Rationale: Atherosclerosis is characterized by lipid accumulation in the vessel wall, inflammation, and both macrophage and vascular smooth muscle cell (VSMC) apoptosis. However, whereas VSMC apoptosis in mice with established atherosclerotic plaques or hyperlipidemia increases serum levels of the proatherogenic cytokines monocyte chemotactic protein (MCP)-1, tumor necrosis factor ␣, and interleukin (IL)-6, the link between hyperlipidemia, apoptosis and inflammation, and the mechanisms by which apoptotic cells promote inflammation in atherosclerosis are unknown. Objective: To determine whether hyperlipidemia affects apoptotic cell clearance, and identify the molecular pathways downstream of VSMC apoptosis that may promote inflammation. Methods and Results: We find that human VSMCs are potent and efficient phagocytes of apoptotic human VSMCs, but phagocytosis is significantly reduced by oxidized low-density lipoprotein in vitro or hyperlipidemia in vivo. Necrotic human aortic VSMCs release IL-1␣, which induces IL-6 and MCP-1 production from viable human VSMCs in vitro. In contrast, secondary necrotic VSMCs release both IL-1␣ and caspase-activated IL-1␤, augmenting IL-6 and MCP-1 production. Conditionally inducing VSMC apoptosis in situ in hyperlipidemic SM22␣-hDTR/ApoE ؊/؊ mice to levels seen in human plaques increases serum MCP-1, tumor necrosis factor ␣, and IL-6, which is prevented by blocking IL-1. Key Words: apoptosis Ⅲ phagocytosis Ⅲ atherosclerosis Ⅲ inflammation Ⅲ hyperlipidemia T he phagocytosis of senescent or dead cells plays a pivotal role in development, normal tissue turnover, regulation of the immune system, and the resolution of inflammation. Phagocytosis of apoptotic cells generally leads to reduced expression of inflammatory cytokines such as tumor necrosis factor (TNF)-␣ and interleukin (IL)-12 1,2 and increased production of antiinflammatory cytokines such as IL-10 1 and transforming growth factor ␤. 2 However, if dying or apoptotic cells are not swiftly phagocytosed they may undergo necrosis, with lysis releasing endogenous "danger signals" 3 able to induce inflammation. Indeed, a growing body of evidence suggests that defective phagocytosis may be involved, or even causative, in many inflammatory diseases including rheumatoid arthritis, 4 lung injury, autoimmune diseases, 5 and, more recently, atherosclerosis. 6,7 Atherosclerosis is a chronic inflammatory disease in which both innate and adaptive immunity modulate disease progression. 8 Many advanced atherosclerotic plaques consist of a fibrous cap of vascular smooth muscle cells (VSMCs), collagen, and extracellular matrix, with macrophages and T lymphocytes present in superficial regions of the plaque. Myocardial infarction occurs when the fibrous cap ruptures to expose the lipid-rich core, with subsequent thrombosis occluding the vessel. Plaque stability is determined by its mechanical properties, in particular the number of VSMCs and their ability to synthesize extracellular matrix. 9 Both apoptosis and necrosis occur in advanced plaques ...

Environmental pollution has the potential to have a significant impact on animal’s health especially on birds due to daily exposure and habitat. This experimental study was carried out for a 60 days period in which, a total of 24 pigeon birds with suitable weight (80-100 g) were kept in Animal house with suitable environmental conditions viz, controlled temperature, humidity & light source to minimize any other stress. Out of twenty-four, eighteen birds were divided into three treatment groups (6 birds in each group). Whole experiment was run in triplicate manner in breeding season. One served as Control (Group 1) and remaining three were experimental groups including Road traffic noise (Group 2), Military noise (Group 3) & Human activities noise (Group 4). Noise was applied as recorded high intensity music (1125 Hz/ 90 dB) through speakers for 5-6 hrs. daily. Blood sampling was done after 20, 40 and 60 days by sacrificing treatment birds. Noise stress significantly (p<0.05) increase the serum levels of corticosterone and thyroid stimulating hormone (TSH) in Group 2 while significantly (p<0.05) decrease the serum levels of luteinizing hormone (LH) and follicle stimulating hormone (FSH) of Group 3 birds. Moreover, major fault bars formation was seen both in Group 2 and Group 3. It was concluded as that Noise stress caused rise in serum levels of Corticosterone and TSH but fall in LH and FSH. Along with fault bars formation was also prominent in all treatment groups due to stress hormone.

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