupts colonization resistance.

    “Antibiotic treatment – especially treatment with broad-spectrum antibiotics – kills members of the gut microbiota and disrupts colonization resistance (Fig. 1).”
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    Premisecitation

    Examples of indirect mechanisms of colonization resistance include interactions between the gut microbiota and the host immune response, changes in the gut microbiota that influence oxygen availability, modulation of the mucus layer by the gut microbiota, and promotion of cytokine release by the gut microbiota.

    “Indirect mechanisms of colonization resistance include interactions between the gut microbiota and the host immune response, changes in the gut microbiota that influence oxygen availability, modulation of the mucus layer by the gut microbiota, and promotion of cytokine release by the gut microbiota [34].”
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    Premisecitation

    Examples of direct mechanisms of colonization resistance include nutrient competition between gut commensals and pathogens, production of inhibitory metabolites by gut commensals, production of bacteriocins by gut commensals, and the presence of bacteriophages.

    “Examples of direct mechanisms of colonization resistance include nutrient competition between gut commensals and pathogens, production of inhibitory metabolites by gut commensals, production of bacteriocins by gut commensals, and the presence of bacteriophages [33, 34].”
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    Administration of Lactobacillus to antibiotic-treated mice increased faecal butyrate levels and decreased intestinal colonization by Klebsiella pneumoniae.

    “Administration of Lactobacillus to antibiotic-treated mice increased faecal butyrate levels and decreased intestinal colonization by Klebsiella pneumoniae [38].”
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    Interpretationreasoning

    A healthy gut microbiota promotes colonization resistance against C. difficile through metabolism of bile acids to both reduce primary bile acids, which promote C. difficile spore germination, and increase secondary bile acids, which inhibit C. difficile vegetative growth.

    “Therefore, a healthy gut microbiota promotes colonization resistance against C. difficile through metabolism of bile acids to both reduce primary bile acids, which promote C. difficile spore germination, and increase secondary bile acids, which inhibit C. difficile vegetative growth.”
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    Premisecitation

    Pathogens must compete with gut commensals for nutrients to colonize the intestine, and pathogens can more easily colonize an intestine with a low diversity gut microbiota that does not utilize all the available nutrients (e.g. following antibiotic treatment).

    “Pathogens must compete with gut commensals for nutrients to colonize the intestine, and pathogens can more easily colonize an intestine with a low diversity gut microbiota that does not utilize all the available nutrients (e.g. following antibiotic treatment).”
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    Premisecitation

    Each gut commensal strain has its own nutrient utilization ability and preference, and competition is high between bacteria with overlapping nutrient utilization abilities.

    “Each gut commensal strain has its own nutrient utilization ability and preference, and competition is high between bacteria with overlapping nutrient utilization abilities [64, 65].”
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    When butyrate is reduced with antibiotic treatment, oxygen availability increases, which promotes the growth of facultatively anaerobic pathogens.

    “When butyrate is reduced with antibiotic treatment oxygen availability increases, which promotes the growth of facultatively anaerobic pathogens [50].”
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    Premisecitation

    Bile salts play an important role in promoting the germination of C. difficile spores or the inhibition of vegetative C. difficile cells.

    “Bile salts play an important role in promoting the germination of C. difficile spores or the inhibition of vegetative C. difficile cells [51].”
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    Butyrate acts as an energy source for colonic epithelial cells, which can improve gut barrier integrity.

    “Butyrate acts as an energy source for colonic epithelial cells, which can improve gut barrier integrity [49].”
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    Premisecitation

    Administering SCFA-producing commensals such as Bifidobacterium longum subspecies infantis to infants reduces intestinal pH from 5.97 to 5.15 and decreased virulence factor gene abundance.

    “For example, administering SCFA-producing commensals such as Bifidobacterium longum subspecies infantis to infants reduces intestinal pH from 5.97 to 5.15 and decreased virulence factor gene abundance [41–43].”
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    Taurocholate promotes the germination of C. difficile spores, which leads to C. difficile colonization in the intestine.

    “Taurocholate promotes the germination of C. difficile spores, which leads to C. difficile colonization in the intestine [52].”
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    Interpretationreasoning

    If nutrients available in the antibiotic-treated gut microbiota are only partially depleted, then a microbiome therapeutic will be ineffective because the pathogen could switch to utilizing alternative available nutrients to support its growth.

