ICAM-1 expression and its role in cigarette smoke inhalationinduced lung inflammation in the mouse.

ICAM-1 表达及其在香烟烟雾吸入诱发小鼠肺部炎症中的作用。

• 批准号: 09670603
• 负责人: MATSUSE Takeshi
• 金额: $ 1.92万
• 依托单位: University of Tokyo
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1997
• 资助国家: 日本
• 起止时间: 1997 至 1998
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09670603/
• 关键词: cigarette; lung inflammation; ICAM-1; bronchoalveolar lavage; immunohistochemistry; immunohistochemistry; Immunohistochemistry

Cigarette smoking induces accumulation of polymorphonuclear leukocytes (PMNs) and mononuclear cells in the peripheral lung. The purpose of this report was to investigate the role of intercellular adhesion molecule-1 (ICAM-1) in a murine model of acute cigarette smoke inhalation-induced lung inflammation. ICR mice were exposed to 100 cigarettes for 2 h pretreated with phosphate buffered saline (Smoke group), an anti-ICAM-1 mAb (ICAMmAb+Smoke group). In the Smoke group, significant increases in total cell, macrophage and PMN counts of bronchoalveolar lavage fluid were observed at 12 h after cigarette smoke exposure. This accumulation of inflammatory cells was significantly reduced by the pretreatment with an anti-ICAM-1 mAb (p<O.O1). Adherence of myeloperoxydase positive PMNs to vascular endothelium and bronchiolar epithelium significantly increased at 12 h after exposure, and this increase of adherent PMNs was attenuated significantly by the pretreatment with anti-ICAM-1 mAb (p<O.O5). The increased expression of ICAM-1 on bronchiolar epithelium was observed after exposure. These observations suggest that the upregulation of ICAM-1 may play an important role in the inflammatory process of airways caused by cigarette smoke inhalation.

吸烟会导致周围肺中多形核白细胞（PMN）和单核细胞的积累。本报告的目的是研究细胞间粘附分子-1 (ICAM-1) 在急性香烟烟雾吸入诱发肺部炎症的小鼠模型中的作用。 ICR小鼠暴露于100支香烟2小时，用磷酸盐缓冲盐水（烟雾组）、抗ICAM-1 mAb（ICAMmAb+烟雾组）预处理。在吸烟组中，暴露于香烟烟雾后12小时观察到支气管肺泡灌洗液的总细胞、巨噬细胞和PMN计数显着增加。抗 ICAM-1 mAb 预处理显着减少了炎症细胞的积累 (p<0.01)。暴露后 12 小时，髓过氧化物酶阳性 PMN 对血管内皮和细支气管上皮的粘附显着增加，并且用抗 ICAM-1 mAb 预处理显着减弱了这种粘附 PMN 的增加 (p<0.05)。暴露后观察到细支气管上皮 ICAM-1 表达增加。这些观察结果表明，ICAM-1的上调可能在吸入香烟烟雾引起的气道炎症过程中发挥重要作用。

项目成果

Matsuse T,Teramoto S,Katayama H,Sudo E,Ekimoto H,Mitsuhashi H,Uejima Y,Fukuchi Y,Ouchi Y.: "ICAM-1 mediates lung leukocyte recruitment, but not pulmonary fibrosis in a murine model of bleomycin-induced lung injury." Eur Respir J. 13. 1-7 (1999)

Matsuse T、Teramoto S、Katayama H、Sudo E、Ekimoto H、Mitsuhashi H、Uejima Y、Fukuchi Y、Ouchi Y.：“在博来霉素诱导的小鼠肺模型中，ICAM-1 介导肺白细胞募集，但不介导肺纤维化

Matsuse T 他8名: "ICAM-1 mediates lung leukocyte recruitment,but not pulmonary fibrosis in a murine model of bleomycin-induced lung injury" Eur Respir J. 13. 1-7 (1999)

Matsuse T 和其他 8 人：“在博莱霉素诱导的肺损伤小鼠模型中，ICAM-1 介导肺白细胞募集，但不介导肺纤维化”Eur Respir J. 13. 1-7 (1999)

Teramoto S,Matsuse T.: "Investigation of effects of anesthesia and age on aspiration in mice vsing Lacz gene transfer by recombinant EI-deleted adenouivus vactors." Am J Respir Care Med. 158. 1914-1919 (1998)

Teramoto S、Matsuse T.：“通过重组 EI 删除的腺病毒载体进行 Lacz 基因转移，研究麻醉和年龄对小鼠抽吸的影响。”

Matsuse T,Ohga E,Teramoto S,Fukayama M,Nagai R,Horiuchi S,Ouchi Y.: "Immunohistochemical localisation of advanced glycation end products in pulmonary fibrosis." J.Clin. Pathol. 51. 515-519 (1998)

Matsuse T，Ohga E，Teramoto S，Fukayama M，Nagai R，Horiuchi S，Ouchi Y.：“肺纤维化中晚期糖基化终产物的免疫组织化学定位。”

Matsuse T,他8名: "ICAM-1 mediates lung leukocyte recruicment,but not pulmonary fibrosis in a murine model of bleomycin-induced lung injury." Eur Respir J. 13. 1-7 (1999)

Matsuse T 等人：“在博莱霉素诱导的肺损伤小鼠模型中，ICAM-1 介导肺白细胞重新聚集，但不介导肺纤维化。”Eur Respir J. 13. 1-7 (1999)