Immunocompetence of macrophages in rats exposed to Candida albicans infection and stress.

RODRIGUEZ GALAN MC; SOTOMAYOR CE; COSTAMAGNA ME; CABANILLAS AM; RENTERIA BS; MASINI-REPISO AM,; CORREA SG

AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY

AMER PHYSIOLOGICAL SOC

Año: 2003 vol. 284 p. 111 - 118

0363-6143

The integration of innate and adaptive immune responses is required for efficient control of Candida albicans. The present work aimed to assess, at the local site of the infection, the immu-nocompetence of macrophages in rats infected intraperitoneally with C. albicans and exposed simultaneously to stress during 3 days (CaS group). We studied the 1) ability to remove and kill C. albicans, 2) tumor necrosis factor-(TNF-alpha) release, 3) balance of the inducible enzymes NOsynthase (iNOS) and arginase, and 4) expression of interleukin (IL)-1betha and IL-1 receptor antagonist (ra) mRNA. Compared with only infected animals (Ca group), the number ofcolony-forming units was significantly higher in CaS rats (P <0.01), and the macrophage candidicidal activity was ~2.5-fold lower (P < 0.01). Release of TNF-alpha was diminishedin both unstimulated and heat-killed C. albicans restimulated macrophages of the CaS group (Ca vs. CaS, P <0.03 and P < 0.05, respectively). In Ca- and CaS-group rats, the rates for both the arginase activity and the NO synthesis were significantly enhanced. However, the stress exposuredownregulated the activity of both enzymes (CaS vs. Ca, P <0.05). After in vitro restimulation, the IL-1ra/IL-1betha ratio was significantly diminished in CaS-group rats (P <0.05). Our results indicate that a correlation exists between early impairment of macrophage function and stress exposure.