The systemic inflammatory response syndrome induces functional changes and relative hyporesponsiveness in neutrophils

Fung, Yoke Lin, Fraser, John F., Wood, Peter, Minchinton, Robyn M. and Silliman, Christopher C. (2008) The systemic inflammatory response syndrome induces functional changes and relative hyporesponsiveness in neutrophils. Journal of Critical Care, 23 4: 542-549. doi:10.1016/j.jcrc.2007.09.004


Author Fung, Yoke Lin
Fraser, John F.
Wood, Peter
Minchinton, Robyn M.
Silliman, Christopher C.
Title The systemic inflammatory response syndrome induces functional changes and relative hyporesponsiveness in neutrophils
Journal name Journal of Critical Care   Check publisher's open access policy
ISSN 0883-9441
1557-8615
Publication date 2008-12
Sub-type Article (original research)
DOI 10.1016/j.jcrc.2007.09.004
Volume 23
Issue 4
Start page 542
End page 549
Total pages 8
Place of publication Philadelphia PA, U.S.
Publisher W. B. Saunders
Language eng
Subject 11 Medical and Health Sciences
1117 Public Health and Health Services
Abstract Purpose: To study the effects of systemic inflammatory response syndrome (SIRS) on polymorhonuclear neutrophil (PMN) function and phenotype by comparing neutrophils from critically ill patients with SIRS against those from healthy blood donors. Material and Methods: Intensive care unit patients (n = 110) who met at least one SIRS criterion were recruited to the study. One hundred healthy blood donors were recruited as normal controls. Results: Polymorphonuclear cells from critically ill patients with SIRS were more resistant to activation than PMNs from healthy donors, but when stimulated had an exaggerated microbicidal response. Buffer-treated PMNs from patients with SIRS had significantly higher CD43 surface expression that may inhibit heterotypic cellular contact or ligand stimulation of membrane receptors, had significantly lower expression of IgG receptor CD16, demonstrated resistance to shedding of L-selectin when primed by platelet-activating factor which could be pro-inflammatory, and had reduced respiratory burst when primed by platelet-activating factor than activated by formyl-Met-Leu-Phe. Conclusion: The phenotypic and functional changes observed in neutrophils in the critically ill indicate that they require a higher level of stimulus to become activated. This may represent an auto-protective mechanism where the neutrophils in the already inflamed host may, by this mechanism, avoid excessive inflammation reducing the risk of further host cell injury and death.
Keyword Neutrophils
Hyporesponsiveness
systemic inflammatory response syndrome (SIRS)
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
School of Medicine Publications
 
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Created: Tue, 05 Jan 2010, 11:13:51 EST by Ms May Balasaize on behalf of Faculty Of Health Sciences