Abstract:
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.
journal_name
Surgeryjournal_title
Surgeryauthors
Muehlstedt SG,Richardson CJ,West MA,Lyte M,Rodriguez JLdoi
10.1067/msy.2001.117105subject
Has Abstractpub_date
2001-10-01 00:00:00pages
602-9; discussion 609-11issue
4eissn
0039-6060issn
1532-7361pii
S0039-6060(01)25951-0journal_volume
130pub_type
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