The inflammatory response: an efficient way of life.
The successive pathophysiological mechanisms that develop in the interstitium of tissues when these undergo acute post-traumatic inflammation are considered increasingly complex trophic functional systems for using oxygen. The nervous or immediate functional system presents ischemia-revascularization and edema, which favor nutrition by diffusion through injured tissue. In this phase of the inflammatory response, while the progression of the interstitial edema produces progressive distancing of the epithelial cells from the capillaries, it simultaneously enhances lymphatic circulation, which assumes an unusually important role. During immune system function, tissue nutrition is carried out by leukocytes through symbiosis with bacteria. Improper use of oxygen persists in this immune phase. Activated phagocytes would require anaerobic glycolysis as the main source of ATP for their functions. During this immune phase, lymphatic circulation still plays a major role. The dilatation of lymphatics may be mediated by cytokines, leuokotrienes, and prostaglandins produced at the trauma site by activated resident and infiltrating cells. Finally, the endocrine functional system facilitates the arrival of oxygen, transported by red blood cells and capillaries. Their trophic potential permits the tissue specialization required for tissue repair to take place. However, if complications occur during the evolution of acute inflammation, the tissues could go back to using more primitive trophic mechanisms. In summary, the ability of the interstitial tissue to express increasingly complex nutritional systems in relation to oxygen use could reflect the importance of this space as a battleground for inflammation and, as a result, for evolution.
Aller
María-Angeles
MA
Surgery Chair, Surgery Department I, School of Medicine, Complutense University of Madrid, Madrid, Spain.
Arias
Jorge-Luis
JL
Sánchez-Patán
Fernando
F
Arias
Jaime
J
D000818:Animals; D004702:Endocrine Glands / Q000502:physiology*; D006801:Humans; D007107:Immune System / Q000502:physiology*; D007249:Inflammation / Q000209:etiology / Q000276:immunology / Q000503:physiopathology*; D019369:Life; D018448:Models, Immunological; D009424:Nervous System Physiological Phenomena