Oral N-acetyl-cysteome increases the production of anti HIV chemokines in peripheral blood mononuclear cells.
The C-C chemokines MIP-1alpha, MIP-1beta and RANTES are specific and powerful inhibitors of HIV infectivity. They appear to work by blocking the interaction of the virus with the receptor (CCR5). The latter is utilized as a coreceptor for cell penetration by macrophage-tropic (R5) HIV strains responsible for the majority of HIV transmissions. A natural high capability to release such chemokines has been proposed as a protection factor against HIV infection in exposed uninfected individuals. We report that oral administration of N-acetyl-cysteine (NAC) to healthy volunteers increases the capability of their peripheral blood mononuclear cells (PBMC) to release such anti HIV chemokines upon stimulation. The data reported may explain at least in part the mechanism of action of NAC as an anti HIV therapeutic agent: By potentiating chemokine production NAC may decrease susceptibility to infection.
Cavallini
L
L
Department of Biological Chemistry, C.N.R. Centro di Studio delle Biomembrane, University of Padova, Italy.
Alexandre
A
A
D000111:Acetylcysteine / Q000494:pharmacology*; D000284:Administration, Oral; D000328:Adult; D000998:Antiviral Agents / Q000494:pharmacology*; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5 / Q000378:metabolism; D018925:Chemokines / Q000378:metabolism*; D005260:Female; D005978:Glutathione / Q000378:metabolism; D006678:HIV / Q000276:immunology*; D006801:Humans; D066298:In Vitro Techniques; D007963:Leukocytes, Mononuclear / Q000187:drug effects* / Q000378:metabolism; D019402:Macrophage Inflammatory Proteins / Q000378:metabolism; D008297:Male
D000998:Antiviral Agents; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D018925:Chemokines; D019402:Macrophage Inflammatory Proteins; D005978:Glutathione; D000111:Acetylcysteine