Smoke inhalation enhances early alveolar leukocyte responsiveness to endotoxin.
ABSTRACT Pulmonary dysfunction after smoke inhalation and thermal injury is associated with excessive morbidity and mortality. The purpose of this study was to evaluate alveolar leukocyte function after thermal injury and smoke inhalation.
Twenty-one patients with thermal injury only (n = 8); thermal injury and smoke inhalation injury (n = 8); and nonburned controls (n = 5) were assessed by means of bronchoscopically directed lavage (bronchoalveolar lavage [BAL]) on the first and fourth days postinjury. BAL-isolated pulmonary leukocytes were assessed for number, composition, viability, and production of tumor necrosis factor (TNF)alpha, interleukin (IL)-8, and IL-6 in response to 100 ng/mL of lipopolysaccharide (LPS) (mean +/- SEM; significance at p < 0.05).
Six of eight Smoke patients had gross evidence of lung injury. On day 1, Smoke and Burn BAL isolates yielded greater cell counts than Control (10.6 vs. 4.5 vs. 2.4 x 10(6)/mL). Smoke macrophages on day 1 produced more TNFalpha (1.2 vs. 0.2 ng/mL), IL-6 (8.0 vs. 1.9 ng/mL), and IL-8 (85 vs. 32 ng/mL) after LPS stimulation compared with respective unstimulated (0 ng/mL of LPS) day-1 Smoke cells. LPS-stimulated Burn cells on day 1 produced more IL-8 (150 vs. 62 ng/mL) but not TNFalpha (0.4 vs. 0.25 ng/mL) or IL-6 (1.8 vs. 0.69 ng/mL), when compared with respective unstimulated Burn cells. By day 4, LPS-stimulated Smoke and Burn cells produced significantly more TNFalpha (Smoke, 0.41 vs. 0.16 ng/mL; Burn, 0.87 vs. 0.51 ng/mL) and IL-6 (Smoke, 2.5 vs. 0.47 ng/mL; Burn, 4.1 vs. 1.47 ng/mL), but not IL-8 (Smoke, 51.1 vs. 51.1 ng/mL; Burn, 54.4 vs. 55.6 ng/mL), compared with respective unstimulated day-4 cells.
Smoke inhalation induces a massive influx of alveolar leukocytes that are primed for an early, enhanced LPS-activated cytokine response compared with alveolar leukocytes isolated after burn injury alone or normal controls.
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ABSTRACT: Acute lung injury (ALI) and its more severe form acute respiratory distress syndrome (ARDS) can result from both direct and indirect pulmonary damage caused by trauma and shock. In the course of ALI/ARDS, mediators released from resident cells, such as alveolar macrophages, may act as chemoattractants for invading cells and stimulate local cells to build up a pro-inflammatory micro-milieu. Depending on the trauma setting, the role of alveolar macrophages is differentially defined. This review focuses on alveolar macrophage function after blunt chest trauma, ischemia/reperfusion, hemorrhagic shock and thermal burns.Shock (Augusta, Ga.) 03/2014; · 2.87 Impact Factor
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ABSTRACT: Purpose While obesity is associated with increased mortality and decreased functional outcomes in adult burn patients, the ramifications of larger than average body size in the pediatric burn population are less well understood. The present study examines whether obesity was associated with poor outcomes following pediatric burn injuries. Methods Thermal injury data for patients ≤ 18 years of age admitted to a Level III burn center over ten years (n = 536) was analyzed. Obesity was defined as ≥ 95th percentile of weight for height according to the WHO growth charts (< 2 years of age) or BMI for age according to the CDC growth charts (2–18 years of age). Outcomes were compared between thermally injured obese (n = 154) and non-obese (n = 382) children. All data was collected in accordance with IRB regulations. Results Obese and non-obese thermally-injured children did not differ in TBSA, percentage of full thickness burn, or overall mortality. However, these groups were significantly different with respect to age (obese = 7.16 ± 0.46 years, non-obese = 9.38 ± 0.32 years, p < 0.001) and days requiring mechanical ventilation (obese = 4.89 ± 1.3 days, non-obese = 2.67 ± 0.49 days, p < 0.05). For thermally injured children admitted to the BICU without inhalation injury (n = 175); the obese (n = 46) and non-obese (n = 129) did not differ significantly with respect to age, TBSA, percentage of full thickness burn or other outcome measures. However, significant differences between these groups were noted for ICU LOS (obese = 18.59 ± 5.18 days, non-obese = 9.51 ± 1.82 days, p < 0.05) and number of days requiring mechanical ventilation (obese = 11.65 ± 3.91 days, non-obese = 3.92 ± 0.85 days, p < 0.05). Conclusion These data show thermally-injured obese pediatric patients required longer and more intensive medical support in the form of BICU care and respiratory intervention. Counter to findings in adult populations, differences in mortality were not observed. Collectively, these findings suggest obesity as a risk factor for increased morbidity in the pediatric burn population.Journal of Pediatric Surgery 03/2014; 49(3):469–473. · 1.31 Impact Factor
- Frontiers in Bioscience 01/2009; Volume(14):4618. · 4.25 Impact Factor