Differential expression of stress proteins in nonhuman primate lung and conducting airway after ozone exposure

The presence of seven stress proteins including various heat shock proteins [27-kDa (HSP27), 60-kDa (HSP60), 70-kDa (HSP70) and its constitutive form HSC70, and 90-kDa (HSP90) HSPs] and two glucose-regulated proteins [75-kDa (GRP75) and 78-kDa (GRP78) GRPs] in ozone-exposed lungs of nonhuman primate s and in cultured tracheobronchial epithelial cells was examined immunohist ochemically by various monoclonal antibodies. Heat treatment (42 degrees C) resulted in increased HSP70, HSP60, and HSP27 and slightly increased HSC70 and GRP75 but no increase in GRP78 in primary cultures of monkey tracheobr onchial epithelial cells. Ozone exposure did not elevate the expression of these HSPs and GRPs. All of these HSPs including HSP90, which was undetecta ble in vitro, were suppressed in vivo in monkey respiratory epithelial cell s after ozone exposure. Both GRP75 and GRP78 were very low in control cells , and ozone exposure in vivo significantly elevated these proteins. These r esults suggest that the stress mechanism exerted on pulmonary epithelial ce lls by ozone is quite different from that induced by heat. Furthermore, dif ferences between in vitro and in vivo with regard to activation of HSPs and GRPs suggest a secondary mechanism in vivo, perhaps related to inflammator y response after ozone exposure.