Abstract
Expression of type I and II interferon (IFN) was evaluated in gut-associated lymphoid tissue (GALT) and peripheral blood mononuclear cells (PBMCs) of HIV-1-positive patients on long-term, suppressive, antiretroviral therapy before and after probiotic supplementation. IFNα subtypes and IFNβ were expressed at higher levels in GALT compared to PBMC, whereas an opposite trend of expression was recorded for IFNγ. An increase of IFNα6, IFNα10, IFNα14, IFNα17, and IFNα21 and a decrease of IFNγ were observed in both anatomical sites after probiotic supplementation.
Highlights
A strong relationship between type I interferon (IFN) response and disease progression in chronic HIV-1 and simian immunodeficiency virus (SIV) infection exists [1]
Four major points emerged from our current analysis of type I/II IFN response in gut-associated lymphoid tissue (GALT) and peripheral blood mononuclear cells (PBMCs) of HIV-1-infected patients before and after probiotic treatment: (1) all IFNα subtypes and IFNβ are more strongly expressed in GALT than in PBMC whereas IFNγ exhibits an opposite trend; (2) IFNα subtype expression signature in GALT is different from the signature in PBMC; (3) levels of the IFNα subtypes and their signature significantly change after probiotic supplementation; and (4) probiotic supplementation is associated with a decrease of the IFNγ levels
The very high endogenous expression of all IFNα/β subtypes in GALT could be sustained by the chronic stimulation of pattern recognition receptors by intestinal bacteria ligands which subsequently drive the production of type I IFN [6]
Summary
A strong relationship between type I interferon (IFN) response and disease progression in chronic HIV-1 and simian immunodeficiency virus (SIV) infection exists [1]. IFNα was recently identified as the predominant type I IFN expressed in plasma during untreated, chronic HIV-1 infection [2]. A recent comprehensive direct study of IFNα subtype expression in HIV-1 infection and of the type I IFN signature in specific anatomical sites, such as the gastrointestinal tract, showed a compartmentalized IFN-I response during chronic untreated HIV-1 infection, with IFNβ being more predominant in the gut. In this regard, it is not completely clear whether constitutive type I IFN production in the intestine is driven by commensal microbial signals and/or modulated by dietary, probiotic, and prebiotic interventions. The protective effects of commensal and probiotic bacteria in the intestine have been shown to be mediated, in part, by the induction of type I IFN, and, more importantly, IFNAR1−/− mice have increased susceptibility to dextran sodium sulfate-induced acute colitis [5, 6]
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