Altered Host-Microbe Interaction in HIV: A Target for Intervention with Pro- and Prebiotics

Figures & data

FIGURE 1  Normal mucosal defenses and homeostasis: The commensal microbiota induces a state of non-responsiveness through interaction with dendritic cells (DC) and subsequent induction of the T-regulatory phenotype and secretion of IL-10 and TGF-β. There is a limited uptake of bacterial antigens, such as lipopolysaccharide (LPS), polysaccharide-A (PSA), and DNA, that induce intestinal defense systems, such as the excretion of β-defensin and secretory IgA.

TABLE 1  Evidence Implicating the Intestinal Microbiota and Epithelial Cell Barrier as a Factor in HIV Progression

• Aberrant intestinal microbiota among HIV patients with fewer lactobacilli and bifidobacteria, and higher numbers of pathogenic P. aeruginosa, and C. albicans present [62, 63]

• Antibiotics can temporarily reduce bacterial translocation in SIV infected macaques [48]

• Increased bacterial translocation among HIV progressors and those not effectively responding to ARV [48, 53]

• Enhanced epithelial inflammation and scarring of GALT among HIV progressors [40]

• Increased epithelial permeability with HIV at all stages of infection [41]

FIGURE 2  Potential benefits of probiotics and prebiotics in HIV-induced intestinal pathogenesis: HIV infection induces effects and positive feedback mechanisms that induce a loss of intestinal homeostasis and promote replication of the virus (triangles). Pro- and prebiotics may ameliorate the HIV-induced intestinal problems through effects on the microbiota and its metabolism, on various cells of the immune system (as represented by the arrow pointing at the sampling DC), and on intestinal epithelial cells.

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