Literature DB >> 1532218

Reduced expression of neutrophil CD11b and CD16 after severe traumatic injury.

C White-Owen1, J W Alexander, G F Babcock.   

Abstract

Overwhelming sepsis continues to be a major source of morbidity and mortality in patients who have sustained severe traumatic injury. Recently, much interest has been focused on the role of the peripheral blood neutrophil (PMN) in infections in these patients. Two surface receptors, CD11b (CR3) and CD16 (Fc gamma RIII), are thought to participate in bacterial phagocytosis and are both present on greater than 85% of normal PMNs. We have previously shown that cells that lack both of these receptors have markedly reduced phagocytic function. The purpose of this study was to determine the effect of severe trauma on the expression of these PMN receptors. Twenty severe trauma patients, age 19-70 years, presenting with an initial APACHE II score of greater than or equal to 10 were arbitrarily divided into two groups to define severity of injury: Group A, initial APACHE II of 10-18 (n = 11) and Group B, initial APACHE II of 19-25 (n = 9). Blood was obtained on admission, on Day 3, and weekly thereafter. PMNs were stained with fluorochrome-labeled monoclonal antibodies directed against CD11b and CD16 and then analyzed by flow cytometry. Controls consisted of 14 normal adults, age 20-65 years. The percentage and absolute numbers of CD11b+/CD16+ PMNs were determined for each patient or control sample. ANOVA and multiple comparison of variables (P = 0.05) were performed for each week. Values for Group A were different from controls at Weeks 0, 1, and 3. Values for Group B were significantly lower than those of controls at all weeks.(ABSTRACT TRUNCATED AT 250 WORDS)

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Year:  1992        PMID: 1532218     DOI: 10.1016/0022-4804(92)90273-3

Source DB:  PubMed          Journal:  J Surg Res        ISSN: 0022-4804            Impact factor:   2.192


  12 in total

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4.  Up-regulation of the dendritic cell marker CD83 on polymorphonuclear neutrophils (PMN): divergent expression in acute bacterial infections and chronic inflammatory disease.

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5.  Reduced PMN beta 2 integrins after trauma: a possible role for colony-stimulating factors.

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6.  Pneumonia in the surgical intensive care unit. Immunologic keys to the silent epidemic.

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7.  Neutrophil CD18 expression and blockade after traumatic shock and endotoxin challenge.

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8.  Isolated blunt chest injury leads to transient activation of circulating neutrophils.

Authors:  T Visser; F Hietbrink; K M Groeneveld; L Koenderman; L P H Leenen
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9.  Trauma: the role of the innate immune system.

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Review 10.  Pathophysiology of the systemic inflammatory response after major accidental trauma.

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Journal:  Scand J Trauma Resusc Emerg Med       Date:  2009-09-15       Impact factor: 2.953

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