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Santos KT. Pharmacological contribution of early-lifetime exposure of mice to 1,2naphthoquinone (1,2-NQ) to increase pulmonary susceptibility of allergic response at a late stage of life [Master thesis]. São Paulo: Instituto de Ciências Biomédicas da Universidade de São Paulo; 2009. There is a close correlation between increasing pollutant emission and maternal immune responses, which seems to increase newborn susceptibility to asthma. However, little is known about the direct influence of pollutants such as 1,2-napththoquinone (1,2-NQ) in the immune system control of neonate. Thus, this study was designed to comparatively investigate whether exposure of neonates and adults mice to 1,2-NQ, a contaminant found in the diesel exhaust particles (PED), increases their susceptibility to allergic inflammation evoked by ovalbumin (OVA) and mechanisms possibly involved. Adults or neonate mice were nebulized with 1,2-NQ (100 nM; 10 mL) or corresponding vehicle ([PBS; 99,008%], Tween 80 and DMSO [both 0.001%]) over 3 days during 15 min. Following 24 h or eight weeks, adult or neonate mice were sensitized (10 μg/mL; 0,2 mL) and challenged with OVA (1%) and both the functional and inflammatory parameters were evaluated 24 h after the last OVA challenge. The allergic challenge in mice exposed to 1,2-NQ as neonates caused a potent influx of leukocytes (lymphocytes and eosinophils) in bronchoalveolar lavage, peripheral blood and increased eosinophil maturation in the bone marrow, without affecting airways hyperresponsiveness (Penh) compared with the allergic group. This response was correlated with increased presentation of splenic CD11c, mast cell activation and increased biosynthesis of inflammatory mediators in the lung (ex.: Th2 cytokines, INF-γ, LTB4 and IgE), independently of costimulatory molecules expression (CD86, CD80, CD40 and MHCII). In contrast, adult mice exposure to 1,2-NQ failed to significantly increase OVAinduced allergic response, Penh and inflammatory mediators production when compared to allergic group. We conclude that exposure to 1,2-NQ during neonatal period is critical to enhance susceptibility of asthma at a later stage of life, and that sensitization of lymphocytes, mast cell and increased expression of splenic CD11c and inflammatory mediators i.e. Th2 cytokines, LTB4 and IgE contribute to this effect.

Contribuição farmacológica do estudo da exposição de camundongos na fase neonatal ao poluente 1,2-naftoquinona (1,2-NQ) e sua repercussão na resposta inflamatória na fase adulta.