Myocardial ischemia-reperfusion (IR) injury complicates all forms of coronary artery revascularization. Circulating interleukin-6 (IL-6) has been implicated in cell death following a variety of stimuli. Macrophages, platelets, neutrophils and the endothelium have been shown to release IL-6 after IR injury. Cardiac mast cells have been implicated in IR; however, their involvement has never been quantified. In this randomized, prospective study, we compared cardiac tissue susceptibility and serum IL-6 changes between mast cell deficient (W/WV) mice and their normallittermates (+/+). Twentyeight male W/Wv mice (n=14) and their +/+ littermates (n=14) were anaesthetized with 2.5% isofluorane. The left coronary artery (LCA) was ligated for 30 minutes or a sham procedure was performed. After 6 hours of reperfusion, the animals were sacrificed. The muscle viability was assessed on fresh wholemount slices by nitroblue tetrazolium (NBT) histochemical assay and serum IL-6 concentrations measured by ELISA. Cardiac muscle viability was significantly higher in W/Wv mice than the +/+ mice. Serum IL-6 levels were higher in the +/+ sham mice (465 ± 32 pg/ml, n=6) than the W/Wv mice (185 ± 31 pg/ml, n=6), p < 0.001. The IL-6levels increased significantly after reperfusion only in the +/+ mice (698 ± 41 pg/ml, n=8, p = 0.001), while it remained similar in the W/wv mice (202 ± 48 pg/ml, n=8, p = 0.783). These results show that the absence of mast cells reduces the myocardial damage associated with IR injury. Furthermore, there is an attenuation in the inflammatory response, as measured by serum IL-6 levels, following this local insult. This finding entertains the prospect of developing prophylactic therapy -targeting selective inhibition of cardiac mast cell activation, in clinical situations involving medical or surgical myocardial revascularization.Coronary Artery Disease (CAD) is the leading cause of morbidity and mortality in the United States; it accounts for 1.5 million of myocardial infarctions (MI) and 500,000 deaths each year. Unfortunately, in spite of earlier predictions, CAD continues to be the leading cause of death globally. CAD is a clinical manifestation of atherosclerosis, which is now considered to be a chronic vascular inflammatory disorder (l). Angioplasty removes cholesterol plaques in CAD and allows reperfusion,

Chemokines are inflammatory proteins acting via G-protein coupled chemokine receptors that trigger different signaling pathways. Monocyte chemoattractant protein-1 (CCL2/MCP-1) and regulated on activation, normal T expressed and secreted (CCL5/RANTES) are the two major members of the CC chemokine beta subfamily. The roles of RANTES and MCP-1 are emerging in regulating the recruitment of inflammatory cells into tissue during inflammation. The inhibition of MCP-1 and RANTES with corresponding antibodies or other inhibitors may provide benefits in different clinical scenarios including cancer, inflammation, CNS disorders, parasitic disease, autoimmune and heart diseases. RANTES and MCP-1 may represent targets for diagnostic procedures and therapeutic intervention, and may be useful as a prognostic factor in the above diseases.

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Host resistance against pathogens depends on a complex interplay of innate and adaptive immune mechanisms. Acting as an early line of defence, the immune system includes activation of neutrophils, tissue macrophages, monocytes, dendritic cells, eosinophils and natural killer (NK) cells. NK cells are lymphoid cells that can be activated without previous stimulation and are therefore like macrophages in the first line of defence against tumor cells and a diverse range of pathogens. NK cells mediate significant activity and produce high levels of proinflammatory cytokines in response to infection. Their cytotoxicity production is induced principally by monocyte-, macrophage- and dendritic cell-derived cytokines, but their activation is also believed to be cytokine-mediated. Recognition of infection by NK cells is accomplished by numerous activating and inhibitory receptors on the NK cells' surface that selectively trigger the cytolytic activity in a major histocompability complex-independent manner. NK cells have trypanocidal activity of fibroblast cells and mediate direct destruction of extracellular epimastigote and trypomastigote forms of T. cruzi and T. lewisi in vitro; moreover, they kill plasmodia-infected erythrocytes directly through cell-cell interaction. This review provides a more detailed analysis of how NK cells recognize and respond to parasites and how they mediate cytotoxicity against tumor cells. Also the unique role of NK cells in innate immunity to infection and the relationship between parasites and carcinogenesis are discussed.

Background:Abdominal exploration followed by vascular bypass has been the standard of care for acute mesenteric ischemia (AMI), but there is increasing use of endovascular treatment with selective exploratory laparotomy.Methods:We performed a retrospective review of patients diagnosed with AMI who underwent mesenteric artery angioplasty or stenting at a single institution from 2010-2017. Patients were divided into 3 groups: those who did not undergo exploratory laparotomy; those who received endovascular treatment before laparotomy (post-reperfusion laparotomy group); and those who had endovascular treatment after laparotomy (pre-reperfusion laparotomy group).Results:Patients who did not undergo exploratory laparotomy showed 85.7% (12/14) survival, compared with 63.6% (7/11) in the post-reperfusion group and 25.0% (2/8) in the pre-reperfusion group, P=0.077). Time to reperfusion was significant (P=0.009) in predicting survival for patients who underwent exploratory laparotomy.Conclusion:Emergent endovascular treatment prior to laparotomy seems to be associated with a higher survival.