Shedding of Soluble Receptor for Tumor Necrosis Factor Alpha Induced by M. leprae or LPS from Human Mononuclear Cells

Access this Article

Search this Article

Author(s)

Abstract

Cell surface expression and release of the tumor necrosis factor receptor (TNFR type I) was analyzed after stimulation of peripheral blood mononuclear cells (PBMC) with <I>Mycobacterium leprae</I> (<I>M. leprae</I>) or lipopolysaccharide (LPS). A transient spontaneous expression of TNFR type I on the surface of PBMC was observed. Two hr after activation with LPS, a significant reduction of TNFR type I expression was detected: Release of TNFR type I by <I>M. leprae</I> or LPS-stimulated PBMC was evaluated with an enzyme-linked immunoabsorbent assay. This release occurred relatively later (20 to 40 hr) than the secretion of TNF alpha which reached high levels between 8 to 20 hr after activation. <BR>Thalidomide, a potent drug for the treatment of erythema nodosum leprosum episodes by inhibiting TNF alpha production, had no influence on the TNFR type I expression. Similar results were obtained with pentoxifylline. <BR>It is concluded that the release of TNFR type I by <I>M. leprae</I> or LPS-stimulated PBMC may counteract the pro-inflammatory activities of TNF alpha, by reducing the systemic toxicity of this cytokine in leprosy.

Journal

  • JAPANESE JOURNAL OF LEPROSY

    JAPANESE JOURNAL OF LEPROSY 68(3), 185-193, 1999-11-30

    Japanese Leprosy Association

References:  31

Codes

  • NII Article ID (NAID)
    10008625826
  • NII NACSIS-CAT ID (NCID)
    AN10559906
  • Text Lang
    ENG
  • Article Type
    ART
  • ISSN
    13423681
  • Data Source
    CJP  J-STAGE 
Page Top