{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T19:49:01Z","timestamp":1792180141808,"version":"4.4.0"},"reference-count":208,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T00:00:00Z","timestamp":1783987200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Nutr."],"abstract":"<jats:p>\n                    Damage to the mucosal layer of the gut is a central feature of chronic inflammatory diseases, often resulting in gut dysbiosis, microbial imbalances, and dysregulated immunometabolism. Gut dysfunction significantly impacts human health, disrupting metabolic, cardiovascular, and neurological systems, and leading to metabolic syndrome. Here, we discuss two clinical entities that are apparently unrelated but actually share similar alterations to gut mucosal barrier integrity: inflammatory bowel disease (IBD) and human immunodeficiency virus (HIV). We use the particular cases of pediatric IBD and nonhuman primate models of HIV infection to compare and contrast the impact of these diseases on gut integrity and microbiome composition. We also explore potential therapies, focusing on dietary interventions. Both HIV infection and IBD cause gut barrier disruption, but via different mechanisms. HIV rapidly depletes mucosal CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells (especially Th17 cells), weakening epithelial defenses, leading to a loss of tight junctions (\u201cleaky gut\u201d), microbial translocation, and systemic inflammation. In IBD (Crohn\u2019s disease and ulcerative colitis), chronic immune attacks on the gut lining produce ulcers and tight-junction defects. These ulcerations trigger immune-cell infiltration and markedly increase permeability. In both conditions, impaired mucus and epithelial integrity result in higher circulating lipopolysaccharides (LPS), macrophage activation, and systemic inflammation. HIV and IBD also induce distinct yet overlapping dysbioses. HIV infection is associated with markedly reduced bacterial diversity and an overgrowth of potentially inflammatory taxa (e.g., Proteobacteria, Prevotella). Similarly, IBD patients have low diversity and loss of beneficial Firmicutes (notably\n                    <jats:italic>Faecalibacterium prausnitzii<\/jats:italic>\n                    ) with relative\n                    <jats:italic>Proteobacteria<\/jats:italic>\n                    overabundance. In both diseases, the gut flora shifts away from fiber-fermenting commensals to \u201cpathobionts,\u201d fueling local inflammation. While the therapeutic potential of targeting metabolic products is widely explored, there is also a push towards discovering nondrug solutions, particularly through diet and nutrition. We present the effects of micronutrient intake, feeding mechanisms (exclusive enteral nutrition), and different diets (high fiber, Mediterranean, high fat) on disease progression and cellular metabolism. As a low-intervention approach, nutrition has enormous potential to improve human health by reducing inflammation and associated metabolic disturbances. Finally, we emphasize the capabilities of using animal models to elucidate the complexities of disease mechanics in IBD and HIV.\n                  <\/jats:p>","DOI":"10.3389\/fnut.2026.1878885","type":"journal-article","created":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T05:38:19Z","timestamp":1784007499000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Gut feelings and sweet teeth: nutritional solutions to the gut damage in inflammatory bowel disease and HIV infection"],"prefix":"10.3389","volume":"13","author":[{"given":"Anna","family":"Labiner","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, School of Medicine, University of Pittsburgh","place":["Pittsburgh, PA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena-Lia","family":"Spoiala","sequence":"additional","affiliation":[{"name":"Grigore T. Popa University of Medicine and Pharmacy","place":["Iasi, Romania"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cristian","family":"Apetrei","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, School of Medicine, University of Pittsburgh","place":["Pittsburgh, PA, United States"]},{"name":"Department of Infectious Diseases and Microbiology, School of Public Health, University of Pittsburgh","place":["Pittsburgh, PA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura Mihaela","family":"Trandafir","sequence":"additional","affiliation":[{"name":"Grigore T. Popa University of Medicine and Pharmacy","place":["Iasi, Romania"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ivona","family":"Pandrea","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases and Microbiology, School of Public Health, University of Pittsburgh","place":["Pittsburgh, PA, United States"]},{"name":"Division of Experimental Pathology, Department of Pathology, Department of Medicine, School of Medicine, University of Pittsburgh","place":["Pittsburgh, PA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,7,14]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","first-page":"1822","DOI":"10.1038\/s41591-019-0675-0","article-title":"Chronic inflammation in the etiology of disease across the life span","volume":"25","author":"Furman","year":"2019","journal-title":"Nat 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