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Chemotactic mediator requirements in lung injury following skin burns in rats.

Authors: Piccolo, MT  Wang, Y  Sannomiya, P  Piccolo, NS  Piccolo, MS  Hugli, TE  Ward, PA  Till, GO 
Citation: Piccolo MT, etal., Exp Mol Pathol. 1999 Aug;66(3):220-6.
Pubmed: (View Article at PubMed) PMID:10486240
DOI: Full-text: DOI:10.1006/exmp.1999.2263

Partial-thickness skin burns have been shown to induce neutrophil-dependent microvascular injury both locally (skin) and systemically (lung). In the present study, interventional measures to block inflammatory chemoattractants were employed to define the pathophysiologic role of these mediators in the development of secondary lung injury following thermal injury of skin. Rats were treated with blocking antibodies to either C5a or to the alpha-chemokines, keratinocyte-derived cytokine (KC), or macrophage inflammatory protein-2 (MIP-2). To study the role of platelet activating factor, a receptor antagonist (PAF-Ra) was utilized. The development of lung vascular injury following thermal injury to skin was significantly attenuated by treatment with anti-C5a (84%), anti-KC (67%), and anti-MIP-2 (77%), but treatment with PAF-Ra had no protective effects. Protective interventions were paralleled by significant reductions in the tissue buildup of myeloperoxidase. When bronchoalveolar lavage fluids from thermally injured rats were evaluated, elevations in TNF;ZA and IL-1 were found and were determined to be C5a-dependent (but unaffected by treatment with PAF-Ra). These studies indicate that lung tissue injury after thermal skin burns is dependent on chemotactic mediators. The data also suggest that lung expression of TNFalpha and IL-1 after thermal injury of skin is C5a-dependent.

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RGD Object Information
RGD ID: 1600658
Created: 2007-03-22
Species: All species
Last Modified: 2007-03-22
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.