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Effet protecteur de la modulation de TREM-1 au cours du sepsis et de l'infarctus du myocarde expérimental

Abstract : The most frequent cardiovascular diseases people in charge of the death at the man are the septic shock and the myocardial infarction. Septic shock is the most caricatural illustration of the fatal consequences, which the development of a deregulated inflammatory response can involve. Just like for the myocardial infarction, of many pharmacological experimental inhibitions of the innate response during the septic shock appeared beneficial, and led to the installation of clinical studies of great width studied the effectiveness of various molecules anti-inflammatory drugs. Unfortunately, no significant effectiveness could be shown in terms of mortality. One of the actors essential with the development of this inflammatory response is TREM-1 (Triggering Receptor Expressed one Myeloid cells-1 (TREM-1). TREM-1 is a receptor of the superfamily of the immunoglobulin expressed by the neutrophils and monocytes/macrophages. TREM-1 is an amplifier of the inflammatory response in the inflammatory and infectious pathology. According to our results, we noted that TREM-1 seemed to have a role of sensor for various signals of danger, with like resultant the amplification of the inflammatory response. The pharmacological modulation of TREM-1 by a peptide of synthesis (LR12) thus appears promising in the sense that it is never accompanied by a complete inhibition of the inflammatory response. Results in the septic shock and the myocardial infarction certainly experimental, confirm the effectiveness of this approach
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Submitted on : Thursday, March 29, 2018 - 12:40:59 PM
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  • HAL Id : tel-01750223, version 1



Amir Boufenzer. Effet protecteur de la modulation de TREM-1 au cours du sepsis et de l'infarctus du myocarde expérimental. Médecine humaine et pathologie. Université de Lorraine, 2013. Français. ⟨NNT : 2013LORR0156⟩. ⟨tel-01750223⟩



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