Abstract
Microbicidal functions of the circulating neutrophil are well known to be temporally compromised following thermal or blunt traumatic injury. One function of the neutrophil grossly affected by injury is chemotaxis, or the ability to exit the vasculature and migrate directionally in response to one or more chemical signals generated at a site of inflammation. Defective patient neutrophil chemotactic function ex vivo has been reported by multiple laboratories using a variety of techniques [1–3] and has been reproduced in an animal model [4]. A decrease in the chemotactic response of neutrophils in vivo has also been documented for patients and animals with severe burns [5–7]. A defect in chemotactic function limits emigration of neutrophils from the circulation and likely contributes to the increased susceptibility to infection associated with thermal and traumatic injuries.
Supported in part by grants from the St. Paul-Ramsey Foundation, St. Paul-Ramsey Medical Center, St. Paul, Minnesota, by grant AI 22374 from the National Institutes of Health, DHHS, and by a grant from the International Fire Fighters Union.
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Nelson, R.D., Hasslen, S.R., Ahrenholz, D.H., Solem, L.D. (1989). Polymorphonuclear Leukocyte Function Following Burn and Mechanical Injury: Regulation and Kinetics. In: Faist, E., Ninnemann, J.L., Green, D.R. (eds) Immune Consequences of Trauma, Shock, and Sepsis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-73468-7_25
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DOI: https://doi.org/10.1007/978-3-642-73468-7_25
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