title: Role of chemotactic factors in neutrophil activation after thermal injury in rats.
abstract: Acute thermal trauma is well known to produce evidence of a "systemic inflammatory response" in vivo, as manifested by evidence of complement activation, appearance in plasma of a variety of inflammatory factors, and development of multi-organ injury. The current studies were focused on acute thermal injury of rat skin and factors responsible for accompanying activation of blood neutrophils. Acute thermal injury of rat skin resulted in a time-dependent loss of L-selectin and up-regulation of Mac-1 (CD11b/CD18) on blood neutrophils, with no changes in LFA-1 (CD11a/CD18). The loss of L-selectin was prevented by blockade of C5a but not by blockade of the alpha-chemokine, macrophage inflammatory protein-2 (MIP-2). C5a, the alpha chemokines, MIP-2 and keratinocyte-derived cytokine (KC), and platelet activating factor (PAF) contributed to up-regulation of blood neutrophil Mac-1. Blocking interventions against these mediators also blunted the degree of neutropenia developing after thermal trauma. These data suggest that activation of blood neutrophils after thermal trauma is related to the role of several chemotactic mediators. These studies may provide clues regarding factors responsible for development of the "systemic inflammatory response syndrome" after thermal injury in the experimental model employed.
authors.affiliation: Department of Pathology, University of Michigan Medical School, Ann Arbor 48109, USA.
authors.forename: M T
authors.initials: MT
authors.lastname: Piccolo
authors.forename: Y
authors.initials: Y
authors.lastname: Wang
authors.forename: S
authors.initials: S
authors.lastname: Verbrugge
authors.forename: R L
authors.initials: RL
authors.lastname: Warner
authors.forename: P
authors.initials: P
authors.lastname: Sannomiya
authors.forename: N S
authors.initials: NS
authors.lastname: Piccolo
authors.forename: M S
authors.initials: MS
authors.lastname: Piccolo
authors.forename: T E
authors.initials: TE
authors.lastname: Hugli
authors.forename: P A
authors.initials: PA
authors.lastname: Ward
authors.forename: G O
authors.initials: GO
authors.lastname: Till
mesh_terms: D000818:Animals; D019138:Antibodies, Blocking / Q000494:pharmacology; D002056:Burns / Q000276:immunology* / Q000378:metabolism / Q000628:therapy; D018845:CD11 Antigens / Q000096:biosynthesis; D018821:CD18 Antigens / Q000096:biosynthesis; D015815:Cell Adhesion Molecules / Q000096:biosynthesis; D054426:Chemokine CXCL2; D018925:Chemokines; D002630:Chemotactic Factors / Q000502:physiology*; D015936:Complement C5a / Q000037:antagonists & inhibitors / Q000276:immunology / Q000502:physiology; D016207:Cytokines / Q000037:antagonists & inhibitors / Q000502:physiology; D007106:Immune Sera / Q000494:pharmacology; D019041:L-Selectin / Q000096:biosynthesis; D007958:Leukocyte Count; D008297:Male; D015846:Monokines / Q000037:antagonists & inhibitors / Q000276:immunology / Q000502:physiology; D018375:Neutrophil Activation / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism; D010980:Platelet Membrane Glycoproteins / Q000037:antagonists & inhibitors; D051381:Rats; D020318:Rats, Long-Evans; D011956:Receptors, Cell Surface; D043562:Receptors, G-Protein-Coupled; D015854:Up-Regulation / Q000276:immunology
chemical_list: D019138:Antibodies, Blocking; D018845:CD11 Antigens; D018821:CD18 Antigens; D015815:Cell Adhesion Molecules; D054426:Chemokine CXCL2; D018925:Chemokines; D002630:Chemotactic Factors; D016207:Cytokines; D007106:Immune Sera; D015846:Monokines; D010980:Platelet Membrane Glycoproteins; D011956:Receptors, Cell Surface; D043562:Receptors, G-Protein-Coupled; C039351:platelet activating factor receptor; D019041:L-Selectin; C074302:keratinocyte-derived chemokines; D015936:Complement C5a