Assessment of the pulmonary adaptive immune response to Cladosporium cladosporioides infection using an experimental mouse model

Abstract Cladosporium cladosporioides causes asthma and superficial and deep infections, mostly in immunodeficient individuals and animals. This study aimed to investigate whether C. cladosporioides spores can enter the lungs through pulmonary circulation and influence pulmonary immune response. We...

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Autores principales:	Xiaoping Ma, Jing Hu, Yan Yu, Chengdong Wang, Yu Gu, Sanjie Cao, Xiaobo Huang, Yiping Wen, Qin Zhao, Rui Wu, Zhicai Zuo, Junliang Deng, Zhihua Ren, Shumin Yu, Liuhong Shen, Zhijun Zhong, Guangneng Peng
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/d8f8f1288b2146dbb28a36c3942571dc
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spelling	oai:doaj.org-article:d8f8f1288b2146dbb28a36c3942571dc2021-12-02T15:23:01ZAssessment of the pulmonary adaptive immune response to Cladosporium cladosporioides infection using an experimental mouse model10.1038/s41598-020-79642-y2045-2322https://doaj.org/article/d8f8f1288b2146dbb28a36c3942571dc2021-01-01T00:00:00Zhttps://doi.org/10.1038/s41598-020-79642-yhttps://doaj.org/toc/2045-2322Abstract Cladosporium cladosporioides causes asthma and superficial and deep infections, mostly in immunodeficient individuals and animals. This study aimed to investigate whether C. cladosporioides spores can enter the lungs through pulmonary circulation and influence pulmonary immune response. We intravenously injected mice with C. cladosporioides spore suspension and conducted several assays on the lungs. Pulmonary hemorrhage symptoms and congestion were most severe on days 1, 2, and 3 post-inoculation (PI). Extensive inflammatory cell infiltration occurred throughout the period of infection. More spores and hyphae colonizing the lungs were detected on days 1, 2, and 3 PI, and fewer spores and hyphae were observed within 21 d of infection. Numerous macrophages, dendritic cells, and neutrophils were observed on day 5 PI, along with upregulation of CD54, an intercellular adhesion molecule. Th1 and Th2 cells increased after infection; specifically, Th2 cells increased considerably on day 5 PI. These results suggest that days 2 and 5 PI represent the inflammatory peak in the lungs and that the Th2 and Th1 signaling pathways are potentially involved in pulmonary immune responses. In conclusion, the further adaptive immune responses played important roles in establishing effective pulmonary immunity against C. cladosporioides systemic infections based on innate immune responses.Xiaoping MaJing HuYan YuChengdong WangYu GuSanjie CaoXiaobo HuangYiping WenQin ZhaoRui WuZhicai ZuoJunliang DengZhihua RenShumin YuLiuhong ShenZhijun ZhongGuangneng PengNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-13 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Xiaoping Ma Jing Hu Yan Yu Chengdong Wang Yu Gu Sanjie Cao Xiaobo Huang Yiping Wen Qin Zhao Rui Wu Zhicai Zuo Junliang Deng Zhihua Ren Shumin Yu Liuhong Shen Zhijun Zhong Guangneng Peng Assessment of the pulmonary adaptive immune response to Cladosporium cladosporioides infection using an experimental mouse model
description	Abstract Cladosporium cladosporioides causes asthma and superficial and deep infections, mostly in immunodeficient individuals and animals. This study aimed to investigate whether C. cladosporioides spores can enter the lungs through pulmonary circulation and influence pulmonary immune response. We intravenously injected mice with C. cladosporioides spore suspension and conducted several assays on the lungs. Pulmonary hemorrhage symptoms and congestion were most severe on days 1, 2, and 3 post-inoculation (PI). Extensive inflammatory cell infiltration occurred throughout the period of infection. More spores and hyphae colonizing the lungs were detected on days 1, 2, and 3 PI, and fewer spores and hyphae were observed within 21 d of infection. Numerous macrophages, dendritic cells, and neutrophils were observed on day 5 PI, along with upregulation of CD54, an intercellular adhesion molecule. Th1 and Th2 cells increased after infection; specifically, Th2 cells increased considerably on day 5 PI. These results suggest that days 2 and 5 PI represent the inflammatory peak in the lungs and that the Th2 and Th1 signaling pathways are potentially involved in pulmonary immune responses. In conclusion, the further adaptive immune responses played important roles in establishing effective pulmonary immunity against C. cladosporioides systemic infections based on innate immune responses.
format	article
author	Xiaoping Ma Jing Hu Yan Yu Chengdong Wang Yu Gu Sanjie Cao Xiaobo Huang Yiping Wen Qin Zhao Rui Wu Zhicai Zuo Junliang Deng Zhihua Ren Shumin Yu Liuhong Shen Zhijun Zhong Guangneng Peng
author_facet	Xiaoping Ma Jing Hu Yan Yu Chengdong Wang Yu Gu Sanjie Cao Xiaobo Huang Yiping Wen Qin Zhao Rui Wu Zhicai Zuo Junliang Deng Zhihua Ren Shumin Yu Liuhong Shen Zhijun Zhong Guangneng Peng
author_sort	Xiaoping Ma
title	Assessment of the pulmonary adaptive immune response to Cladosporium cladosporioides infection using an experimental mouse model
title_short	Assessment of the pulmonary adaptive immune response to Cladosporium cladosporioides infection using an experimental mouse model
title_full	Assessment of the pulmonary adaptive immune response to Cladosporium cladosporioides infection using an experimental mouse model
title_fullStr	Assessment of the pulmonary adaptive immune response to Cladosporium cladosporioides infection using an experimental mouse model
title_full_unstemmed	Assessment of the pulmonary adaptive immune response to Cladosporium cladosporioides infection using an experimental mouse model
title_sort	assessment of the pulmonary adaptive immune response to cladosporium cladosporioides infection using an experimental mouse model
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/d8f8f1288b2146dbb28a36c3942571dc
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Assessment of the pulmonary adaptive immune response to Cladosporium cladosporioides infection using an experimental mouse model

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