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Updated: Aug 8, 2025
Chronic Salmonella Infection Induced Intestinal Fibrosis
Published on: September 22, 2019
Experimental bacterial dysbiosis with consequent immune alterations increase intrarectal SIV acquisition
Alexandra M Ortiz1, Phillip J Baker1, Charlotte A Langner1
1Barrier Immunity Section, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Abstract:
Variations in the composition of the intestinal bacterial microbiome correlate with acquisition of some sexually transmitted pathogens. To experimentally assess the contribution of intestinal dysbiosis to rectal lentiviral acquisition, we induce dysbiosis in rhesus macaques (RMs) with the antibiotic vancomycin prior to repeated low-dose intrarectal challenge with simian immunodeficiency virus (SIV) SIVmac239X. Vancomycin administration reduces T helper 17 (TH17) and TH22 frequencies, increases expression of host bacterial sensors and antibacterial peptides, and increases numbers of transmitted-founder (T/F) variants detected upon SIV acquisition. We observe that SIV acquisition does not correlate with measures of dysbiosis but rather associates with perturbations in the host antimicrobial program. These findings establish a functional association between the intestinal microbiome and susceptibility to lentiviral acquisition across the rectal epithelial barrier.
Insights
Intestinal microbiome changes impact rectal lentiviral acquisition. Antibiotic-induced gut dysbiosis in macaques altered immune responses, increasing susceptibility to simian immunodeficiency virus (SIV) infection.
Area of Science:
- Microbiology
- Immunology
- Virology
Background:
- Intestinal microbiome composition is linked to susceptibility to certain sexually transmitted pathogens.
- Understanding the role of intestinal dysbiosis in rectal lentiviral acquisition is crucial for developing prevention strategies.
Purpose of the Study:
- To experimentally assess how intestinal dysbiosis influences rectal lentiviral acquisition.
- To investigate the relationship between antibiotic-induced gut dysbiosis and simian immunodeficiency virus (SIV) infection in rhesus macaques.
Main Methods:
- Induction of intestinal dysbiosis in rhesus macaques using the antibiotic vancomycin.
- Repeated low-dose intrarectal challenge with simian immunodeficiency virus (SIV) SIVmac239X.
- Analysis of immune cell frequencies (T helper 17 and T helper 22), host bacterial sensor expression, and transmitted-founder (T/F) viral variants.
Main Results:
- Vancomycin treatment reduced T helper 17 (TH17) and T helper 22 (TH22) cell frequencies.
- Increased expression of host bacterial sensors and antibacterial peptides was observed.
- SIV acquisition correlated with perturbations in the host antimicrobial program, not directly with measures of dysbiosis.
Conclusions:
- Intestinal dysbiosis, induced by vancomycin, influences host immune responses and susceptibility to lentiviral acquisition.
- The study establishes a functional link between the intestinal microbiome and rectal epithelial barrier susceptibility to lentiviral infection.
- Perturbations in the host antimicrobial program, rather than dysbiosis itself, are associated with increased SIV acquisition risk.
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