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Abstract
Eicosanoids, lymphokines, and free radicals are known to participate in the pathogenesis
of inflammation. Tumour necrosis factor (TNF), interluekin-1 and 6 (IL-1 and IL-6)
and colony stimulating factor-1 (CSF-1) are secreted mainly by activated macrophages,
whereas T-cells secrete IL-2, IL-3, IL-4 and interferon-γ (IFN-γ). In addition, activated
macrophages and lymphocytes can also produce eicosanoids and free radicals which have
potent pro-inflammatory actions. Eicosanoids, lymphokines, and free radicals can modulate
the immune response, cell proliferation, stimulate collagenase and proteases secretion
and induce bone resorption; events which are known to be associated with various collagen
vascular diseases. On the other hand transforming growth factor-β (TGF-β) produced
by synovial tissue, platelets and lymphocytes can inhibit collagenase production,
suppress T-cell and NK-cell proliferation and activation and block free radical generation
and seems to be of benefit in rheumatoid arthritis. Drugs such as cyclosporine, 1,25,dihydroxycholecalciferol
and pentoxyfylline can block lymphokine and TNF production and thus, may inhibit the
inflammatory process. Essential fatty acids, the precursors of eicosanoids, are suppressors
of T-cell proliferation, IL-1, IL-2 and TNF production and have been shown to be of
benefit in rheumatoid arthritis, systemic lupus erythematosus and glomerulonephritis.
Thus, the interactions between essential fatty acids, eicosanoids, lymphokines, TGF-β
and free radicals suggest that new therapeutic strategies can be devised to modify
the course of collagen vascular diseases.
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rats.Article info
Publication history
Accepted:
July 3,
1991
Received:
April 17,
1991
Identification
Copyright
© 1991 Published by Elsevier Inc.
