COMPARTMENTALIZATION OF INTRAALVEOLAR AND SYSTEMIC LIPOPOLYSACCHARIDE-INDUCED TUMOR NECROSIS FACTOR AND THE PULMONARY INFLAMMATORY RESPONSE
COMPARTMENTALIZATION OF INTRAALVEOLAR AND SYSTEMIC LIPOPOLYSACCHARIDE-INDUCED TUMOR NECROSIS FACTOR AND THE PULMONARY INFLAMMATORY RESPONSE
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DOI：
10.1093/infdis/159.2.189
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发表时间：
1989-02-01
影响因子：
6.4
通讯作者：
SUMMER, WR
中科院分区：
文献类型：
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作者：
NELSON, S;BAGBY, GJ;SUMMER, WR
肿瘤坏死因子-α。肿瘤坏死因子(TNF)是由脂多糖(LPS)刺激的巨噬细胞产生的一种单核细胞因子，是吞噬功能的激活剂，可能调节宿主在感染过程中的反应。为了确定内毒素对体内肿瘤坏死因子活性和肺部炎症反应的影响，我们用内毒素对大鼠进行了全身或气管内攻击。经气管内注射内毒素后，对照组小鼠肺泡灌洗液和肺泡巨噬细胞中的肿瘤坏死因子水平显著升高，接近检测不到水平。肿瘤坏死因子水平的增加仅限于内毒素刺激的隔室。静脉注射脂多糖导致外周血中性粒细胞的数量减少，并使这些细胞隔离在肺血管内。相反，气管内的内毒素可引起明显的肺泡内炎症反应。
Tumor necrosis factor-.alpha. (TNF), a monokine produced by lipopolysaccharide (LPS)-stimulated macrophages, is an activator of phagocytic functions and may modulate host responses during infection. To determine the effects of LPS on TNF activity and the pulmonary inflammatory response in vivo, we challenged rats systemically or intratracheally with LPS. Intravenous LPS significantly increased serum TNF content from nondetectable levels in control specimens to peak levels at 90 min, which declined to baseline by 3 h. In response to intratracheal LPS, levels of TNF both in bronchoalveolar lavage fluid and associated with alveolar macrophages increased significantly from near nondetectable levels in control animals. Increases in TNF levels were confined to the LPS-challenged compartment. Intravenous LPS resulted in a decrease in the number of peripheral blood neutrophils and in sequestration of these cells within the pulmonary vasculature. In contrast, intratracheal LPS elicited a marked intraalveolar inflammatory response.