Neuropeptide regulation of proinflammatory cytokine responses
Autor: | Richard A. Winchurch, Brandon Bullock, Camille Dickerson, Bradley J. Undem |
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Rok vydání: | 1998 |
Předmět: |
Lipopolysaccharides
Quinuclidines medicine.medical_specialty Time Factors Transcription Genetic Lipopolysaccharide Immunology Neuropeptide Substance P Inflammation Proinflammatory cytokine Mice chemistry.chemical_compound Neurokinin-1 Receptor Antagonists Piperidines Tachykinins Internal medicine medicine Animals Immunology and Allergy Receptor Mice Inbred BALB C Tumor Necrosis Factor-alpha business.industry Cell Biology Endotoxins Nociception Endocrinology Gene Expression Regulation Liver chemistry Cytokines Female Tumor necrosis factor alpha Capsaicin medicine.symptom business Spleen |
Zdroj: | Journal of Leukocyte Biology. 63:602-605 |
ISSN: | 1938-3673 0741-5400 |
DOI: | 10.1002/jlb.63.5.602 |
Popis: | Severe traumatic injuries and infections are frequently accompanied by life-threatening shock and are associated with increases in the proinflammatory cytokines, particularly tumor necrosis factor α (TNF-α). The body's first perception of injury is the nociceptive or pain response. This response is induced at the site of injury and is transmitted systemically by sensory neuropeptides, the tachykinins, released from sensory afferent c-fiber neurons. We studied the role of tachykinins in regulating the production of proinflammatory cytokines induced by the administration of bacterial lipopolysaccharide. Destruction of terminal sensory nerve endings before lipopolysaccharide administration abrogates tachykinin synthesis and down-regulates TNF-α transcription and secretion. In contrast, the responses of interleukins-1 and -6 are unaffected. Pretreating animals with an antagonist for the substance P-specific NK-1 receptor also down-regulated the TNF-α response, whereas blockade of the NK-2 receptor had no effect. These findings indicate that substance P contributes to the induction of those cytokines that are involved in precipitating the shock response. |
Databáze: | OpenAIRE |
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