Vaccine-enhanced competition permits rational bacterial strain replacement in the gut.
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| Title: | Vaccine-enhanced competition permits rational bacterial strain replacement in the gut. |
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| Authors: | Lentsch, Verena, Woller, Aurore, Rocker, Andrea, Aslani, Selma, Moresi, Claudia, Ruoho, Niina, Larsson, Louise, Fattinger, Stefan A., Wenner, Nicolas, Barazzone, Elisa Cappio, Hardt, Wolf-Dietrich, Loverdo, Claude, Diard, Médéric, Slack, Emma |
| Source: | Science. 4/4/2025, Vol. 388 Issue 6742, p74-81. 8p. |
| Subjects: | Pathogenic bacteria, Oral vaccines, Escherichia coli, Salmonella, Homeostasis |
| Abstract: | Colonization of the intestinal lumen precedes invasive infection for a wide range of enteropathogenic and opportunistic pathogenic bacteria. We show that combining oral vaccination with engineered or selected niche-competitor strains permits pathogen exclusion and strain replacement in the mouse gut lumen. This approach can be applied either prophylactically to prevent invasion of nontyphoidal Salmonella strains, or therapeutically to displace an established Escherichia coli. Both intact adaptive immunity and metabolic niche competition are necessary for efficient vaccine-enhanced competition. Our findings imply that mucosal antibodies have evolved to work in the context of gut microbial ecology by influencing the outcome of competition. This has broad implications for the elimination of pathogenic and antibiotic-resistant bacterial reservoirs and for rational microbiota engineering. Editor's summary: The gut has essential microbial assemblages that need conservation during treatment to maintain homeostasis, but they can also be manipulated to good effect to exclude pathogens. Whole-cell inactivated oral vaccines are safe and stimulate high-affinity immunoglobulin A responses, but alone they may not eliminate infection. Lentsch et al. recognized that such host responses put specific bacterial pathogens at a competitive disadvantage compared with more benign bacteria occupying the same metabolic niche. After oral vaccination of mice, the authors found that a benign niche competitor, which can be supplied as a probiotic supplement, could outgrow and replace or exclude pathogenic variants consistently and permanently without provoking inflammation. —Caroline Ash [ABSTRACT FROM AUTHOR] |
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| Database: | Psychology and Behavioral Sciences Collection |
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| Abstract: | Colonization of the intestinal lumen precedes invasive infection for a wide range of enteropathogenic and opportunistic pathogenic bacteria. We show that combining oral vaccination with engineered or selected niche-competitor strains permits pathogen exclusion and strain replacement in the mouse gut lumen. This approach can be applied either prophylactically to prevent invasion of nontyphoidal Salmonella strains, or therapeutically to displace an established Escherichia coli. Both intact adaptive immunity and metabolic niche competition are necessary for efficient vaccine-enhanced competition. Our findings imply that mucosal antibodies have evolved to work in the context of gut microbial ecology by influencing the outcome of competition. This has broad implications for the elimination of pathogenic and antibiotic-resistant bacterial reservoirs and for rational microbiota engineering. Editor's summary: The gut has essential microbial assemblages that need conservation during treatment to maintain homeostasis, but they can also be manipulated to good effect to exclude pathogens. Whole-cell inactivated oral vaccines are safe and stimulate high-affinity immunoglobulin A responses, but alone they may not eliminate infection. Lentsch et al. recognized that such host responses put specific bacterial pathogens at a competitive disadvantage compared with more benign bacteria occupying the same metabolic niche. After oral vaccination of mice, the authors found that a benign niche competitor, which can be supplied as a probiotic supplement, could outgrow and replace or exclude pathogenic variants consistently and permanently without provoking inflammation. —Caroline Ash [ABSTRACT FROM AUTHOR] |
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| ISSN: | 00368075 |
| DOI: | 10.1126/science.adp5011 |
