The role of inflammation in vascular diseases

Abstract

When the body responds to an infectious insult, it initiates an immune response to eliminate the pathogen. The hallmark of the immune response is an inflammatory cascade that can also do extensive damage to host tissues. Inflammation is a major contributing factor to many vascular events, including atherosclerotic plaque development and rupture, aortic aneurysm formation, angiogenesis, and ischemia/reperfusion damage. The immune response is mediated by both circulating and resident leukocytes and the cells with which they interact (e.g., vascular endothelium and smooth muscle cells). The process is orchestrated by the activity of a changing series of released and displayed mediators. These include the expression of adhesion molecules on leukocytes and underlying vascular endothelium and the release of cytokines, chemokines, and tissue-destructive metalloproteases and reactive oxygen species. This review focuses on the causes, the inflammatory processes involved, and possible strategies for decreasing vascular disease through regulation of the inflammatory response.

Autophagy Contributes to Caspase-independent Macrophage Cell Death

“…The importance of macrophages in this defense system is evident by the fact that the virulence of some bacteria is due to their ability to overcome the protective responses of the host by triggering the death of activated macrophages (2)(3)(4). However, prolonged activation of macrophages is also believed to be dangerous because it can cause extensive local tissue damage if uncontrolled (5)(6)(7). The death of activated macrophages could also be beneficial in controlling the level of inflammation.…”

The relation between delivery type and cord blood levels of chitotriosidase and Troponin T

“…Recent data suggest that the balance between reactive oxygen species (ROS) and nitric oxide (NO) plays a role in microvascular response to hypoxia. A study by Steiner et al [28] showed that ROS formation increased in the mesenteric microcirculation during hypoxia. ROS formation, as well as leukocyte adherence and migration, was shown to decrease with an antioxidant pretreatment before the hypoxia.…”

“…Another potential result of the oxidative stress that results from the imbalance between ROS and NO is an increase in local inflammatory mediators, which are readily formed from arachidonic acid; these substances play a role in the microvascular rapid response to hypoxia [27,28]. Circulatory levels of cytokines, such as leukotriene B4 (LTB4), have been shown to increase during hypoxia [29].…”

Garlic Extract Ameliorates Renal and Cardiopulmonary Injury in the Rats with Chronic Renal Failure

“…60 In many inflammatory disorders, important components of the pathological processes are linked to the ability of neutrophils to release several agents that can destroy normal cells and dissolve connective tissue. It has been shown that activated phagocytic neutrophils, when suitably stimulated, secrete enzymes (e.g., MPO, elastase, and proteases) and liberate oxygen radicals, 61 and thus further aggravate tissue injury indirectly through activated neutrophils. MPO, an essential enzyme for normal neutrophil function, is released from the neutrophils when they are stimulated by various stimulants.…”