Abstract
Neutrophils which are isolated in the lung adhere to endothelial cells due to chemotactic factors, and release various proteases, superoxide anions and prostanoids in inflammatory processes. However, this host defense mechanism can cause tissue damage. Excessive adherent neutrophils are not always derived from lung injury. We have previously reported that an increase in cell density in human neutrophils attenuates superoxide anion generation by cell to cell communication (autoregulation). Autoregulation of the protein kinase c stimulator, phorbol myristate acetate, and also of the cell membrane receptor stimulator, N-formyl-methionyl-leucyl-phenyl-alanine was observed. The autoregulation was not related to the presence of extracellular Ca2+ not to a change of [Ca2+]i induced by stimulants.
These results suggest that neutrophils accumulated in the lung tissue have a built-in defense mechanism induced by membrane to membrane contact of neutrophils, which protects tissues from an excessive inflammatory response.
