EFFECT OF RIFAMPICIN AND ADRENAL STEROIDS ON HUMAN MACROPHAGES STIMULATED WITH Mycobacterium tuberculosis.

DÍAZ ARIANA ; IMHOFF MATILDE ; , MASSA ESTEFANÍA 1,3; , GALLUCCI GEORGINA; DIAB MAGDALENA ; BONGIOVANNI BETTINA ; DERIO MARISA ; DATTILIO LUCIANO; BAY MARÍA LUISA

Mar del Plata . Buenos Aires

Congreso; REUNIÓN CONJUNTA SAIC SAI&FAIC SAFIS 2022; 2022

Sociedad Argentina de Inmunología

Tuberculosis (TB) is a major health problem worldwide. The etiologic agent,Mycobacterium tuberculosis (Mtb) is transmitted by air and captured by lungmacrophages (Mf). Mf activation along with an efficient cellular immune response (IR)are required for Mtb elimination, which at the same time can mediate tissue damage. Weearly found that newly diagnosed TB patients showed an immune-endocrine imbalance:high plasma levels of pro- and anti-inflammatory mediators and cortisol (Gc), as well aslowered Dehydroepiandrosterone (DHEA) levels. During specific anti-TB treatment, theproinflammatory mediators and DHEA levels reached values like those found in healthycontrols. Rifampicin (R) is a potent antimicrobial agent and a major drug in TBtreatment. There is evidence that R also modulates the host IR, influencing lymphocytemigration, cytokine production, and phagocytosis. Accordingly, we analyzed the effectof R (15 µg/ml) on the proinflammatory response of Mf stimulated with Mtbi (irradiatedMtb), added or not with DHEA (10 -7 M) and/or cortisol (10 -6 M). All Mf cultures(adherent human THP-1 cells, activated with 30 ng/ml of phorbol-12-myristate-13-acetate -PMA- for 24hs) were stimulated and treated for 24 hrs. Culture supernatants ofMtbi-stimulated Mf had increased contents of IL-1β and IL-10, compared to non-stimulated Mf (p