Person:
Luevano, Jesus-Mario

Profile Picture

Email Address

AA Acceptance Date

Birth Date

Research Projects

Organizational Units

Job Title

Last Name

Luevano

First Name

Jesus-Mario

Name

Luevano, Jesus-Mario
Author's Publications: search.filters.isAuthorOfPublication.e55a5786-0c59-4be8-8922-b5b24745bbae

Search Results

Now showing 1 - 2 of 2
  • Thumbnail Image
    Publication
    HIV-associated changes in the enteric microbial community: potential role in loss of homeostasis and development of systemic inflammation
    (Lippincott Williams & Wilkins, 2017) Gootenberg, David; Paer, Jeffrey M.; Luevano, Jesus-Mario; Kwon, Douglas
    Purpose of review Despite HIV therapy advances, average life expectancy in HIV-infected individuals on effective treatment is significantly decreased relative to uninfected persons, largely because of increased incidence of inflammation-related diseases, such as cardiovascular disease and renal dysfunction. The enteric microbial community could potentially cause this inflammation, as HIV-driven destruction of gastrointestinal CD4+ T cells may disturb the microbiota–mucosal immune system balance, disrupting the stable gut microbiome and leading to further deleterious host outcomes. Recent findings Varied enteric microbiome changes have been reported during HIV infection, but unifying patterns have emerged. Community diversity is decreased, similar to pathologies such as inflammatory bowel disease, obesity, and Clostridium difficile infection. Many taxa frequently enriched in HIV-infected individuals, such as Enterobacteriaceae and Erysipelotrichaceae, have pathogenic potential, whereas depleted taxa, such as Bacteroidaceae and Ruminococcaceae, are more linked with anti-inflammatory properties and maintenance of gut homeostasis. The gut viral community in HIV has been found to contain a greater abundance of pathogenesis-associated Adenoviridae and Anelloviridae. These bacterial and viral changes correlate with increased systemic inflammatory markers, such as serum sCD14, sCD163, and IL-6. Summary Enteric microbial community changes may contribute to chronic HIV pathogenesis, but more investigation is necessary, especially in the developing world population with the greatest HIV burden (Video, Supplemental Digital Content 1, which includes the authors’ summary of the importance of the work).
  • No Thumbnail Available
    Publication
    HIV-Associated Changes in the Human Gut Microbiome and Impact on Disease Progression
    (2018-05-15) Luevano, Jesus-Mario
    Human immunodeficiency virus (HIV) infection is associated with increased intestinal translocation of microbial products, enteropathy, and alterations in gut bacterial communities. Whether this is the same in developed and developing nations, and if the status of a human host as an immunological controller affects disease progression remains unknown. We characterized the enteric bacterial microbiome in two geographical cohorts, Boston and Uganda, which included HIV-uninfected controls or HIV-infected subjects on anti-retroviral treated (ART) and individuals with chronic untreated disease that are either immunologically controlled or have progressive disease. In both of the cohorts, serum immune markers were measured as well as a collection of cohort and clinical metadata. Dietary information was collected for Boston patients. It was found that HIV infection was the predominant correlative factor for the Boston cohort, with significant shifts in the communities after HIV acquisition that were not ameliorated by ART. These changes included decrease of both richness and bacteria from the phyla Firmicutes, Bifidobacterium, and Bacteroidetes; with proportional expansion of the family Prevotellaceae. These changes correlated with serum markers of inflammation, but there was a dichotomy in the controller patients. Controllers had low levels of bacterially mediated inflammatory markers sCD14, MCP-1, and MIP-1 alpha/beta similar to healthy controls, while having markers of general inflammation, like sCD163 and IP-10, more similar to their infected counterparts. Diet and clinical cohort data were not found to be significant correlation factors in the Boston cohort. Our Ugandan cohort did not have the same significant shifts from HIV infection that were seen in the Boston cohort. All of Ugandan communities already had significant enrichment of Prevotella compared to the Boston patients, possibly driven by differences in geography, and agrarian versus westernized diets. The potential inflammatory nature of selected microbes enriched in either healthy or HIV infected communities were found not to be damaging to Caco2 colonic adenocarcinoma cells, by measure of their transepithelial resistance (TER), when co-cultured. This is in contrast to the presumed model that changes in community structure select for bacteria that are sufficient in inducing damage to the epithelial barrier and promoting bacterial product translocation. Moving towards a ‘two-hit’ model, when cells were cultured with bacteria and exposed to a chemical irritant, Prevotella copri, (enriched after HIV-infection) did not lower TER. Rather Prevotella performed better at mitigating damage from the chemical irritant than Bacteroides caccae did, a species enriched in HIV-negative controls. When predictive gene expression was assigned to bacterial communities the functional microbiome was found to shift with HIV infection. All of this suggests that the model for HIV induced changes in the enteric bacterial communities is complex. Although HIV infection does perturb the bacterial community, so that it resembles the Prevotella rich structure common in the developing world, this alone does not mean it is strictly pro-inflammatory. Rather, both HIV infection, whether immunologically or therapeutically controlled, and commensal bacterial changes influence each other to modify the physiologic changes seen in HIV disease progression.