| Abstract: | Summary In normal conditions, alveolar macorphage (AM) is the main cell that respond against to bacteria that reach lower airways.
However, if the microbial inoculum is too high or too virulent to be stopped by AM alone, these cells recruit polymorphonuclear
neutrophils (PMN) into the alveoli from the vascular compartment. Cytokines, such as tumor necrosis factor-alpha (TNF-α), interleukin-1-beta (IL-1β), interleukin-6 (IL-6), and interleukin-8 (IL-8), secreted by the AM are able to attract PMN enhanced for phagocytosis are
ready to destroy the invading pathogens. However, excessive cytokine production has deleterious effects, with a systemic inflammatory
response (sepsis) that can lead to multiorganic failure and death. Other cytokines like interleukin-10 (IL-10) balance this
response attenuating several inflammatory mechanisms. The inflammatory lung response in pneumonia has been well studied in
animals and more recently in humans using bronchoalveolar lavage to measure some inflammatory mediators (TNF-α, IL-1β, IL-6, IL-8). From these studies, it seems that first, the inflammatory response to pneumonia is compartmentalized for most
cytokines (in contrast to ARDS), except for IL-6 which is a general marker of inflammation. On the other hand, C-Reactive-Protein
is an acute-phase protein synthesized by the liver through the stimuli of IL-6 that may be also an easy to measure marker
of inflammation directly related to IL-6; second, some of these cytokines may be useful as prognostic markers; third, there
is no clear relationship between the local lung bacterial burden and the intensity of the inflammatory response; fourth, the
administration of G-CSF is a promising therapeutic approach still under clinical investigation. In the future the therapeutic
goal in severe pneumonia will probably be to find the exact point at which inflammation is beneficial but not deleterious.
The measurement of the inflammatory response could serve for this purpose.
Received: 20 August 1997 Accepted: 2 December 1997 |
