Abstract
Macrophages play an essential role not only in the defense against the infection, but are involved in many various pathological processes. They take an important part e.g. in the development of hypoxic pulmonary hypertension (HPH).
The production of reactive oxygen species (ROS) by macrophages causes the pulmonary tissue damage, which seems to play a key role in this process. This paper is focused on the NADPH-oxidase derived ROS production in alveolar macrophages and ways of its modification.
NADPH-oxidase is activated via two different pathways by many stimulators. The role of the trigger can play, besides others, integrins, molecules mediating the adherence of cells.
To test a role of adherence, we compared ROS production (measured as the amount of released hydrogen peroxide by the luminoldependent chemiluminescence (LDCL)) in alveolar and peritoneal macrophages. The adherence itself triggered significantly the H2O2 production only in the alveolar macrophages.
Thus we suppose that the adherence is recognised as the pathological signal only in the alveolar macrophages and it can modify macrophages response to further stimuli.