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

Horrocks, Victoria; King, Olivia; Marques, Isabela G.; McDonald, Julie A. K.

doi:10.1099/mic.0.001377

Cited by 18 publications

(9 citation statements)

References 134 publications

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“…6D). Cumulatively these results suggest that metabolic competition is the mechanism by which the probiotic cocktail suppressed C. difficile growth, which is consistent with the emerging consensus in the field 9,43,45 . Finally, we found that certain probiotic strains were more or less likely to engraft in an individual (Fig.…”

Section: Resultssupporting

confidence: 85%

PersonalizedClostridioides difficileengraftment risk prediction and probiotic therapy assessment in the human gut

Carr

Baliga

Diener

et al. 2023

Preprint

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Clostridioides difficile colonizes up to 30-40% of community-dwelling adults without causing disease. C. difficile infections (CDIs) are the leading cause of antibiotic-associated diarrhea in the U.S. and typically develop in individuals following disruption of the gut microbiota due to antibiotic or chemotherapy treatments. Further treatment of CDI with antibiotics is not always effective and can lead to antibiotic resistance and recurrent infections (rCDI). The most effective treatment for rCDI is the reestablishment of an intact microbiota via fecal microbiota transplants (FMTs). However, the success of FMTs has been difficult to generalize because the microbial interactions that prevent engraftment and facilitate the successful clearance of C. difficile are still only partially understood. Here we show how microbial community-scale metabolic models (MCMMs) accurately predicted known instances of C. difficile colonization susceptibility or resistance. MCMMs provide detailed mechanistic insights into the ecological interactions that govern C. difficile engraftment, like cross-feeding or competition involving metabolites like succinate, trehalose, and ornithine, which differ from person to person. Indeed, three distinct C. difficile metabolic niches emerge from our MCMMs, two associated with positive growth rates and one that represents non-growth, which are consistently observed across 14,862 individuals from four independent cohorts. Finally, we show how MCMMs can predict personalized engraftment and C. difficile growth suppression for a probiotic cocktail (VE303) designed to replace FMTs for the treatment rCDI. Overall, this powerful modeling approach predicts personalized C. difficile engraftment risk and can be leveraged to assess probiotic treatment efficacy. MCMMs could be extended to better understand personalized engraftment of other opportunistic bacterial pathogens, beneficial probiotic organisms, or more complex microbial consortia.

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Section: Resultssupporting

confidence: 85%

PersonalizedClostridioides difficileengraftment risk prediction and probiotic therapy assessment in the human gut

Carr

Baliga

Diener

et al. 2023

Preprint

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“…29 On the other hand, numerous commensal mucin-degrading bacteria, such as Fusobacterium, Prevotella, and Streptococcus, can stabilize the TJ barrier, eg, regulating the expression of ZO-1, occludin, claudin-1, and E-cadherin. [116][117][118] Importantly, the sinonasal epithelium acts not only as a passive barrier but also actively coordinates both innate and adaptive responses through pathogen-recognition receptors (PRRs), such as Toll-like receptors (TLRs), N-formyl peptide receptors (FPRs), and Taste Receptor Family 2 receptors (T2Rs). 12 It should be emphasized that the function of PPRs is far beyond pathogen recognition.…”

Section: Dovepressmentioning

confidence: 99%

Remodeling of Paranasal Sinuses Mucosa Functions in Response to Biofilm-Induced Inflammation

