Upregulated IL-32 Expression And Reduced Gut Short Chain Fatty Acid Caproic Acid in People Living With HIV With Subclinical Atherosclerosis.

However, these differences did not reach statistical significance except for the caproic acid (hexanoic acid), which was less abundant in the HIV+plaque+ group (p=0.049).

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By using this analysis in the HIV+ individuals, we observed that expression of IL-32D and IL-32θ, IL-18, VEGF-A and IFNβ remained significantly associated with coronary artery atherosclerosis independently of age, smoking or statin treatment (p=0.031, p=0.042, p=0.001, p=0.029 and p=0.046, respectively), whereas TRAIL, IL-1β and FLT3L showed borderline significance (p=0.052, p=0.055, and 0.059, respectively).

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While we did not observe systemic outlier samples, statistical analysis of three analytes (IL-1β, FGF-23, and FSH) became marginally significant, only in the HIV+ group (p=0.053, 0.068 and 0.085, Table 2 ).

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Since our data showed a highly significant potential role for IL-32 in atherogenesis, it was important to identify the underlying mechanisms by which IL-32 upregulation is sustained in ART-treated PLWH.

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