作者: Brian J. Macneil , Dwight M. Nance
DOI: 10.1016/S1567-7443(01)80042-9
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摘要: Abtract Spinal cord injury (SCI) is associated with an elevated risk of infection as well increased mortality from septicemia. Pressure ulcers the skin, a frequent complication after SCI, are major source these infections. Reports suppressed immune function in otherwise healthy SCI humans suggests that altered immunity may be part sequela SCI. Therefore, we examined whether impaired inflammation and could demonstrated animal model complete In initial study, rats given at T1–T2 level were challenged lipopolysaccharide (LPS) 2 weeks spleen, production tumor necrosis factor-alpha (TNF-α) mRNA protein above control animals whereas interleukin-1 beta (IL-1β) synthesis was not effected. These changes specific to organ, since cytokines liver effected by To extend studies site antigen entry pressure ulcers, tested how skin generate inflammatory response. Injection turpentine into produced robust which fully established tow hours injection. contrast, showed little or no sign until 12–24 The cutaneous response further characterized measuring cytokine two A significant reduction TNF-α, IL-1β, IL-6, MCP seen below compared same rats. results demonstrate limited affected We propose dysregulated neural input following primary mediator increase susceptibility infection.