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Background: Many health issues prevalent in African American (AA) populations are associated with chronic inflammation and related health conditions, including autoimmune diseases, infectious diseases, neurologic disorders, metabolic syndromes, and others. The current study aims to understand plasma microbiome translocation as a potential trigger for chronic inflammation. Methods: In this study, 16 Caucasian American (CA) and 22 African American (AA) healthy individuals were recruited. Microbial DNA was isolated from the plasma samples and sequenced via microbial 16S rRNA V3-4 sequencing. The plasma levels of 33 cytokines and chemokines were evaluated. The proinflammatory microbiomes were verified using human THP-1 cells in vitro. Results: The plasma levels of IL-6, IL-15, MIP-1α, MIP-1β, and MIP-3α were higher in the AA people, whereas IL-1α and IL-27 were elevated in the CA people. The plasma microbiomes exhibited eight bacterial genera/phyla differentially enriched in the CA and AA people. Given the critical role of IL-6 in chronic inflammation and associated diseases, we identified five bacteria genera significantly associated with IL-6. The abundance of Actinomyces was positively correlated with the plasma IL-6 level (r = 0.41, p = 0.01), while the abundance of Kurthia (r = −0.34, p = 0.04), Noviherbaspirillum (r = −0.34, p = 0.04), Candidatus Protochlamydia (r = −0.36, p = 0.03), and Reyranella (r = −0.39, p = 0.02) was negatively correlated with this. Finally, the THP-1 cells treated with heat-killed bacteria produced higher levels of IL-6 in vitro in response to the Actinomyces species compared to the species in the genus either uncorrelated or negatively correlated with IL-6. Conclusions: This is the first study to report potential blood microbiome translocation as a driver for persistently elevated IL-6 levels in the periphery in healthy AA versus CA people. Understanding the plasma microbiome linked to the IL-6 levels in people with different racial backgrounds is essential to unraveling the therapeutic approaches to improve precision medicine. [ABSTRACT FROM AUTHOR]

Autoantibodies binding on CD4+ T cells may mediate CD4+ T cell death, and prevent CD4+ T cell recovery in aviremic HIV‐infected patients under ART. Although effective antiretroviral therapy (ART) suppresses HIV viral replication, prevents AIDS‐related complications, and prolongs life, a proportion of patients fails to restore the patients' CD4+ T cell number to the level of healthy individuals. Increased mortality and morbidity have been observed in these patients. In the current study, we have investigated the role of auto‐IgGs in CD4+ T cell apoptosis and recovery in a cross‐sectional study. All HIV+ subjects were on viral‐suppressive ART treatment with a different degree of CD4+ T cell reconstitution. Total auto‐IgG binding on CD4+ T cell surfaces and its associated apoptosis and CD4+ T cell recovery were analyzed by flow cytometry ex vivo. Total IgGs from plasma were tested for their binding capacities to CD4+ T cell surfaces and their mediation to CD4+ T cell death through NK cell cytotoxicity in vitro. HIV+ subjects had increased surface binding of auto‐IgGs on CD4+ T cells compared with healthy controls, and IgG binding was associated with elevated CD4+ T cell apoptosis in HIV+ subjects but not in healthy controls. Plasma IgGs from HIV+ subjects bound to CD4+ T cells and induced cell apoptosis through NK cytotoxicity in vitro. Soluble CD4 (sCD4) preincubation prevented NK cell‐mediated CD4+ T cell death. Our results suggest that plasma autoantibodies may play a role in some HIV+ patients with poor CD4+ T cell recovery under viral‐suppressive ART. [ABSTRACT FROM AUTHOR]