Introduction: Pulmonary dysfunction following thermal injury with smoke mh! is frequently complicated by early infection. Early, smoke-induced changes in alveolar leukocyte number, composition and function may contribute to pulmonary sepsis and mortality. The purpose of this study was to evaluate the differential cytokine response of a fixed tissue (alveolar) macrophage population isolated from burn patients with/without smoke inhalation to an in vitro LPS challenge. .Methods: Sixteen patients with severe thermal injury requiring endotncheal intubation were studied. The diagnosis of inhalation injury was based on clinical history and bronchoscopy. All patients underwent bronchoscopic alveolar lavage (BAL) on the first (O/A) and third (72 hrs) day post injury. BAL leukocytes were assessed in vitro for cell number, composition, viability and responsiveness to LPS stimulation. Cell cultures were assayed at 24 hrs by EIA for production of TNFa and IL-6. Results: Seven patients had bronchoscopic evidence of inhalation injury. BAL of Bum/Inhalation (B/ln) patients yielded significantly more leukocytes O/A (8.42.2x10vs. 4.5±1.5×106 cells) with significantly fewer alveolar macrophages (51 vs. 85%) than Bum only (B/O). By 72 hrs, BAL cell recovery was similar (6.0±1.4×106 vs. 6.9±2.0×106 cells) but die proportion of alveolar macrophages diminished in both groups (38 vs. 51%). AU unstimulated cells produced detectable TNFα (O/A:135±41 vs. 133±16pg/ml) and (72hrs:173±49 vs. 516±305pg/ml). LPS stimulation enhanced TNFa production from all O/A cells, with B/In cells producing significantly more TNFα compared to B/O cells (1682±497 vs. 460±129pg/ml with 100ng/ml LPS). All cells isolated at 72 hrs had minimal TNFa response to LPS. All ceus produced detectable IL6, but unstimulated B/In cells produced significantly less IL-6 (O/A:87.4±69 vs. 719±456pg/ml) and (72hrs:430±176 vs. 1244±538pg/ml) than B/O. LPS stimulated IL-6 production from O/A cells was minimal. At 72 hrs, IL-6 response to LPS from both groups was significant compared to unstimulated cells, but no difference between groups was noted. B/In had a significantly higher mortality rate than B/O (42.8 vs. 11.1%). (MeantSEM; significance at p<0.05 between groups by Students t-test and ANOVA). Conclusions: Smoke inhalation may contribute to pulmonary morbidity by causing an early enhancement of LPS-stimulated TNFa production, a disproportionate reduction in fixed tissue alveolar macrophage populations and an increase in porymorphonuclear cells (PMN) within the alveoli.
|Original language||English (US)|
|Journal||Critical care medicine|
|Issue number||1 SUPPL.|
|State||Published - Dec 1 1998|
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine