Bcl-2 in LPS- and allergen-induced hyperplastic mucous cells in airway epithelia of Brown Norway rats

Environmental toxins, infection, and allergens lead to a transient mucous c ell hyperplasia (MCH) in airway epithelia; however, the mechanisms for redu cing mucous cell numbers during recovery are largely unknown. This study in vestigated Bcl-2 expression in mucous cells induced by a neutrophilic or eo sinophilic inflammatory response. Brown Norway rats intratracheally instill ed with lipopolysaccharide (LPS) showed an inflammatory response characteri zed primarily by neutrophils. Secreted mucin was increased fourfold at 1 da y, and the number of mucous cells was increased fivefold 2, 3, and 4 days p ost-LPS instillation compared with those in noninstilled rats. None of the mucous cells in non- or saline-instilled control animals expressed Bcl-2, w hereas 20-30% of mucous cells were Bcl-2 positive 1 and 2 days post-LPS ins tillation. Brown Norway rats immunized and challenged with ovalbumin (OVA) for 2, 4, and 6 days showed an inflammatory response characterized primaril y by eosinophils. Secreted mucin increased fivefold, and mucous cell number increased fivefold after 4 and 6 days of OVA exposure compared with water- immunized control rats challenged with OVA aerosols. Approximately 10-25% o f mucous cells were Bcl-2 positive in OVA-immunized and -challenged rats. T hese data demonstrate Bcl-2 expression in hyperplastic mucous cells of Brow n Norway rats regardless of the type of inflammatory response and indicate that apoptotic mechanisms may be involved in the resolution of MCHs.