Kaliniak,

Fiedoruk,

Spałek

et al. 2024

JIR

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Rhinosinusitis (RS) is an acute (ARS) or chronic (CRS) inflammatory disease of the nasal and paranasal sinus mucosa. CRS is a heterogeneous condition characterized by distinct inflammatory patterns (endotypes) and phenotypes associated with the presence (CRSwNP) or absence (CRSsNP) of nasal polyps. Mucosal barrier and mucociliary clearance dysfunction, inflammatory cell infiltration, mucus hypersecretion, and tissue remodeling are the hallmarks of CRS. However, the underlying factors, their priority, and the mechanisms of inflammatory responses remain unclear. Several hypotheses have been proposed that link CRS etiology and pathogenesis with host (eg, "immune barrier") and exogenous factors (eg, bacterial/fungal pathogens, dysbiotic microbiota/biofilms, or staphylococcal superantigens). The abnormal interplay between these factors is likely central to the pathophysiology of CRS by triggering compensatory immune responses. Here, we discuss the role of the sinonasal microbiota in CRS and its biofilms in the context of mucosal zinc (Zn) deficiency, serving as a possible unifying link between five host and "bacterial" hypotheses of CRS that lead to sinus mucosa remodeling. To date, no clear correlation between sinonasal microbiota and CRS has been established. However, the predominance of Corynebacteria and Staphylococci and their interspecies relationships likely play a vital role in the formation of the CRS-associated microbiota. Zn-mediated "nutritional immunity", exerted via calprotectin, alongside the dysregulation of Zn-dependent cellular processes, could be a crucial microbiota-shaping factor in CRS. Similar to cystic fibrosis (CF), the role of SPLUNC1-mediated regulation of mucus volume and pH in CRS has been considered. We complement the biofilms' "mechanistic" and "mucin" hypotheses behind CRS pathogenesis with the "structural" one -associated with bacterial "corncob" structures. Finally, microbiota restoration approaches for CRS prevention and treatment are reviewed, including pre-and probiotics, as well as Nasal Microbiota Transplantation (NMT).

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“…The composition and activity of the gut microbiota affect host health by causing changes in metabolic activity or changes in local distribution [ 22 ]. For instance, certain symbiotic bacteria, such as Bifidobacterium, can prevent colonization of pathogenic bacteria by reducing the intestinal pH [ 23 ]. Also, with the recent enhanced understanding of the important role of the gut microbiome, there are researches on the relationship of host inflammation response and the pathogenesis of ocular diseases [ 24 ].…”

Section: Introductionmentioning

confidence: 99%

Consumption of Limosilactobacillus fermentum Inhibits Corneal Damage and Inflammation in Dry Eye Disease Mouse Model through Regulating the Gut Microbiome

Lee,

Gwon,

Shim

et al. 2024

IJMS

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The present study investigated the effect of orally administered Limosilactobacillus fermentum HY7302 (HY7302) on the relationship between ocular tissue and the microbiome in a corneal injury dry eye mouse model. Specifically, 0.1% benzalkonium chloride (BAC) was applied to the ocular surface for 14 days to induce corneal injury in male Balb/c mice. During the BAC treatment period, HY7302 (1 × 108 CFU/kg/day or 1 × 109 CFU/kg/day) or an omega-3 positive control (400 mg/kg/day) were administered orally (n = eight/group). To examine the signaling pathways affected by the HY7302 treatment, the in vitro effects of HY7302 on the tight junctions and the inflammatory response were investigated in the mouse colon epithelial cell line, CMT-93. BAC exposure decreased tear production, induced ocular inflammation and corneal epithelial detachment, and altered the gut microbiota. However, oral administration of HY7302 restored tear secretion and decreased corneal epithelial detachment in BAC-treated corneal injury mice. Further, HY7302 alleviated corneal inflammation via modulation of matrix metalloproteinase-9 (MMP-9) expression and affeted alterations in gut microbiota composition. These findings suggest that the gut–eye axis interaction between gut microbiota and corneal tissue affects disease severity in corneal injury, and that the alteration of the microbiota by HY7302 could improve eye health by regulating the inflammatory response.

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

Cited by 18 publications

References 134 publications

PersonalizedClostridioides difficileengraftment risk prediction and probiotic therapy assessment in the human gut

PersonalizedClostridioides difficileengraftment risk prediction and probiotic therapy assessment in the human gut

Remodeling of Paranasal Sinuses Mucosa Functions in Response to Biofilm-Induced Inflammation

Consumption of Limosilactobacillus fermentum Inhibits Corneal Damage and Inflammation in Dry Eye Disease Mouse Model through Regulating the Gut Microbiome

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