Dockrell, D. H. and Whyte, M. K. B. (2006) Regulation of phagocyte lifespan in the lung during bacterial infection. Journal of leukocyte biology, 79 (5). pp. 904-8. ISSN 0741-5400Full text not available from this repository.
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.
|Institution:||The University of Sheffield|
|Academic Units:||The University of Sheffield > Faculty of Medicine, Dentistry and Health (Sheffield) > School of Medicine (Sheffield)|
|Depositing User:||Miss Anthea Tucker|
|Date Deposited:||29 Mar 2012 09:49|
|Last Modified:||29 Mar 2012 09:49|
|Publisher:||Society for Leukocyte Biology|