Modulation of apoptosis during infection with Chlamydia

ORCiD

David M. Ojcius: 0000-0003-1461-4495

Department

Biomedical Sciences

Document Type

Article

Publication Title

Methods in Enzymology

ISSN

0076-6879

Volume

358

DOI

10.1016/S0076-6879(02)58099-X

First Page

334

Last Page

344

Publication Date

1-1-2002

Abstract

This chapter describes methods used to measure apoptosis or inhibition of apoptosis during infection, particularly techniques that reveal host cell morphological changes, caspase activation, mitochondrial membrane depolarization, cytochrome c release, and DNA fragmentation. Apoptosis is apparently blocked through inhibition of cytochrome c release from mitochondria and subsequent caspase-3 activation, In contrast, induction of host cell apoptosis has also been observed in macrophages and epithelial cells infected by C. psittaci during late stages of the infection, and the apoptosis requires intracellular bacterial replication. C. psittaci-induced apoptosis may require secretion of a bacterial apoptotic factor, potentially via the type III secretion apparatus and/or may be a stress response in the infected cell. Furthermore, the hallmarks of apoptosis are condensation of the nuclear chromatin and cytoplasm, activation of proteases (caspases) and endonucleases, loss of plasma membrane phosphatidylserine (PS) asymmetry, cleavage of the DNA into 200 base-pair oligonucleosomal fragments, and segmentation of the dying cell into membrane-bound apoptotic bodies. Intracellular microbes can also modulate apoptosis of the host cell, either inhibiting or promoting cell death, and it has been proposed that the persistence and pathogenesis of several pathogenic microbes may be related to their ability to dysregulate apoptosis.

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