title: Bcl-2 in LPS- and allergen-induced hyperplastic mucous cells in airway epithelia of Brown Norway rats.
abstract: Environmental toxins, infection, and allergens lead to a transient mucous cell hyperplasia (MCH) in airway epithelia; however, the mechanisms for reducing mucous cell numbers during recovery are largely unknown. This study investigated Bcl-2 expression in mucous cells induced by a neutrophilic or eosinophilic inflammatory response. Brown Norway rats intratracheally instilled with lipopolysaccharide (LPS) showed an inflammatory response characterized primarily by neutrophils. Secreted mucin was increased fourfold at 1 day, and the number of mucous cells was increased fivefold 2, 3, and 4 days post-LPS instillation compared with those in noninstilled rats. None of the mucous cells in non- or saline-instilled control animals expressed Bcl-2, whereas 20-30% of mucous cells were Bcl-2 positive 1 and 2 days post-LPS instillation. Brown Norway rats immunized and challenged with ovalbumin (OVA) for 2, 4, and 6 days showed an inflammatory response characterized primarily 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% of mucous cells were Bcl-2 positive in OVA-immunized and -challenged rats. These data demonstrate Bcl-2 expression in hyperplastic mucous cells of Brown Norway rats regardless of the type of inflammatory response and indicate that apoptotic mechanisms may be involved in the resolution of MCHs.
authors.affiliation: Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87185, USA. ytesfaig@lrri.org
authors.forename: Y
authors.initials: Y
authors.lastname: Tesfaigzi
authors.forename: M J
authors.initials: MJ
authors.lastname: Fischer
authors.forename: A J
authors.initials: AJ
authors.lastname: Martin
authors.forename: J
authors.initials: J
authors.lastname: Seagrave
mesh_terms: D000336:Aerosols; D000485:Allergens / Q000276:immunology / Q000494:pharmacology; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000276:immunology; D004804:Eosinophils / Q000276:immunology; D006965:Hyperplasia; D008070:Lipopolysaccharides / Q000276:immunology / Q000494:pharmacology; D008297:Male; D009092:Mucous Membrane / Q000737:chemistry / Q000166:cytology / Q000276:immunology; D009093:Mucus / Q000276:immunology / Q000378:metabolism; D009504:Neutrophils / Q000276:immunology; D010047:Ovalbumin / Q000276:immunology / Q000494:pharmacology; D011014:Pneumonia / Q000139:chemically induced / Q000473:pathology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000032:analysis*; D051381:Rats; D011914:Rats, Inbred BN; D020545:Respiratory Mucosa / Q000737:chemistry* / Q000166:cytology* / Q000276:immunology; D012965:Sodium Chloride / Q000494:pharmacology
chemical_list: D000336:Aerosols; D000485:Allergens; D008070:Lipopolysaccharides; D019253:Proto-Oncogene Proteins c-bcl-2; D012965:Sodium Chloride; D010047:Ovalbumin