Literature DB >> 27865699

TNF-α inhibits the growth of Legionella pneumophila in airway epithelial cells by inducing apoptosis.

Yasuhide Kawamoto1, Yoshitomo Morinaga2, Yumiko Kimura1, Norihito Kaku1, Kosuke Kosai1, Naoki Uno1, Hiroo Hasegawa1, Katsunori Yanagihara1.   

Abstract

BACKGROUND: TNF-α plays an important role in the pathogenesis of Legionella pneumophila (Lp)-induced pneumonia. Patients undergoing anti-TNF-α therapy are at an increased risk of Lp infection. Lp infects both phagocytic and non-phagocytic cells such as airway epithelial cells; however, the role of TNF-α in airway epithelial cells is unknown.
METHODS: Human airway epithelial cell line NCI-H292 was infected with Lp NUL1 strain. After infection, both intracellular growth of Lp and cell death were evaluated after treating the cells with or without TNF-α. Apoptosis was examined by performing activated caspase-3/7 staining and by using a pan-caspase inhibitor.
RESULTS: Lp infected and replicated in NCI-H292 cells in a time-dependent manner, and TNF-α treatment of Lp-infected NCI-H292 cells inhibited Lp replication. Inhibitory effects of TNF-α on Lp replication were suppressed after treatment with a TNF-α-neutralizing antibody. Lp infection increased extracellular lactate dehydrogenase levels and decreased the number of living cells. Increased number of Lp-infected NCI-H292 cells showed caspase-3/7 activation, indicating they underwent apoptosis. TNF-α treatment inhibited Lp replication by increasing the apoptosis of NCI-H292 cells.
CONCLUSIONS: Thus, our results suggested that airway epithelial cells were involved in the pathogenesis of Lp infection and that TNF-α played a protective role by inhibiting the intracellular replication of Lp and by increasing the apoptosis of Lp-infected airway epithelial cells. However, Lp infection should be investigated further in patients undergoing anti-TNF-α therapy who develop pneumonia.
Copyright © 2016 Japanese Society of Chemotherapy and The Japanese Association for Infectious Diseases. Published by Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  Anti-TNF-α therapy; Caspase 3; Caspase 7; Cell death; Lung epithelial cells

Mesh:

Substances:

Year:  2016        PMID: 27865699     DOI: 10.1016/j.jiac.2016.09.010

Source DB:  PubMed          Journal:  J Infect Chemother        ISSN: 1341-321X            Impact factor:   2.211


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