Cytokines and the pathogenesis of nosocomial pneumonia.
BACKGROUND
Nosocomial pneumonia (NP) in injured patients is a significant clinical problem. We hypothesize that the pathogenesis of NP in injured patients involves an imbalanced cytokine response within the alveolar airspace that may inhibit effector cell function.


METHODS
Proinflammatory (IL-8) and anti-inflammatory (IL-10) levels were measured in bronchoalveolar lavage (BAL) fluid from multitrauma patients on admission, 24, 48, and 72 hours post-injury and following lipopolysaccharide (LPS) induction of alveolar cells. Patients were compared based on IL-8 levels and the development of NP.


RESULTS
A high level of IL-8 on admission was associated with the development of NP. In addition, levels of IL-8 were significantly greater in NP-positive patients at all time points. The IL-10 levels decreased from admission values in NP-negative patients but increased in NP-positive patients. Furthermore, a high level of IL-10 ( > 120 pg/mL) at 72 hours post-injury was associated with the development of NP. Alveolar cells from NP-positive patients produced significantly more IL-10 in response to LPS than cells from NP-negative patients.


CONCLUSIONS
The pathogenesis of NP in injured patients involves an early and severe IL-8 process within the lung followed by an exaggerated IL-10 response that may inhibit effector cell function.
Muehlstedt
S G
SG
Department of Surgery, Hennepin County Medical Center, University of Minnesota Medical School, Minneapolis 55415, USA.
Richardson
C J
CJ
West
M A
MA
Lyte
M
M
Rodriguez
J L
JL
D000328:Adult; D000368:Aged; D003428:Cross Infection / Q000209:etiology*; D005260:Female; D006801:Humans; D016753:Interleukin-10 / Q000032:analysis / Q000502:physiology*; D016209:Interleukin-8 / Q000032:analysis / Q000502:physiology*; D008070:Lipopolysaccharides / Q000633:toxicity; D008297:Male; D008875:Middle Aged; D018410:Pneumonia, Bacterial / Q000209:etiology*
D016209:Interleukin-8; D008070:Lipopolysaccharides; D016753:Interleukin-10