Liu Jian-Xing, Zhang Ying, An Miao, Wu Qing-Guang, Zhao Ya, Li Xiong, Li Geng
Guangzhou University of Chinese Medicine, Guangzhou, China.
Guangdong Provincial Academy of Chinese Medical Sciences, Guangzhou, China.
J Infect Dev Ctries. 2019 Jun 30;13(6):536-544. doi: 10.3855/jidc.10338.
The polarization of T helper (Th) cells plays an important role in the inflammatory response, pathogen removal, and tissue damage processes of infectious acute lung injury (ALI). However, Th cell polarization in viral- or bacterial-mediated ALI is not well defined. Herein, an influenza virus (A/FM/1/47, H1N1) and lipopolysaccharide (LPS) were chosen to induce ALI in mice, and the resultant diversity of Th-cell polarization was explored.
BALB/c mice were challenged intranasally with the influenza virus or LPS. Edema of the lung, infiltration of inflammatory cells (macrophages, neutrophils, and lymphocytes), oxidative stress, and signature cytokines of Th1 and Th2 cells were detected at 2 days post virus or LPS challenge.
The mice exhibited increased capillary permeability accompanied by lung edema and protein-rich alveolar exudation after virus or LPS challenge. Additionally, excessive infiltration of inflammatory cells, robust oxidative stress, and cytokine production were observed in both mouse groups. However, there was conspicuous disparity in the inflammatory cell infiltration and cytokines between the virus- and LPS-challenged mice, where the infiltration in virus-challenged mice was mainly of macrophages and accompanied by robust Th1 cytokine elevation, whereas the infiltration in LPS-challenged mice was primarily of neutrophils and accompanied by robust Th2 cytokine elevation.
The Th cell polarization was skewed depending on whether ALI was induced by the influenza virus or LPS. The polarization in the virus-challenged mice was primarily toward a Th1 response, whereas that in the LPS-challenged mice was mainly toward Th2.
辅助性T（Th）细胞的极化在感染性急性肺损伤（ALI）的炎症反应、病原体清除及组织损伤过程中发挥着重要作用。然而，病毒或细菌介导的ALI中Th细胞极化情况尚不明确。在此，选用甲型流感病毒（A/FM/1/47，H1N1）和脂多糖（LPS）诱导小鼠ALI，并探究由此产生的Th细胞极化多样性。
将流感病毒或LPS经鼻内接种BALB/c小鼠。在病毒或LPS攻击后2天，检测肺水肿、炎性细胞（巨噬细胞、中性粒细胞和淋巴细胞）浸润、氧化应激以及Th1和Th2细胞特征性细胞因子。
病毒或LPS攻击后，小鼠出现毛细血管通透性增加，伴有肺水肿和富含蛋白质的肺泡渗出。此外，两组小鼠均观察到炎性细胞过度浸润、强烈的氧化应激和细胞因子产生。然而，病毒攻击组和LPS攻击组小鼠在炎性细胞浸润和细胞因子方面存在显著差异，病毒攻击组小鼠的浸润主要为巨噬细胞，并伴有Th1细胞因子显著升高，而LPS攻击组小鼠的浸润主要为中性粒细胞，并伴有Th2细胞因子显著升高。
Th细胞极化因ALI是由流感病毒还是LPS诱导而发生偏移。病毒攻击组小鼠的极化主要朝向Th1反应，而LPS攻击组小鼠的极化主要朝向Th2。
