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Lookup NU author(s): Dr Ahmed Chishti, Dr Brian Shenton, Emeritus Professor John Kirby, Dr Simon Baudouin
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Objective: To examine the hypothesis that neutrophil chemotaxis to interleukin-8 (IL-8) is reduced in septic shock. Surface expression of neutrophil CXC chemokine receptors and the adhesion molecule CD11b were also examined and associations between disease severity, gas exchange and receptor expression were studied. Design: Prospective cohort clinical study. Setting: Intensive care unit in a tertiary referral teaching hospital. Patients: Patients with septic shock (n=15) and healthy controls (n=8) were studied. Measurements and results: Daily (for 5 consecutive days) flow cytometric measurements of chemokine and β integrin surface expression. "In vitro" neutrophil chemotaxis to IL-8 was also compared between patients with sepsis and healthy controls. CXCR2 expression significantly fell, CD11b expression increased and CXCR1 expression was unchanged throughout the study in the septic group compared with healthy controls. CD11b positively correlated with increasing APACHE II scores (p<0.0001) and worsening PaO2/FIO 2 ratios (p<0.0001). CXCR2 expression negatively correlated with both APACHE II scores (p=0.016) and PaO2/FIO2 ratios (p=0.01). There was no correlation between CXCR1 expression and either APACHE II score or PaO2/FIO2 ratios. Chemotaxis to IL-8 was reduced in patients with sepsis compared with healthy volunteers. Conclusions: Surface expression of the chemokine receptor CXCR2 and the β-integrin CD11b, but not CXCR1, were reduced on neutrophils isolated from patients with septic shock compared with healthy controls. Chemotaxis to IL-8 was also reduced in neutrophils from septic patients compared with healthy controls. The changes in receptor expression correlated with measures of disease severity. © Springer-Verlag 2004.
Author(s): Chishti AD, Shenton BK, Kirby JA, Baudouin SV
Publication type: Article
Publication status: Published
Journal: Intensive Care Medicine
Year: 2004
Volume: 30
Issue: 4
Pages: 605-611
ISSN (print): 0342-4642
ISSN (electronic): 1432-1238
Publisher: Springer
URL: http://dx.doi.org/10.1007/s00134-004-2175-y
DOI: 10.1007/s00134-004-2175-y
PubMed id: 14991094
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