Pathogen-Mediated Inhibition of Anorexia Promotes Host Survival and Transmission
Open accessAbstract
Sickness-induced anorexia is a conserved behavior induced during infections. Here, we report that an intestinal pathogen, Salmonella Typhimurium, inhibits anorexia by manipulating the gut-brain axis. Inhibition of inflammasome activation by the S. Typhimurium effector, SlrP, prevented anorexia caused by IL-1β-mediated signaling to the hypothalamus via the vagus nerve. Rather than compromising host defenses, pathogen-mediated inhibition of anorexia increased host survival. SlrP-mediated inhibition of anorexia prevented invasion and systemic infection by wild-type S. Typhimurium, reducing virulence while increasing transmission to new hosts, suggesting that there are trade-offs between transmission and virulence. These results clarify the complex and contextual role of anorexia in host-pathogen interactions and suggest that microbes have evolved mechanisms to modulate sickness-induced behaviors to promote health of their host and their transmission at the expense of virulence.
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SlrP also promotes survival of the host and microbial transmission to other hosts.
“It also promotes survival of the host, and from the microbial point of view microbial transmission to other hosts (212).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [212]
Salmonella leucine-rich repeat protein (SlrP) inhibits Salmonella virulence and the typical host anorexic response induced by the infection.
“An evidence for intestinal inflammasome activation and its effects on the brain comes from the discovery that Salmonella leucine-rich repeat protein (SlrP) inhibits Salmonella virulence and the typical host anorexic response induced by the infection (212).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [212]
Intestinal inflammasome activation by the microbiota might lead to the production of effector molecules which have an effect in the CNS via the vagus nerve.
“These data show that intestinal inflammasome activation by the microbiota might lead to the production of effector molecules which have an effect in the CNS via the vagus nerve (212).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [212]
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References 57 · Cited by 167
- Authors
- Rao, S., Schieber, A. M. P., O’Connor, C. P., Leblanc, M., Michel, D., & Ayres, J. S.
- Affiliations
- Salk Institute for Biological Studies (US)
- Corresponding author
- Ayres, Janelle S.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2017-01
- Volume
- 168
- Issue
- 3
- Pages
- 503-516.e12
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC5324724
- OpenAlex
- W2580150325
- Cited by
- 167
- References
- 57
- Citations by year
- 2026: 9 · 2025: 19 · 2024: 18 · 2023: 15 · 2022: 15 · 2021: 24 · 2020: 22 · 2019: 19 · 2018: 16 · 2017: 10
- FWCI
- 9.13
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (P30CA014195)
- National Institute of Allergy and Infectious Diseases (R01AI114929)
- Topics
- Life Sciences › Neuroscience › Neurology › Vagus Nerve Stimulation Research
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Agricultural and Biological Sciences › Food Science › Salmonella and Campylobacter epidemiology
- Keywords
- Salmonella typhimurium, gut-brain axis, inflammasome inhibition, IL-1β signaling, vagus nerve, hypothalamus, host survival, host-pathogen interaction, bacterial virulence
- MeSH terms
- Animals, Anorexia, Bacterial Proteins, Humans, Mice, Inbred C57BL, Neural Pathways, Salmonella Infections, Salmonella typhimurium, Specific Pathogen-Free Organisms, Virulence, Mice, Interleukin-1beta, Host-Pathogen Interactions, Inflammasomes
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