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首页> 外文期刊>Experimental Lung Research >Characteristics of alveolar macrophages from murine models of OVA-induced allergic airway inflammation and LPS-induced acute airway inflammation
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Characteristics of alveolar macrophages from murine models of OVA-induced allergic airway inflammation and LPS-induced acute airway inflammation

机译：OVA诱发的过敏性气道炎症和LPS诱发的急性气道炎症的小鼠模型中的肺泡巨噬细胞的特征

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Background:Macrophages include the classically activated pro-inflammatory M1 macrophages (M1s) and alternatively activated anti-inflammatory M2 macrophages (M2s). The M1s are activated by both interferon- and Toll-like receptor ligands, including lipopolysaccharide (LPS), and have potent pro-inflammatory activity. In contrast, Th2 cytokines activate the M2s, which are involved in the immune response to parasites, promotion of tissue remodeling, and immune regulatory functions. Although alveolar macrophages (AMs) play an essential role in the pulmonary immune system, little is known about their phenotypes. Methods:Quantitative reverse transcription polymerase chain reaction and flow cytometry were used to define the characteristics of alveolar macrophages derived from untreated naive mice and from murine models of both ovalbumin (OVA)-induced allergic airway inflammation and LPS-induced acute airway inflammation. AMs were co-cultured with CD4(+) T cells and were pulsed with tritiated thymidine to assess proliferative responses. Results:We characterized in detail murine AMs and found that these cells were not completely consistent with the current M1 versus M2-polarization model. OVA-induced allergic and LPS-induced acute airway inflammation promoted the polarization of AMs towards the current M2-skewed and M1-skewed phenotypes, respectively. Moreover, our data also show that CD11c(+) CD11b(+) AMs from the LPS-treated mice play a regulatory role in antigen-specific T-cell proliferation in vitro. Conclusions:These characteristics of AMs depend on the incoming pathogens they encounter and on the phase of inflammation and do not correspond to the current M1 versus M2-polarization model. These findings may facilitate an understanding of their contributions to the pulmonary immune system in airway inflammation.
机译：背景：巨噬细胞包括经典激活的促炎性M1巨噬细胞（M1s）和其他激活的抗炎性M2巨噬细胞（M2s）。 M1被干扰素和Toll样受体配体（包括脂多糖（LPS））激活，并具有有效的促炎活性。相反，Th2细胞因子激活M2，这些M2参与对寄生虫的免疫反应，促进组织重塑和免疫调节功能。尽管肺泡巨噬细胞（AMs）在肺部免疫系统中起重要作用，但对其表型了解甚少。方法：采用定量逆转录聚合酶链反应和流式细胞仪来确定未经处理的幼鼠和卵清蛋白（OVA）诱发的过敏性气道炎症和LPS诱发的急性气道炎症的鼠模型的肺泡巨噬细胞的特征。 AMs与CD4（+）T细胞共培养，并用ti化胸苷脉冲处理以评估增殖反应。结果：我们对鼠类AM进行了详细表征，发现这些细胞与当前的M1对M2极化模型并不完全一致。 OVA引起的变态反应和LPS引起的急性气道炎症分别促进了AMs向当前M2偏斜和M1偏斜的表型分化。此外，我们的数据还显示，来自LPS处理的小鼠的CD11c（+）CD11b（+）AMs在体外抗原特异性T细胞增殖中起调节作用。结论：AMs的这些特征取决于它们遇到的传入病原体以及炎症的阶段，并不符合当前的M1对M2极化模型。这些发现可能有助于了解它们对气道炎症中肺免疫系统的作用。

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