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实验性过敏性肺炎：单核细胞趋化蛋白-1的作用

Experimental hypersensitivity pneumonitis: role of MCP-1.

作者信息

Schuyler Mark, Gott Katherine, Cherne Amy

机构信息

Department of Medicine, Albequerque Veterans Affairs Medical Center, University of New Mexico, 87108, USA.

出版信息

J Lab Clin Med. 2003 Sep;142(3):187-95. doi: 10.1016/S0022-2143(03)00107-0.

DOI:10.1016/S0022-2143(03)00107-0
PMID:14532907
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7126991/
Abstract

Inhalation of Saccharopolyspora rectivirgula causes "farmer's lung" disease, a classic example of hypersensitivity pneumonitis (HP). Monocyte chemoattractant protein-1 (MCP-1) is increased in the bronchoalveolar lavage fluid of mice challenged with S rectivirgula, and S rectivirgula induces MCP-1 secretion by alveolar macrophages. We tested the hypothesis that MCP-1 and its receptor CC chemokine receptor-2 (CCR2) are essential to the development of experimental HP by treating mice with MCP-1 antibody and using CCR2(-/-) mice. Administration of anti-MCP-1 did not change the response to intratracheally administered S rectivirgula. CCR2(-/-) animals responded in a fashion similar to that of wild-type animals to intratracheally administered.S rectivirgula. To determine the influence of the MCP-1-CCR2 interaction in vitro, we transferred S rectivirgula-cultured spleen cells from S rectivirgula-sensitized mice, to naïve recipients. Later, challenge of the recipients with intratracheal S rectivirgula and examination of both lung histology and bronchoalveolar lavage fluid characteristics were used to determine whether adoptive transfer had occurred. We found that cultured cells from CCR2(-/-) animals were fully capable of adoptive transfer. We conclude that interaction of MCP-1 with CCR2 is not necessary for the development of pulmonary inflammation in response to intratracheally administered S rectivirgula or cells able to adoptively transfer experimental HP.

摘要

吸入直丝糖多孢菌会引发“农民肺”疾病，这是超敏性肺炎（HP）的一个典型例子。单核细胞趋化蛋白-1（MCP-1）在受到直丝糖多孢菌攻击的小鼠支气管肺泡灌洗液中含量增加，且直丝糖多孢菌可诱导肺泡巨噬细胞分泌MCP-1。我们通过用MCP-1抗体处理小鼠并使用CCR2基因敲除（CCR2(-/-)）小鼠，来检验MCP-1及其受体CC趋化因子受体2（CCR2）对实验性HP发展至关重要这一假设。给予抗MCP-1抗体并未改变小鼠对气管内给予直丝糖多孢菌的反应。CCR2(-/-)动物对气管内给予直丝糖多孢菌的反应方式与野生型动物相似。为了确定MCP-1-CCR2相互作用在体外的影响，我们将来自经直丝糖多孢菌致敏小鼠的经直丝糖多孢菌培养的脾细胞转移至未致敏的受体小鼠体内。随后，通过对受体小鼠进行气管内给予直丝糖多孢菌攻击，并检查肺组织学和支气管肺泡灌洗液特征，来确定是否发生了过继转移。我们发现来自CCR2(-/-)动物的培养细胞完全能够进行过继转移。我们得出结论，对于气管内给予直丝糖多孢菌或能够过继转移实验性HP的细胞所引发的肺部炎症发展而言，MCP-1与CCR2的相互作用并非必需。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0570/7126991/6a88c5f3431f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0570/7126991/01175338d1de/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0570/7126991/fcc36e1d8954/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0570/7126991/817026287826/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0570/7126991/68a33bb5d8a2/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0570/7126991/b06df9a13b0c/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0570/7126991/6a88c5f3431f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0570/7126991/01175338d1de/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0570/7126991/fcc36e1d8954/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0570/7126991/817026287826/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0570/7126991/68a33bb5d8a2/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0570/7126991/b06df9a13b0c/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0570/7126991/6a88c5f3431f/gr6.jpg

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