Nitric oxide-dependent killing of Candida albicans by murine peritoneal cells during an experimental infection

• Published in: FEMS immunology and medical microbiology 1995-06, Vol.11 (3), p.157-162
• Main Authors: Rementería, Aitor, García-Tobalina, Roberto, Sevilla, María Jesús
• Format: Article
• Language: English
• Subjects: Animals; Arginine - analogs & derivatives; Arginine - pharmacology; Biological and medical sciences; Candida albicans; Candida albicans - immunology; Candidacidal activity; Candidiasis - immunology; Candidiasis - physiopathology; Experimental mycoses and models; Female; In Vitro Techniques; Infectious diseases; Medical sciences; Mice; Murine peritoneal cell; Mycoses; Nitric oxide; Nitric Oxide - biosynthesis; Nitric Oxide - physiology; Nitric Oxide Synthase - antagonists & inhibitors; omega-N-Methylarginine; Peritoneal Cavity - cytology; Phagocytes - drug effects; Phagocytes - physiology; Phagocytic activity; Phagocytosis - physiology; Reactive Oxygen Species - metabolism
• ISSN: 0928-8244; 1574-695X
• DOI: 10.1016/0928-8244(95)00019-4

The phagocytic and candidacidal activities of the peritoneal cells of Candida albicans-infected mice were studied 20 days following experimental infection. Both activities were enhanced during infection. The production of nitric oxide (NO) by the peritoneal cells of infected mice was determined, and an increase in the nitrite concentration in supernatants of peritoneal cell cultures was detected. The period of NO production by the peritoneal cells coincided partially with the period of enhanced C. albicans killing. The inhibition of NO synthesis by N-monomethyl- l-arginine was concomitant with inhibition of candidacidal activity. We conclude that NO systhesis is the primary candidacidal mechanism of the murine peritoneal cells activated by C. albicans infection.