Despite recent advances in understanding macrophage activation, little is known regarding how human alveolar macrophages in health calibrate its transcriptional response to canonical TLR4 activation. In this study, we examined the full spectrum of LPS activation and determined whether the transcriptomic profile of human alveolar macrophages is distinguished by a TIR-domain-containing adapter-inducing interferon-β (TRIF)-dominant type I interferon signature. Bronchoalveolar lavage macrophages were obtained from healthy volunteers, stimulated in the presence or absence of ultrapure LPS in vitro, and whole transcriptomic profiling was performed by RNA sequencing (RNA-Seq). LPS induced a robust type I interferon transcriptional response and Ingenuity Pathway Analysis predicted interferon regulatory factor (IRF)7 as the top upstream regulator of 89 known gene targets. Ubiquitin-specific peptidase (USP)-18, a negative regulator of interferon α/β responses, was among the top up-regulated genes in addition to IL10 and USP41, a novel gene with no known biological function but with high sequence homology to USP18. We determined whether IRF-7 and USP-18 can influence downstream macrophage effector cytokine production such as IL-10. We show that IRF-7 siRNA knockdown enhanced LPS-induced IL-10 production in human monocyte-derived macrophages, and USP-18 overexpression attenuated LPS-induced production of IL-10 in RAW264.7 cells. Quantitative PCR confirmed upregulation of USP18, USP41, IL10, and IRF7. An independent cohort confirmed LPS induction of USP41 and IL10 genes. These results suggest that IRF-7 and predicted downstream target USP18, both elements of a type I interferon gene signature identified by RNA-Seq, may serve to fine-tune early cytokine response by calibrating IL-10 production in human alveolar macrophages.

Acute pancreatitis (AP) is a rare complication of hemorrhagic fever with renal syndrome (HFRS), and is difficult to diagnose. In this study, we retrospectively analyzed the clinical characteristics of 7 cases of HFRS complicated with AP and 105 cases of acute biliary pancreatitis (ABP). Medical records of 83 hospitalized patients with HFRS and 105 hospitalized patients with ABP in the affiliated Yijishan Hospital of Wannan Medical College were reviewed. The comparative analysis of patients between the 2 groups was conducted in terms of sex, age, duration of hospital stay, fever, hemorrhage, proteinuria, oliguria, laboratory results, radiologic examinations, and prognosis. A total of 83 patients were diagnosed with HFRS during study period. Only 8.43% (7/83) of the total HFRS patients were diagnosed with AP. The differences in the gender, age, and duration of hospital stay between the 2 investigated groups of patients were not statistically significant. The major symptoms for all 7 patients with HFRS complicated with AP and 105 patients with ABP were fever and upper abdominal pain. During the disease course of HFRS complicated with AP, 6 patients experienced hemorrhaging, and 7 patients underwent an oliguric stage, but none of the ABP patients experienced hemorrhaging and oliguria. Among the laboratory results of all patients, the differences in alanine aminotransferase and glycemia were not statistically significant. The other laboratory results (leucocyte count, platelet count, amylase, lipase, total bilirubin, direct bilirubin, creatinine, blood urea nitrogen, prothrombin time, activated partial thromboplastin time, and serum calcium level) were significantly different during hospitalization. All 7 patients with HFRS complicated with AP received conservative medical treatment and hemodialysis. In the patients with ABP, 21 patients were discharged from the hospital after conservative treatment, 53 patients were treated by endoscopic invasive treatment after stabilization, and 31 patients were treated by surgery after stabilization. AP is not a frequent complication in patients with HFRS. There are differences in clinical manifestations and laboratory findings between the HFRS complicated with AP group and the ABP group; these differences may help in the differential diagnosis and treatment of these 2 types of pancreatitis.

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This study demonstrates that genetic variants in the promoter regions of the IL-6 and IL-10 genes are associated with lumbar disc herniation risk in this Northern Chinese Han population.

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There is no association between rs1130864 or rs3093059 and ischaemic stroke in Chinese Han population.

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Objective. The aim of this study is to explore the relationship between neuron-specific enolase (NSE) gene polymorphism and delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) and provide a theoretical basis for DEACMP pathogenesis, diagnosis, and prognosis. Methods. To investigate this relationship, we screened 6 NSE single nucleotide polymorphisms (SNPs), based on the results of the previous genome-wide association studies (GWAS). A total of 1,201 patients, including 416 in the DEACMP group and 785 in the acute carbon monoxide poisoning (ACMP) group, were detected by the Sequenom MassARRAY® method. The genotype frequencies and alleles of the 6 NSE SNPs (rs2071074, rs2071417, rs2071419, rs11064464, rs11064465, and rs3213434) were compared using different genetic models. Results. In the SNPs rs2071419 and rs3213434, we found that the genotypes and allele frequencies in the two groups significantly correlated with the grouping of patients ( χ 2 = 6.596 , p = 0.037 ; χ 2 = 8.769 , p = 0.012 ). The haplotypes GGTTTC and CCTTTC of ACMP and DEACMP were different ( χ 2 = 6.563 , p = 0.010 ; χ 2 = 4.151 , p = 0.042 ). We also observed that rs2071419 and rs3213434 significantly correlated with DEACMP-increased risk in the dominant, codominant, and overdominant genetic models. In addition, we speculated that the C allele of the rs2071419 polymorphism and the T allele of the rs3213434 polymorphism in NSE may increase the DEACMP risk ( p = 0.011 , p = 0.006 ). Conclusions. The results show that rs2071419 and rs3213434 are susceptible sites of DEACMP. The NSE C allele of rs2071419 and T allele of rs3213434 and the haplotypes GGTTTC and CCTTTC may be risk factors for DEACMP.