Modulation of renal inflammation: therapeutic strategies.
Inflammation is a complex process that reflects the local and systemic responses to different immunological and non-immunological stimuli, enable resistance to disease, repair of tissue damage, and restoration of normal function with the least possible tissue damage. This is achieved by intact regulatory immune system, which includes pro- and anti-inflammatory cytokines, chemokines, growth factors, complement cascade system, renin-angiotensin system, and different sets of adhesion molecules expressed on leukocytes and vascular endothelium, in addition to neutrophils, monocytes/macrophages, and different subsets of T-lymphocytes. Once imbalance occurs in the different factors of the inflammatory response to injurious stimuli, inflammation will proceed and exacerbate tissue damage. Inflammation can be initiated by different stimuli such as deposition or formation of antibody-antigen immune complexes, sensitized T-cells, trauma, tissue necrosis, or infection. It is characterized by activation of acute phase response and release of reactants/markers such as C-reactive protein. Renal inflammation can occur either as an isolated local acute inflammatory reaction or as part of a systemic inflammatory disorder. Recently, there have been tremendous advancements in the fields of immunology and molecular biology that helped in exploring the mechanisms of renal inflammation. This has been accompanied by extensive in vitro and in vivo studies that led to a better understanding of phenotypic changes and multifunctional potentials of local and infiltrating cells, role and control of different inflammatory mediators, adhesion molecules, and the rennin-angiotensin system within the site of inflammation. These achievements helped in researching into ways to modulate renal inflammation, control the severity of renal injury, promote regeneration and tissue repair, and induce tolerance.
Karkar
Ayman
A
D058186:Acute Kidney Injury / Q000276:immunology / Q000503:physiopathology* / Q000628:therapy; D002908:Chronic Disease; D016207:Cytokines / Q000502:physiology; D005921:Glomerulonephritis / Q000276:immunology / Q000503:physiopathology / Q000628:therapy; D018380:Hematopoietic Stem Cell Transplantation; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000503:physiopathology*; D007668:Kidney / Q000276:immunology / Q000503:physiopathology*; D007674:Kidney Diseases / Q000276:immunology / Q000503:physiopathology / Q000628:therapy; D008264:Macrophages / Q000502:physiology; D016176:T-Lymphocyte Subsets / Q000276:immunology
D016207:Cytokines