CCPG1 involved in corneal Aspergillus fumigatus infection

To investigate whether non-canonical autophagy transport receptor cell cycle progression 1 (CCPG1) is involved in the corneal antifungal immune response. Human corneal epithelial cells (HCECs) and human myeloid leukemia mononuclear cells (THP-1) macrophages stimulated by ( ) were used as cell models...

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Published inInternational journal of ophthalmology Vol. 15; no. 4; pp. 541 - 546
Main Authors Wang, Li-Mei, Chen, Xiao-Meng, Yan, Hai-Jing, Yan, Shu, Sun, Xiao-Yan, Zhang, Da-Wei, Yang, Hua, Lu, Dan-Li, Che, Cheng-Ye
Format Journal Article
LanguageEnglish
Published China International Journal of Ophthalmology Press 18.04.2022
Press of International Journal of Ophthalmology (IJO PRESS)
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Summary:To investigate whether non-canonical autophagy transport receptor cell cycle progression 1 (CCPG1) is involved in the corneal antifungal immune response. Human corneal epithelial cells (HCECs) and human myeloid leukemia mononuclear cells (THP-1) macrophages stimulated by ( ) were used as cell models. The expression of CCPG1 mRNA was detected by qRT-PCR. Western blot was used to determine the protein expression of CCPG1 and interleukin-1β (IL-1β). The dectin-1 neutralizing antibody was used to detect the association between dectin-1 and CCPG1. Immunofluorescence was used to observe the colocalization of CCPG1 and C-type lectin-like receptor-1 (CLEC-1) in THP-1 macrophages. The expression of CCPG1 started to increase at 4h after infection and increased in a time-dependent manner in HCECs and THP-1 macrophages. With dectin-1 neutralizing antibody pretreatment, the expression of IL-1β was down-regulated. CCPG1 up-regulation in response to infection was independent of dectin-1. Immunofluorescence showed the colocalization of CCPG1 and CLEC-1 in THP-1 macrophages. As a specific autophagy protein of non-canonical autophagy pathway, CCPG1 is involved in corneal infection with .
Bibliography:ObjectType-Article-1
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Co-first authors: Li-Mei Wang, Xiao-Meng Chen, and Hai-Jing Yan
ISSN:2222-3959
2227-4898
DOI:10.18240/ijo.2022.04.03