Important note: Information in this article was accurate in 2000. The state of the art may have changed since the publication date.
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Abstr Gen Meet Am Soc Microbiol. 1999 May 30-Jun 3;99:305 (abstract no. F-48). Unique Identifier : AIDSLINE AIDS/20712144
Rivera J; Mukherjee J; Weiss L; Casadevall A; Albert Einstine Coll. of Med., Bronx, NY.
Abstract: Nitric oxide (NO) is important for defense against various pathogens, including Cryptococcus neoformans. In vitro, Fc receptor activation elicits NO production. This study evaluated the susceptibility of iNOS deficient mice (iNOS-/- ) to C. neoformans infection and efficacy of passive mAb administration in intratracheal (IT) infection. iNOS-/- and the wildtype (WT) mice were infected IT with 1 x 10(6) yeast cells. MAb 2H1 (IgGI), which binds capsular polysaccharide, was administered 24h prior to infection. The severity of cryptococcal infection was assessed by measurement of survival, lung colony forming units (CFUs) and degree of inflammation in the lung. mAb administration polonged survival in WT mice but not iNOS-/- mice. In the absence of mAb, infected iNOS-/- and WT mice do not exhibit significant differences with respect to survival. In the absence of mAb, there was moe intense inflammation in iNOS-/- mice relative to WT mice. MAb administration significantly decreased CFUs in iNOS-/- mice, but this did not result in prolonged survival. No differences were noted in the phagocytosis of C. neoformans by alveolar macrophages from iNOS-/- and WT mice in the presence and absence of mAb 2H1. In summary, (i) iNOS-/- mice are more susceptible to C. neoformans infection; (ii) passive antibody administration has little or no efficacy for iNOS-/- mice survival; (iii) C. neoformans infection results in more intense inflammatory responses in the lungs of iNOS-/- mice. These results suggest that antibody efficacy in mice requires NO and support a role for NO in the regulation of pulmonary inflammation.
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