Marriott, H. M. and Dockrell, D. H. (2006) Streptococcus pneumoniae: the role of apoptosis in host defense and pathogenesis. The International Journal of Biochemistry & Cell Biology, 38 (11). pp. 1848-1854. ISSN 1357-2725Full text not available from this repository.
Programmed cell death or apoptosis is a recognised feature of infection with Streptococcus pneumoniae, and is observed during pneumococcal meningitis and pneumonia. The cholesterol-dependent cytolysin, pneumolysin, is a major trigger of apoptosis in the brain in association with pneumococcal production of hydrogen peroxide. Pneumococcal cell wall is also an important stimulus for apoptosis. Microbial factors and host factors combine in causing apoptosis in the brain, with hippocampal neurons being particularly susceptible. In pulmonary infection epithelial cell apoptosis contributes to tissue injury but macrophage apoptosis may benefit the host, aiding microbial killing and downregulating the inflammatory response. During sepsis lymphocyte apoptosis may be harmful to the host while dendritic cell apoptosis may limit the generation of an adaptive immune response during infection. Apoptosis induction may be harmful or potentially beneficial during pneumococcal infection and understanding its function in each setting is essential to allow specific therapeutic intervention.
|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|
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