Canadá
Cy tokines are important soluble signalling molecules that dict ate and coordinate inflammatory and immune res ponses. Furth e r understandin g th e role of cy to kin es in th e pa th o bi o log ic mecha nisms o f pulmonary inflammatory and immune diseases holds the key to the development of effecti ve proph ylacti c and therapeutic strategies. In the last several yea rs, the use of models of human pulmonary diseases established either in norm al adult animals, mi ce defi cient for a give n immune ce ll type or cy tokine, or mice engineered to overex press a given cytokine, has remarkably facilitated o ur und e rstandin g o f th e mech ani sms ope ratin g in hum an disease . Cy to kin es th at a re in vo lve d in pulmonary infl ammatory and immune conditions may be generally divided into groups of pro-inflammatory, antiinflammatory and growth-stimulatory cytokines. While pro-inflammatory cy tokines ca n be detrimental under such eve re conditions as endotoxemia and fibrosis, they are required in host resistance against infectious agents.
Anti-inflammatory cytokines play an import ant role in controlling th e ex tent of tissue infl ammatory/immune res po nses. Ove rex pressio n o f g row th-stimul ato ry cyto kin es a re oft en directl y associated with tiss ue fibrotic responses. In this review, the findin gs attained fro m exp erime nt al models by us a nd ot he rs we re discussed with emphasis on cellular and histopathologic alterations, cy tokine-medi ated molecul ar mechanisms and th e pros pec ts of cy to kin e-b ase d th e ra peut ic strategies. Due to the restricted space, we chosc to focus onl y on models for endotoxic lung, endotoxemia, acute pulmonary infections by extrace llular Gram-negative bacteri a, chronic pulmonary in fections by intracellular myco -bac te ri a, all e rg ic a irw ays infl amm ati on and pulmonary fib rosis.
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