Role of surfactant protein a and its oxidation in the susceptibility to experimental pneumonia

Surfactant protein A (SP-A) plays a host-defense function in the lung, increasing bacterial phagocytosis. Tropospheric ozone is one of the factors of anthropogenic air pollution. SP-A oxidation in vitro reduces its phagocytic activity. The purpose of this work was to study the influence of SP-A blocking (by elimination of SP-A gene in SP-A (-/-) mice or by SP-A oxidation) on susceptibility of male and female mice to experimental pneumonia after ozone exposure. Wild type С57BL/6J and SP-A knockout male and female Известия Самарского научного центра Российской академии наук, т. 12, № 1(7), 2010 1772 mice were used. Animals were first exposed to ozone (or air, as a control), and then infected intratracheally with K. pneumoniaе bacteria (ATCC 43816). Mouse survival after pneumonia was analyzed during 14 days, and in vivo phagocytosis was assessed after 1 h followed by infection. Also, using wild type mice, the level of SP-A oxidation was analyzed after 1 h followed by injection of PBS (as a sham control). Results showed that: 1) ozone exposure reduced both survival of SP-A (-/-) mice and in vivo phagocytosis level; females were more affected than males, and SP-A (-/-) mice were affected more than wild type mice; 2) ozone exposure increased SP-A oxidation in BAL; SP-A oxidation level was higher in females compared to males. Thus, these results demonstrated that blocking of SP-A function in SP-A (-/-) mice or reducing of functional activity of SP-A due to its oxidation by ozone increases susceptibility of mice to pneumonia, and in both cases females are more affected then males.