ArticleJournal of the International AIDS Society2021
Condomless receptive anal intercourse is associated with markers of mucosal inflammation in a cohort of men who have sex with men in Atlanta, Georgia.
Article in Journal of the International AIDS Society, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 11 citations in OpenAlex.
- Variation in antiviral immunity and inflammation pathways precedes HIV-1 infection in a high-risk African cohort.The Journal of clinical investigation · 2026Article
- Douching Is Associated With Dysregulated Rectal Mucosal Immunity in Sexual Minority Men.The Journal of infectious diseases · 2026Article
- The Biosocial Microbiome: Gender Identity, Geography, and Mucosal Microbial Phenotypes.Research square · 2026Article
- Gut microbiome composition influences immunologic alterations in the blood and gut of HIV-positive and HIV-negative men who have sex with men.Frontiers in immunology · 2025Article
- The spatial biology of HIV infection.PLoS pathogens · 2025Review
- Nuclear Factor Kappa B p65: A Possible Biomarker for Persistent Inflammation in HIV-1 Infection?Cureus · 2024Review
- Sexual behavior is linked to changes in gut microbiome and systemic inflammation that lead to HIV-1 infection in men who have sex with men.Communications biology · 2024Article
- Pleasurable and problematic receptive anal intercourse and diseases of the colon, rectum and anus.Nature reviews. Gastroenterology & hepatology · 2024Review
- The effect of sexual behavior on HIV-1 seroconversion is mediated by the gut microbiome and proinflammatory cytokines.Research square · 2024Article
- Article
- A Summary of the Sixth International Workshop on Microbiome in HIV Pathogenesis, Prevention, and Treatment.AIDS research and human retroviruses · 2022Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
introductionWe previously showed that the rectal mucosal immune environment among men who have sex with men (MSM) engaging in condomless receptive anal intercourse (CRAI) is immunologically distinct from that of men who do not engage in anal intercourse (AI). Here, we further examined these differences with quantitative immunohistochemistry to better understand the geographic distribution of immune markers of interest.
methodsWe enrolled a cohort of MSM engaging in CRAI (n = 41) and men who do not engage in AI (n = 21) between October 2013 and April 2015. Participants were healthy, HIV-negative men aged 18-45 from the metro Atlanta area. We performed rectal mucosal sampling via rigid sigmoidoscopy during two study visits separated by a median of nine weeks and timed with sexual activity for MSM engaging in CRAI. We used standardized, automated immunohistochemistry and quantitative image analysis to investigate the rectal mucosal distribution of neutrophils (MPO), IL-17-producing cells (IL-17) and T
resultsRelative to the colonic crypt base, IL-17, FOXP3, and MPO expression increased towards the rectal lumen, while Ki67 decreased and E-cadherin was more uniformly distributed. Throughout the rectal mucosa distribution examined, MSM engaging in CRAI had higher mean lamina propria MPO expression (p = 0.04) and epithelial Ki67 (p = 0.04) compared to controls. There were no significant differences in IL-17, FOXP3 or E-cadherin expression. We found no significant associations of the five biomarkers with the global rectal microbiota composition or the individual taxa examined.
conclusionsUnderstanding the mucosal distribution of inflammatory mediators can enhance our knowledge of the earliest events in HIV transmission. Neutrophil enrichment and crypt epithelial cell proliferation likely represent sub-clinical inflammation in response to CRAI in the rectal mucosa of MSM, which could increase the risk for HIV acquisition. However, the contributory role of the microbiota in mucosal inflammation among MSM remains unclear. HIV prevention may be enhanced by interventions that reduce inflammation or capitalize on the presence of specific inflammatory mechanisms during HIV exposure.
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