Last but not least our ROFA also contained smaller particles that could induce lung lesions. Our study was done considering the same time lag after exposure, as previously reported in the literature (Laks et al., 2008, Mazzoli-Rocha et al., 2008, Rhoden et al., 2004 and Wegesser et al., 2009). The dose of ROFA utilized in this study was about 2.5 times smaller than the average daily exposure to PM in many cities such as São Paulo, where our ROFA was collected. Buparlisib In spite of this, after a single exposure to ROFA, we observed a pronounced infiltration of PMN cells with an increased fraction of collapsed air

spaces (Table 1). These alterations in cellularity and morphometry were associated selleck kinase inhibitor with an impairment of lung mechanics similar to that observed after exposure to other particulate matter (Laks et al., 2008, Mazzoli-Rocha et al., 2008 and Riedel et

al., 2006). Decays in respiratory function and histology similar to those produced by ROFA were observed in the chronic allergic inflammation model induced by ovalbumin (Fig. 1 and Table 1). It is known that ovalbumin sensitization followed by an ovalbumin challenge can induce an experimental condition that mimics asthma in many aspects, but not all (Kucharewicz et al., 2008). We found that ovalbumin increased pulmonary resistances, as expressed by Rinit (central), Rdiff (peripheral) and Rtot (central and peripheral), and elastance (Fig. 1), as previously Cyclin-dependent kinase 3 reported (Xisto et al., 2005). Other authors also found increased total pulmonary resistance using different methods (Hessel et al., 1995 and Wagers et al., 2002). It is accepted that both central and peripheral airways are inflamed, as well as lung tissue (Bousquet et al., 2000). The inflammatory

process results from a complex interaction between inflammatory mediators and cells (Kay, 2005). In this study, the animals sensitized and challenged with ovalbumin presented an increased number of PNM cells (Table 1). Additionally, mast cells potentially modulate the levels of airway inflammation and remodeling (Broide, 2008). Studies on airway remodeling in mast cell-deficient mice chronically challenged with allergen reveal that mast cells mediate chronic airway inflammation as well as remodeling features (Yu et al., 2006). We observed an increased proliferation of mast cell in animals with chronic allergic inflammation (Table 1) as well as an increased bronchoconstriction (Fig. 3B, insert) index (Table 1). This bronchoconstriction most probably responds for the increased pulmonary resistance, expressed in this study as Rinit (central airways) and Rtot (central and peripheral resistances) (Fig. 1). In summary, these findings suggest that acute ROFA exposure or chronic OVA can independently impair pulmonary mechanical properties and yield lung inflammation.