The following is a summary of “Resistance to Prostaglandin E2 Promotes Monocyte Activation During Chronic HIV Infection,” published in the February 2023 issue of Infectious Diseases by Garcia, et al.
When HIV infection is chronic, monocyte activation is a major contributor to inflammation. Tumor necrosis factor-α (TNF-α) generation by monocytes is known to be inhibited by prostaglandin E2 (PGE2), which is known to have anti-inflammatory properties. The impact of PGE2 on monocyte activation in chronic HIV infection and the mechanisms by which PGE2 modifies their inflammatory hallmark were the subjects of the study.
Researchers matched healthy, uninfected individuals with a group of people with HIV (PWH). Monocyte activation, plasma levels of PGE2, and the susceptibility of monocytes to PGE2-mediated inhibitory effects were all compared.
In PWH, compared to uninfected people, they discovered elevated plasma levels of PGE2 and an activated phenotype in circulating monocytes. When compared to uninfected controls, PGE2 concentrations in PWH were 10 times higher than those necessary to inhibit 50% of the production of TNF-α by lipopolysaccharide-stimulated monocytes. This indicated that PWH monocytes exhibited significant resistance to the inhibitory effects mediated by PGE2. In addition, PWH monocytes showed a substantial rise in the expression of phosphodiesterase 4B, a regulator of PGE2 activity.
The inflammatory character of circulating monocytes in PWH may be partially or entirely explained by resistance to the inhibitory effects mediated by PGE2.
Reference: academic.oup.com/jid/article-abstract/227/3/423/6884250?redirectedFrom=fulltext
