title: [The pathogenesis of the systemic inflammatory response syndrome and compensatory antiinflammatory response syndrome following surgical stress].
abstract: The inflammation charge cells such as the macrophages, neutrophils, endothelial cells, and fibroblasts are activated in surgical sites when tissue injury occurs due to the operation. Proinflammatory cytokines such as tumor necrosis factor alpha, interleukin (IL)-1, IL-6, and IL-8 are induced from the activated inflammation charge cells. These cytokines amplify the information by autocrine and paracrine action, induce the production of other cytokines, and send the information to the whole body. Increases in body temperature, pulse rate, and leukocyte counts are then observed. This condition is called the systemic inflammatory response syndrome (SIRS) clinically. On the other hand, the production of antiinflammatory cytokines against SIRS is induced simultaneously. The condition in which antiinflammatory cytokines are produced in excess and become dominant systemically is called the compensatory antiinflammatory response syndrome (CARS). No standard concrete diagnosis for CARS has been established, although CARS is a pathogenetic concept. However, recently the analysis of cytokine production and various types of surface molecules in the inflammation charge cells became possible with the development of molecular biological methods. As a result, it was found that the immune system is controlled by the balance between proinflammatory and antiinflammatory cytokine production, and if the compensatory antiinflammatory reaction is sufficiently severe, it will manifest clinically as anergy, with increased susceptibility to infection. In this manuscript, we explain the pathogenesis of SIRS and CARS following surgical stress by analyzing cytokine production and surface membrane molecules in the inflammation charge cells.
authors.affiliation: Department of Surgery I, National Defense Medical College, Tokorozawa, Japan.
authors.forename: Satoshi
authors.initials: S
authors.lastname: Ono
authors.forename: Takashi
authors.initials: T
authors.lastname: Ichikura
authors.forename: Hidetaka
authors.initials: H
authors.lastname: Mochizuki
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D016207:Cytokines / Q000096:biosynthesis* / Q000276:immunology; D013505:Digestive System Surgical Procedures; D004381:Duodenal Ulcer / Q000276:immunology*; D005260:Female; D006684:HLA-DR Antigens / Q000096:biosynthesis; D006801:Humans; D007416:Intestinal Perforation / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology* / Q000276:immunology
chemical_list: D016207:Cytokines; D006684:HLA-DR Antigens