    “If nutrients available in the antibiotic-treated gut microbiota are only partially depleted, then the microbiome therapeutic will be ineffective as the pathogen could switch to utilizing alternative available nutrients to support its growth.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S4 (based).

    Interpretationnone given

    Exogenous micro-organisms can only colonize the intestine if they can occupy an available nutrient niche.

    “Exogenous micro-organisms can only colonize the intestine if they can occupy an available nutrient niche.”
    Quote in the paperNot a substantial claim

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    The nutrient niche theory proposed that the composition of the gut microbiota is dictated by nutrient availability and that a micro-organism will only colonize the intestine if it can utilize one or more limiting nutrients with greater efficiency than its competitors.

    “The nutrient niche theory was first described by Rolf Freter in 1983 and proposed that the composition of the gut microbiota is dictated by nutrient availability. It also proposed that a micro-organism will only colonize the intestine if it can utilize one or more limiting nutrients with greater efficiency than its competitors [71].”
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    Interpretationreasoning

    The healthy gut microbiota prevents pathogen intestinal colonization through multiple mechanisms, including nutrient competition.

    “The healthy gut microbiota fully occupies these niches and prevents pathogen intestinal colonization through multiple mechanisms, including nutrient competition.”
    Quote in the paperSubstantial claim
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  • The paper relies on this without support.

    Findings from mouse models of antibiotic-treated gut microbiota and pathogen colonization can be extrapolated to humans.

    “In a mouse model, probiotic E. coli Nissle 1917 engineered to be deficient in nitrate-respiration were less efficient at restricting S. Typhimurium growth than strains, which could utilize nitrate, demonstrating the importance of nutrient competition in maintaining colonization resistance [96].”
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Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • The decrease in Enterococcus could potentially be attributed to carbon source depletion promoted by Bifidobacterium specialised human milk oligosaccharide utilisation in the human milk-fed gut environment, which may inhibit pathobiont colonisation and growth.

    “This decrease could potentially be attributed to the carbon source depletion promoted by Bifidobacterium specialised HMO utilisation in human milk-fed gut environment, which may inhibit pathobiont colonisation and growth39,40.”

    From Impact of early life antibiotic and probiotic treatment on gut microbiome and resistome of very-low-birth-weight preterm infants. (2025) · cites this paper as [40]

    Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Mucin is classified as both a dietary and a host substrate

    Minor

    Table 1 labels its listed polysaccharides as dietary and includes mucin, but the text explicitly identifies mucin as a host substrate.

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Cites

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Research works printed but not linked: 1

  1. 10.1038/srep15782 · DOI · Paper page

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Related

Authors
Horrocks, V., King, O. G., Yip, A. Y. G., Marques, I. M., & McDonald, J. A. K.
Affiliations
  • Imperial College London (GB)
  • Centre for Bacterial Resistance Biology, Department of Life Sciences, Imperial College London, London SW7 2AZ, UK
Corresponding author
McDonald, Julie A. K.
ORCID
Venue
Microbiology
Publisher
Microbiology Society
Published
2023-08-25
Volume
169
Issue
8
ISSN
  • 1350-0872 (ISSN-L)
  • 1465-2080
DOI
10.1099/mic.0.001377
PMC
PMC10482380
OpenAlex
W4385564664
Semantic Scholar
e00eef01437bca8e344216a8bd28b46d31fef9cf
Cited by
104
References
137
Citations by year
2026: 41 · 2025: 42 · 2024: 18 · 2023: 3
FWCI
2.74
Type
journal article
Language
en
Open access
Licence
Locations
  • Microbiology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Spiral (Imperial College London) (submittedVersion, other-oa)
Funders
Medical Research Council (MR/W025655/1)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
  • Health Sciences › Medicine › Infectious Diseases › Clostridium difficile and Clostridium perfringens research
  • Life Sciences › Agricultural and Biological Sciences › Food Science › Probiotics and Fermented Foods
Keywords
gut microbiota, colonization resistance, nutrient competition, enteric pathogens, antibiotic therapy, antibiotic resistance, commensal bacteria, microbiota-based therapy, invasive infections, pathogen colonization
MeSH terms
Gastrointestinal Microbiome, Nutrients, Anti-Bacterial Agents, Humans, Microbiota

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