Augmented Effect of Hyperoxia and Tumour Necrosis Factor-α on Leukosequestration and Pro-inflammatory Cytokines Release in Rat Airways

合併暴露於高氧與腫瘤壞死因子對嗜中性白血球之聚集與腫瘤壞死因子和介白質-1β釋放的影響

余志騰(Chih-Teng Yu) ； 唐家駿(Chia-Chun Tang) ； 黃國雄(Kuo-Hsiung Huang) ； 王圳華(Chun-Hua Wang) ； 劉劍英(Chien-Ying Liu) ； 郭漢彬(Han-Pin Kuo) ； 林鴻銓(Horng-Chyuan Lin)

《胸腔醫學》 17卷4期 (2002/12) Pp. 354-363

摘要

Background: Although oxygen is an important adjunct to therapy in hypoxemic respiratory failure from diverse causes, exposure to high oxygen tension may contribute to exacerbate acute lung injury as a result of increased production of reactive oxygen metabolites. Moreover, tumour necrosis factor-α (TNF-α) is though to be implicated in the many pulmonary and airway diseases, especially in neutrophil mediated lung injury.
Objective: To investigate the augmented effects of hyperoxia on TNF-α - induced leukosequestration and pro-inflammatory cytokines release in rat airways. A prospective, randomized, controlled animal study was conducted.
Methods: Male Sprague-Dawley rats weighing 350-500 g. were pretreated with intratracheal administration of saline, TNF-α or 95% O2, or both. Bronchoalveolar lavage fluid was recovered from the airway of S-D rats after exposure to 95% O2 and TNF-α for 6 hours under ventilator support. Cells in lavage fluid were isolated and examined for total and differential counts by haematocytometer. TNF-α and IL-1β in lavage fluid were measured by ELISA.
Results: The percentage of neutrophils in BAL fluid was significantly higher in rats exposure to hyperoxia+ TNF-α (29.7±12.5%) compared with rats with hyperoxia (16.3±1.2%), TNF-α (4.2±1.1%) or room air (5.0±1.8%) alone (p＜0.05, respectively). Rats exposure to hyperoxia+ TNF-α significantly produced higher level of TNF-a and IL-1β, compared with rats with TNF-α , hyperoxia or room air alone. There was a significant correlation between TNF-α and IL-1β (p＜0.05, rs=0.62, n=20). The total cells and the percentage of neutrophils were also significantly correlated with TNF-α and IL-1β respectively.
Conclusions: The combined exposure to hyperoxia and TNF-α contributes to leukocyte recruitment and subsequently TNF-α and IL-1β release.

關鍵字

高氧 ； 腫瘤壞死因子 ； 介白質-1β ； 嗜中性白血球

並列摘要

Background: Although oxygen is an important adjunct to therapy in hypoxemic respiratory failure from diverse causes, exposure to high oxygen tension may contribute to exacerbate acute lung injury as a result of increased production of reactive oxygen metabolites. Moreover, tumour necrosis factor-α (TNF-α) is though to be implicated in the many pulmonary and airway diseases, especially in neutrophil mediated lung injury.
Objective: To investigate the augmented effects of hyperoxia on TNF-α - induced leukosequestration and pro-inflammatory cytokines release in rat airways. A prospective, randomized, controlled animal study was conducted.
Methods: Male Sprague-Dawley rats weighing 350-500 g. were pretreated with intratracheal administration of saline, TNF-α or 95% O2, or both. Bronchoalveolar lavage fluid was recovered from the airway of S-D rats after exposure to 95% O2 and TNF-α for 6 hours under ventilator support. Cells in lavage fluid were isolated and examined for total and differential counts by haematocytometer. TNF-α and IL-1β in lavage fluid were measured by ELISA.
Results: The percentage of neutrophils in BAL fluid was significantly higher in rats exposure to hyperoxia+ TNF-α (29.7±12.5%) compared with rats with hyperoxia (16.3±1.2%), TNF-α (4.2±1.1%) or room air (5.0±1.8%) alone (p＜0.05, respectively). Rats exposure to hyperoxia+ TNF-α significantly produced higher level of TNF-a and IL-1β, compared with rats with TNF-α , hyperoxia or room air alone. There was a significant correlation between TNF-α and IL-1β (p＜0.05, rs=0.62, n=20). The total cells and the percentage of neutrophils were also significantly correlated with TNF-α and IL-1β respectively.
Conclusions: The combined exposure to hyperoxia and TNF-α contributes to leukocyte recruitment and subsequently TNF-α and IL-1β release.

並列關鍵字

hyperoxia ； tumor necrosis factor-α ； interleukin-1β ； neutrophils