Sepsis and immune response / 世界急诊医学杂志（英文）

@#BACKGROUND: Sepsis and secondary multiple organ failure in critically ill patients are the major cause of death, but the pathogenesis of sepsis is not clear, especially the dysfunction of the immune system. In this paper, we review the response and regulation of the immune system and the functions of a variety of inflammatory mediators in sepsis. DATA SOURCES: Studies were identified by searching MEDLINE and PubMed for articles using the keywords "sepsis", "immune response", and "inflammatory mediator" up to October 2010. Additional papers were identified by a manual search of the references from the key articles. RESULTS: This systematic review was conducted of: 1) the immune response; 2) immune regulation; 3) inflammatory mediators; 4) high-mobility group box 1 protein; 5) the complement system; and 6) the autonomic nervous system. There are no therapeutic approaches available for sepsis that target inflammatory response; the mortality of sepsis has not been significantly reduced. CONCLUSIONS: Sepsis is complex and dynamic, and it has a group of heterogeneous syndromes. Since different patients with sepsis have different etiology, susceptibility, and responses, treatment should be prescribed individually.

Helicobacter pylori infection enhances atherosclerosis in high-cholesterol diet fed C57BL/6 mice / 中华心血管病杂志

<p><b>OBJECTIVE</b>To evaluate the impacts of Helicobacter pylori (H. pylori) infection on atherosclerosis and plasma lipid levels in high-cholesterol diet fed C57BL/6 mice.</p><p><b>METHOD</b>Female C57BL/6 mice were randomly divided into 4 groups (n = 12 each): fed with normal chow diet (A), infected with H. pylori (B), fed with high-cholesterol diet (C) and infected with H. pylori and fed with high-cholesterol diet (D). After 52 weeks, plasma levels of lipids were measured and aortic atherosclerosis was observed. The ureA, ureC, cagA and vacA DNA were also detected by PCR in the aortic arteries.</p><p><b>RESULT</b>(1) Prevalence of atherosclerosis was similar between group C and D (91.6% vs. 100%, P > 0.05) while there was no atherosclerosis in group A and B. H. pylori infected mice showed more obvious inflammation in gastric mucosa than mice without H. pylori infection. (2) The plasma levels of triglyceride, total cholesterol and LDL were higher and HDL was lower in group B, C and D than those in group A and in group D than in group C (all P < 0.05). (3) Roberts & Thompson scores and number of foam cells in plaques were significantly higher in group D compared with those in group C (all P < 0.05). (4) ureC DNA was detected in 5 out of 12 aortic arteries of mice in group D but not in group A, B and C.</p><p><b>CONCLUSION</b>Our results suggested that H. pylori infection might enhance the atherosclerotic lesion formation in this mouse model.</p>