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Originally published online as doi:10.1189/jlb.1005555 on February 14, 2006

Published online before print February 14, 2006
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(Journal of Leukocyte Biology. 2006;79:904-908.)
© 2006 by Society for Leukocyte Biology

Regulation of phagocyte lifespan in the lung during bacterial infection

David H. Dockrell and Moira K. B. Whyte1

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

1Correspondence: Academic Unit of Respiratory Medicine, University of Sheffield, Royal Hallamshire Hospital, Sheffield S10 2JF, UK. E-mail: m.k.whyte{at}sheffield.ac.uk

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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