The stress response and NO production in reprogrammed proinflammatory or antiinflammatory alveolar macrophages were studied after lipopolysaccharide treatment. Experiments with macrophages not containing HSP70 showed that lipopolysaccharide in a dose of 500 ng/ml induced stress response in cells with the proinflammatory phenotype (as distinct from an antiinflammatory phenotype). The stress response was not observed in HSP70-containing lipopolysaccharide-stimulated proinflammatory macrophages, but occurred in cells with antiinflammatory phenotype. Hence, the presence of HSP70 in alveolar macrophages results in the inversion of the phenomenon of reprogramming of the stress response. Independently on the phenotype, stimulation with lipopolysaccharide was accompanied by a 60-70% increase in NO production by macrophages not containing HSP70. However, NO production by HSP70-containing macrophages did not increase in response to lipopolysaccharide treatment. Our results indicate that reprogramming of the cell response in macrophages does not concern the system for NO synthesis. HSP70 prevents the lipopolysaccharide-induced activation of NO synthesis in alveolar macrophages.