[Local cellular response to stress of the lower lung]

The cell populations in the alveoli are exposed to the environment and react differently to each type of challenge (mineral particles, toxic gases, infections, antigenic substances. . .). Amongst the best studied of these irritant factors is tobacco smoke which in the long term leads to a number of changes both in the distribution of alveolar cells and also their function and morphology. Amongst acute and sub-acute pathogens, bacterial infections produce a rapid poly-morpho-nuclear neutrophilia and then a lymphocytosis; oxygen and oxidising agents in general lead to a neutrophilia which amplifies the pulmonary parenchymal changes related to the release of toxic metabolites of oxygen. The inhalation of antigenic substances also disturbs the behaviour of alveolar cells: activation of macrophages in the presence of allergy in those sensitized to IgE and immediate attraction of neutrophils preceding a T lymphocyte alveolitis in hypersensitivity pneumonia. It is possible to categorise several patterns of reaction in intra-pulmonary cells when challenged by some insult, a direct cytotoxic action, the accumulation of inflammatory cells and immunological competence corresponding to the concept of "a neutrophil alveolitis" or a "T cell alveolitis" with the development of emphysematous lesions. An understanding of the cellular make-up present in the alveoli when reacting to an external pathogen enables a better approach to the pathophysiological mechanisms in question.