Abstract
Objective To investigate the expression of triggering receptor-1 on myeloid cells (TREM-1) and inflammatory cytokines in acute lung injury (ALI) incurred by severe acute pancreatitis (SAP).Methods Twenty-four male SD rats were randomly (random number) divided into sham operation (SO) group,SAP group and SAP + LP17 (synthesized TREM-1) group (n =8 in each group),and SAP model was established by retrograde injection of sodium taurocholate into the bile-pancreatic duct.Twelve hours after modeling,all rats of three groups were sacrificed,and the pancreas and lung of rats were harvested.The histopathological changes of pancreas and lung tissue stained with hematoxylin-eosin staining (HE staining) were observed under light microscope.The lung tissue was marked with macrophage-specific antibody CD68 to detect macrophage infiltration by using immunohistochemistry.The expressions of TREM-1 mRNA、interleukin-1β (IL-1β) mRNA and tumor necrosis factor-α (TNF-α) mRNA in lung tissue were detected by fluorescence quantitative polymerase chain reaction (QRT-PCR method).The data were expressed as ((-x) ± s) and SPSS 17.0 software was used to make one-way ANOVA,and P ＜ 0.05 was considered to indicate significant difference.Results Compared with SO group and SAP + LP17 group,the injuries of pancreas and lung tissue in SAP group were significantly more severe (P ＜ 0.05).In SAP group,macrophage infiltration in lung tissue was more evident than that in SO group.Accordantly,the expression of TREM-1 mRNA,IL-1β mRNA and TNF-α mRNA of lung tissue in SAP group were significantly higher than those in SO group and SAP + LP17 group (P ＜ 0.01 or P ＜ 0.05).Conclusions The expression of TREM-1 in the lung injury caused by SAP was significantly higher.It might be an important inflammatory mediator in the mechanism of lung injury caused by SAP.LP17 effectively lowered the expression of TREM-1 and decreased the release of inflammatory cytokines,lessening the lung injury. Key words: Severe acute pancreatitis; Acute lung injury; Triggering receptor-1 on myeloid cells; LP17 ; Interleukin-1β ; Tumor necrosis factor-α
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