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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.1005555

Received for publication October 3, 2005.
Revised December 23, 2005.
Accepted for publication December 28, 2005.

Article

Regulation of phagocyte lifespan in the lung during bacterial infection

David H. Dockrell and Moira K. B. Whyte @

Academic Units of Respiratory Medicine and Infectious Diseases, University of Sheffield, United Kingdom

@ To whom correspondence should be addressed. E-mail: m.k.whyte{at}sheffield.ac.uk.


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Abstract

The innate-immune response to infection is critically dependent on the antimicrobial actions of macrophages and neutrophils. Host and pathogen have evolved strategies to regulate immune-cell antimicrobial functions via alterations in cell death. Modulation of phagocyte death by bacteria is an important pathogenic mechanism. Host benefits of phagocyte apoptosis also exist, and understanding the mechanisms and consequences of apoptosis is essential before we can devise strategies to modulate this element of the innate-immune response to the host’s benefit. This is of particular importance in an organ such as the lung, in which the balance between the need to recruit phagocytes to maintain bacterial sterility and the requirement to clear recruited cells from the alveolar units to preserve physiologic gas exchange must be finely tuned to ensure survival during bacterial infection. Apoptosis clearly plays a critical role in reconciling these physiological requirements.

Key Words: apoptosis • neutrophil • macrophage • Pseudomonas aeruginosa • Streptococcus pneumoniae




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