2. Academic Validation
  3. Chlamydia psittaci Induces Autophagy in Human Bronchial Epithelial Cells via PERK and IRE1α, but Not ATF6 Pathway

Chlamydia psittaci Induces Autophagy in Human Bronchial Epithelial Cells via PERK and IRE1α, but Not ATF6 Pathway

  • Infect Immun. 2022 May 19;90(5):e0007922. doi: 10.1128/iai.00079-22.
Li Chen  # 1 2,  Qiaoling Huang  # 1 3 4,  Qinqin Bai 1 3 4,  Ting Tong 1 3 4,  You Zhou 1 3 4,  Zhongyu Li 5,  Cui Xiao 1 3 4,  Lili Chen 1 3 4
Affiliations

Affiliations

  • 1 Department of Public Health Laboratory Sciences, School of Public Health, Hengyang Medical School, University of South Chinagrid.412017.1, Hengyang, Hunan, China.
  • 2 Department of Laboratory Medicine, Kweichou Moutai Hospital, Zunyi, Guizhou, China.
  • 3 Hunan Key Laboratory of Typical Environmental Pollution and Health Hazards, School of Public Health, Hengyang Medical School, University of South Chinagrid.412017.1, Hengyang, Hunan, China.
  • 4 Hengyang Engineering Technology Research Center, Hengyang, Hunan, China.
  • 5 Institute of Pathogenic Biology, Hengyang medical school, University of South Chinagrid.412017.1, Hengyang, Hunan, China.
  • # Contributed equally.
PMID: 35435728 DOI: 10.1128/iai.00079-22
Abstract

Chlamydia psittaci is an important pathogen that causes chronic and atypical pneumonia in humans. Autophagy and the unfolded protein response (UPR) are important mechanisms for regulating the growth of infectious parasitic pathogens in living cells. Here, we explored whether C. psittaci Infection induced Autophagy via the UPR and the effect of these cellular responses on the survival and replication of C. psittaci in human bronchial epithelial cells (HBEs). Not only were the numbers of autophagosomes and the expression of LC3-II and Beclin1 increased following C. psittaci Infection of HBEs, but also the expression of p62 (also called sequestosome-1) was downregulated. Moreover, after C. psittaci Infection, the UPR and UPR sensors PERK/eIF2α and IRE1α/XBP1 were activated, but not the ATF6 pathway. When either Bip siRNA was used to block normal initiation of the UPR, or activation of the PERK and IER1α pathways was blocked with specific inhibitors GSK2606414 and 4μ8C, the level of Autophagy caused by C. psittaci Infection was significantly inhibited. Furthermore, blocking activation of the UPR and associated pathways significantly reduced the number of C. psittaci inclusions. Our research suggests that the UPR, via the PERK and IRE1α, but not ATF6 signaling pathways, regulates HBE-cell Autophagy induced by C. psittaci Infection and the replication of C. psittaci.

Keywords

ATF6; Chlamydia psittaci; IRE1α; PERK; autophagy; unfolded protein reaction.

Figures
Products
嗨！很高兴为您提供帮助！

尊敬的 MCE 客户您好，
请您选择所在区域，我们将转接对应客服为您服务！

热门区域

A

B

C

F

G

H

J

L

N

Q

S

T

X

Y

Z

热 A B C F G H J L N Q S T X Y Z