Mast cells (M.C) were identified over one century ago. They have been implicated in allergic, as well as various fibrotic processes. (Jr Am Acad of Derm 1990;23:615) Pulmonary Fibrosis (PF) induced by Bleomycin and other agents appears to be modulated by M.C(Am Rev Resp Dis 1984;130:797). Our laboratory has previously shown an association between M.C number and indices of Pulmonary Fibrosis induced by hyperoxic exposure in newborn mice (Ped Research 1994;35:343A). The purpose of this investigation was to directly test the hypothesis that M.C. deficiency reduces or protects against Hyperoxic Pulmonary Fibrosis (HPF). Adult mice heterozygous for the Wv allele were bred. One fourth of their offspring were homozygous and thus mast cell deficient. These mast cell deficient mice (MCD) served as the experimental group for this study, while offspring from breeding normal mice served as control (C). Both groups were exposed to either 60% FiO2 (O2) or room air (RA) under controlled temperature and barometric pressure. At 30days the lungs were prepared for histological examination, determination of collagen (CL) and hydroxyproline (OHPR) content. Data are expressed as X± (SD). NA= not applicable, n.s= not significant a=P< 0.01 Control RA vs O2, b=p< 0.01 MCD RA vs MCD O2, c=p<0.01 Control RA vs MCD RA, d=p<0.001 Control O2 vs MCD O2. These results directly implicate Mast Cells as an important effector cell in Hyperoxia induced pulmonary fibrosis. We speculate that MC products may in part mediate the pulmonary fibrosis response to oxygen. Table

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