Relationships between genetic polymorphisms of triggering recptor expressed on myeloid cells―1 and septic shock in a Chinese Han population.docVIP

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2018-07-04 发布于福建
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Relationships between genetic polymorphisms of triggering recptor expressed on myeloid cells―1 and septic shock in a Chinese Han population.doc

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Relationships between genetic polymorphisms of triggering recptor expressed on myeloid cells―1 and septic shock in a Chinese Han population

Relationships between genetic polymorphisms of triggering receptor expressed on myeloid cells―1 and septic shock in a Chinese Han population 　　BACKGROUND： Triggering receptor expressed on myeloid cells-1 （TREM-1） is a cell surface receptor expressed on neutrophils and monocytes. TREM-1 acts to amplify inflammation and serves as a critical mediator of inflammatory response in the context of sepsis. To date， the predisposition of TREM-1 gene polymorphisms to septic shock has not been reported. This study was designed to investigate whether TREM-1 genomic variations are associated with the development of septic shock. 中国论文网 /1/viewhtm　　METHODS： We genotyped two TREM-1 single nucleotide polymorphisms （SNPs， rs2234237 and rs2234246） and evaluated the relationships between these SNPs and septic shock on susceptibility and prognosis. 　　RESULTS： TREM-1 rs2234246 A allele in the promoter region was significantly associated with the susceptibility of septic shock in recessive model （AA， OR=3.10， 95%CI 1.15 to 8.32， P=0.02）， and in codominant model （AG， OR=0.72， 95%CI 0.43?C1.19， P=0.02； AA， OR=2.71， 95%CI 1.00?C7.42； P=0.03）. However， in three inherited models （dominant model， recessive model， and codominant model）， none of the assayed loci was significantly associated with the prognosis of septic shock. The non-survivor group demonstrated higher plasma IL-6 levels （99.7±34.7 pg/mL vs. 61.2±26.5 pg/mL， P 　　Triggering receptor expressed on myeloid cells-1 （TREM-1） is a recently identified cell surface receptor expressed on neutrophils and a subset of monocytes.[8] This receptor belongs to the immunoglobulin superfamily and activates downstream signaling pathways by interaction with an adaptor protein DAP12.[9?C11] Engagement of TREM-1 has been shown to induce the production of proinflammatory chemokines such as interleukin （IL）-8 and cytokines such as tumor necrosis factor （TNF）-α and interleukin （IL）-1β.[9，12] Meanwhile， TREM-1 acts synergistically with Toll-like