Mediators of hypersensitivity pneumonitis.

Mediators of hypersensitivity pneumonitis.
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DOI:
10.1067/mlc.2000.107694
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发表时间:
2000-07
期刊:
The Journal of laboratory and clinical medicine
影响因子:
--
通讯作者:
Mark Schuyler;K. Gott;A. Cherne
Mark Schuyler;K. Gott;A. Cherne
中科院分区:
其他
文献类型:
--
作者:
Mark Schuyler;K. Gott;A. Cherne

文献摘要

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吸入直脉糖多孢菌(S. rectivirgula)引起农民肺病,这是过敏性肺炎(HP)的典型例子。HP的特征是支气管肺泡灌洗液(BALF)嗜中性粒细胞(在吸入后的前48小时内),随后是BALF淋巴细胞增多。我们利用一个描述良好的小鼠HP模型来确定C-C趋化因子单核细胞趋化蛋白-1(MCP-1)和巨噬细胞炎性蛋白-1 α(macrophage inflammatory protein-1 alpha)出现的时间。(MIP-1 α);炎症细胞因子肿瘤坏死因子(TNF)、白细胞介素-1 α(IL-1 α)和白细胞介素-6(IL-6);以及Th 1分化细胞因子白细胞介素-12(IL-12)。单次腹腔注射S.在C57 Bl/6和BALB/c小鼠中,BALF嗜中性粒细胞增多(24 - 48小时达到峰值),随后是BALF淋巴细胞增多(48 - 72小时达到峰值),在此之前,BALF中出现MIP-1 α(4 - 6小时达到峰值)和MCP-1(48小时达到峰值)。在两种品系的小鼠中,BALF IL-12显著增加(峰值48至72小时)。BALF中IL-6、IL-1 α和TNF的增加在BALB/c小鼠中也大于C57 Bl/6小鼠。S. rectivirgula诱导小鼠巨噬细胞系J774A.1分泌MIP-1 α、MCP-1、IL-6、IL-1 α和IL-12;诱导C57 B1/6肺泡巨噬细胞分泌MIP-1 α、IL-6、IL-1 α、IL-12和TNF;诱导BALB/c肺泡巨噬细胞分泌IL-1 α、IL-6和TNF,但不诱导IL-12。结论:腹腔注射S. rectivirgula之前BALF嗜中性粒细胞和淋巴细胞增多症,并可能导致分化的Th 1细胞,我们还得出结论,肺巨噬细胞代表这些物质的潜在来源。
Inhalation of Saccharopolyspora rectivirgula (S. rectivirgula) causes farmer's lung disease, a classic example of hypersensitivity pneumonitis (HP). HP is characterized by bronchoalveolar lavage fluid (BALF) neutrophilia (within the first 48 hours after inhalation), followed by BALF lymphocytosis. We utilized a well-described murine model of HP to determine the timing of the appearance of the C-C chemokines monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1alpha (MIP-1alpha); the inflammatory cytokines tumor necrosis factor (TNF), interleukin-1alpha (IL-1alpha), and interleukin-6 (IL-6); and the Th1 -differentiating cytokine interleukin-12 (IL-12) in BALF. After a single intratracheal administration of S. rectivirgula, there was remarkable BALF neutrophilia (peak 24 to 48 hours), followed by a BALF lymphocytosis (peak 48 to 72 hours) in both C57Bl/6 and BALB/c mice that was preceded by the appearance of MIP-1alpha in BALF (peak 4 to 6 hours) and MCP-1 (peak at 48 hours). In both strains of mice there was a striking increase of BALF IL-12 (peak 48 to 72 hours). There was also an increase in BALF IL-6, IL-1alpha, and TNF that was greater in the BALB/c mice than in the C57Bl/6 mice. S. rectivirgula induced the secretion of MIP-1alpha, MCP-1, IL-6, IL-1alpha, and IL-12 from the murine macrophage cell line J774A.1; MIP-1alpha, IL-6, IL-1alpha, IL-12, and TNF from C57Bl/6 alveolar macrophages; and IL-1alpha, IL-6, and TNF-but not IL-12-from BALB/c alveolar macrophages. We conclude that chemokines and cytokines induced by intratracheal administration of S. rectivirgula precede BALF neutrophilia and lymphocytosis and may cause differentiation of Th1 cells; we also conclude that pulmonary macrophages represent a potential source of these substances.