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Inflammation requires clearance of the inciting pathogen, then orchestrated removal of the burden of leukocytes and other cells influxed into the inflamed site along with dissipation of the pro (or anti) inflammatory mediator cascades. We now recognize that this resolution process is strictly controlled by a number of mediators and adhesion molecules. Apoptotic cell death, when timed appropriately, allows the non-phlogistic clearance of PMNs, monocytes and eosinophils. Macrophage engulfment of these apoptotic cells signals further anti-inflammatory processes, including additional programmed cell death, anti-inflammatory mediator release, and promotes active macrophage emigration which is the final route by which cell clearance is effected. Should these processes evolve successfully, then the tissue will return to its normal structure and function, but should this not proceed effectively then the body will limit further damage by evoking a fibrotic response to ‘heal and seal’ the damaged tissue.

Inflammation requires clearance of the inciting pathogen, then orchestrated removal of the burden of leukocytes and other cells influxed into the inflamed site along with dissipation of the pro (or anti) inflammatory mediator cascades. We now recognize that this resolution process is strictly controlled by a number of mediators and adhesion molecules. Apoptotic cell death, when timed appropriately, allows the non-phlogistic clearance of PMNs, monocytes and eosinophils. Macrophage engulfment of these apoptotic cells signals further anti-inflammatory processes, including additional programmed cell death, anti-inflammatory mediator release, and promotes active macrophage emigration which is the final route by which cell clearance is effected. Should these processes evolve successfully, then the tissue will return to its normal structure and function, but should this not proceed effectively then the body will limit further damage by evoking a fibrotic response to ‘heal and seal’ the damaged tissue.

Inflammation requires clearance of the inciting pathogen, then orchestrated removal of the burden of leukocytes and other cells influxed into the inflamed site along with dissipation of the pro (or anti) inflammatory mediator cascades. We now recognize that this resolution process is strictly controlled by a number of mediators and adhesion molecules. Apoptotic cell death, when timed appropriately, allows the non-phlogistic clearance of PMNs, monocytes and eosinophils. Macrophage engulfment of these apoptotic cells signals further anti-inflammatory processes, including additional programmed cell death, anti-inflammatory mediator release, and promotes active macrophage emigration which is the final route by which cell clearance is effected. Should these processes evolve successfully, then the tissue will return to its normal structure and function, but should this not proceed effectively then the body will limit further damage by evoking a fibrotic response to ‘heal and seal’ the damaged tissue.