Apoptosis and inflammation

Abstract

During the last few decades it has been recognized that cell death is not the consequence of accidental injury, but is the expression of a cell suicide programme. Kerr et al. (1972) introduced the term apoptosis. This form of cell death is under the influence of hormones, growth factors and cytokines, which depending upon the receptors present on the target cells, may activate a genetically controlled cell elimination process. During apoptosis the cell membrane remains intact and the cell breaks into apoptotic bodies, which are phagocytosed. Apoptosis, in contrast to necrosis, is not harmful to the host and does not induce any inflammatory reaction. The principal event that leads to inflammatory disease is cell damage, induced by chemical/physical injury, anoxia or starvation. Cell damage means leakage of cell contents into the adjacent tissues, resulting in the capillary transmigration of granulocytes to the injured tissue. The accumulation of neutrophils and release of enzymes and oxygen radicals enhances the inflammatory reaction. Until now there has been little research into the factors controlling the accumulation and the tissue load of granulocytes and their histotoxic products in inflammatory processes. Neutrophil apoptosis may represent an important event in the control of intlamtnation. It has been assumed that granulocytes disintegrate to apoptotic bodies before their fragments are removed by local macrophages. Removal of neutrophils from the inflammatory site without release of granule contents is of paramount importance for cessation of inflammation. In conclusion, apoptotic cell death plays an important role in inflammatory processes and in the resolution of inflammatory reactions. The facts known at present should stimulate further research into the role of neutrophil, eosinophil and macrophage apoptosis in inflammatory diseases.

Adipocyte Death and Chronic Inflammation in Obesity

“…During the process of apoptosis, dying cells break into apoptotic bodies that are rapidly phagocytosed ; therefore, this type of cell death is not considered to be a cause of inflammation (2). However, previous studies revealed that programmed cell death also affects immunity and induces inflammation, and, in recent years, inappropriate cell death was shown to be involved in metabolic diseases.…”

Apoptosis of polymorphonuclear leukocytes of the juvenile bovine mammary gland during induced influx

“…Apoptosis of PMN differs from necrosis. During the onset of apoptosis, the organelles and the cytoplasmic membrane remain intact and the histotoxic content of granules is not released into the extracellular compartment [6,9,33]. Moreover, apoptotic PMN are promptly removed by the macrophages (MAC) before they can support the development of cellular damage [33].…”

Silibinin, up-regulates chemokine receptor expression in MDA-MB-231 breast cancer cell line

“…Interestingly, the result of this study revealed that silibinin not only had noinhibitory effects on CXCR3, CCR5 and CCR7 genes expression, but also could increase significantly the expressionof these genes in a dose and time-dependent manner. Although there is no study in the literature to be compared with this study,but there is a report that thecellular and molecular mechanisms of silibinin function could be cell-cycle arrest and apoptosis, therefore, the only proposed mechanism for inducing the effects of silibinin in chemokine receptor gene expression might beapoptotic cell death which can play an important role in inflammatory processes and reduction inflammatory reactionsrelated tochemokines receptors genes expression 22 .…”