Inflammatory response, agents affecting

This, in turn, has led to investigation of OP-mediated suppression of the hypothalamic-pituitary-adrenal axis (Pena-Philippides et al., 2007). However, anti-ChEs were also found to initiate acute immune responses. For example, the nerve agent soman induces an increase in the pro-inflammatory cytokine TNFa, IL-lp, and fL-6 in rats, including in the brain, where IL-lp is thought to contribute to irreversible brain damage (Banks and Lein, 2012). This bidirectional impairment of immune functions may reflect systemic responses that affect more than the cholinergic system alone. 

The close association of fibrin d osition and inflammatory response is further supported by several recent experiments. The carrageenin-edema in the rat paw is inhibited by agents such as pival and heparin which affect the formation and resolution of fibrin.xhe moderate vitro fibrinolytic activity of antiinflammatory drugs has been confirmed and attributed to their binding to the fibrin molecule and possibly the release of a fibrinolytic activator. Salicylate and phenylbutazone also inhibit platelet aggregation and adhesion induced by fibrin and collagen fragments. 

Corticosteroids are the most potent anti-inflammatory agents available for the treatment of asthma. The efficacy of corticosteroids is due to their ability to affect multiple inflammatory pathways, resulting in the suppression of inflammatory cell activation and function, prevention of microvascular leakage, decreased mucus production, and upregulation of P2-adrenergic receptors.10,18 Clinically, corticosteroids decrease airway inflammation, decrease AHR, decrease mucus production and secretion, and improve the response to P2-agonists.18 Corticosteroids for the treatment of asthma are available in inhaled, oral, and injectable dosage forms. 

Flavonoids affect the immune system and the body s inflammatory cells. This function is partly accomplished through the effects on enzymes involved in the immune response and the generation of inflammatory cells. Balentine et al. (1999) recently reported that only the aglycon cyanidin, not the anthocyanin glycoside, showed inhibitory effects on enzymes involved in inflammatory activity. The anthocyanins can be metabolized into their glycoside-free constituents either before or after absorption in the gut and may thereby act as anti-inflammatory agents in the body. Middleton and Kandaswami (1994) stress the fact, however, that as most of these studies have been carried out as in vitro experiments, care should be taken not to draw too extensive conclusions for the in vivo actions of flavonoids. Fundamental biochemical research is needed before the mechanisms behind the diverse actions of flavonoids are fully understood. 

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