Brenchley and colleagues demonstrated that microbial translocation and immune activation were higher among HAART-naïve than those on HAART [24].
On the other hand, Brenchley and others suggested that microbial translocation and plasma endotoxemia are a cause of immune activation in HIV[24].
Our results argue in favor of a link between microbial translocation and systemic immune activation [1], [3], and suggest that LPS-induced Mo activation is associated with HIV disease progression.
Another possible reason for eventual disease progression is a breach in the gut-blood barrier, leading to microbial translocation and subsequent immune hyperactivation, as described in acute chronic infection [36].
Given the relationship between microbial translocation and CD4+ reconstitution, we asked whether HIV-infected patients with ongoing microbial translocation despite virologically effective HAART, maintain a polymicrobic flora translocating in peripheral blood possibly with an imbalanced ratio of harmless indigenous organisms to pathogenic species.
These results identify distinct alterations in the HIV plasma lipidome linked to markers of inflammation, microbial translocation, and hepatic function.
Spearman correlations were used to examine relationships between metabolites and markers of inflammation (IFN-α, IL-6, IL2RA, and sCD14), microbial translocation (LPS and LBP), and hepatic function (total bilirubin, bilirubin (E,E), bilirubin (Z,Z), and albumin), and liver enzymes (alanine transaminase (ALT), aspartate transaminase (AST), and alkaline phosphatase (ALP))(p<0.05, FDR≤0.1).
Next, we examined correlations between these lipid subsets and markers of inflammation (IFN-α, IL-6, IL-2RA, and sCD14), microbial translocation (LPS, and LBP), hepatic function (bilirubin and albumin), and liver enzymes (ALT, AST, and ALP).
Factors that predict of poor immune reconstitution include a lower CD4 nadir [6], [7], older age [8], increased immune activation [9], [10], altered T cell homeostasis [7], [11], [12], markers of microbial translocation [13], and HIV co-receptor usage [14].
Blood was collected for markers of microbial translocation, inflammation, and collagen kinetics.
Distinct clusters of altered lipids correlated with markers of inflammation (interferon-α and interleukin-6), microbial translocation (lipopolysaccharide (LPS) and LPS-binding protein), and hepatic function (bilirubin) (p<0.05).
