May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
IL–4 and TGFb2 modulate TNF–alpha– and IL–1beta–induced IL–8 and MCP–1 production by human glaucomatous trabecular meshwork cells.
Author Affiliations & Notes
  • C. Blondin
    Ophthalmology, Quinze Vingts Hospital AP HP University Paris VI, Paris, France
  • A. Pauly
    Ophthalmology, Quinze Vingts Hospital AP HP University Paris VI, Paris, France
  • P. Hamard
    Ophthalmology, Quinze Vingts Hospital AP HP University Paris VI, Paris, France
  • C. Baudouin
    Ophthalmology, Quinze Vingts Hospital AP HP University Paris VI, Paris, France
  • Footnotes
    Commercial Relationships  C. Blondin, None; A. Pauly, None; P. Hamard, None; C. Baudouin, None.
  • Footnotes
    Support  none
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 902. doi:
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      C. Blondin, A. Pauly, P. Hamard, C. Baudouin; IL–4 and TGFb2 modulate TNF–alpha– and IL–1beta–induced IL–8 and MCP–1 production by human glaucomatous trabecular meshwork cells. . Invest. Ophthalmol. Vis. Sci. 2004;45(13):902.

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Abstract

Abstract: : Purpose: To investigate the effects of interleukin 4 (IL–4) and transforming factor beta 2 (TGFb2) on tumor necrosis factor alpha (TNFa)–induced and interleukin 1 beta (IL–1b)–induced chemokine production by human trabecular meshwork (HTM) cells. Methods: A human trabecular cell line derived from a glaucomatous donor (HTM3 cell line) was stimulated with 10 ng/ml IL–4, TGFb, TNFa and IL–1b alone or in combination for 48 hours. Culture supernatants were subjected to enzyme–linked immunosorbent assay (ELISA) for interleukin 8 (IL–8) and monocyte chemotactic protein 1 (MCP–1), and the detected proteins were compared. Results: The respective effects of IL–4, TGFb2 and the combination of IL–4 and TGFb2 were similar for TNFa–induced and IL–1b–induced IL–8 and MCP–1 production by HTM3 cells. Specifically, IL–4 induced no significant change in IL–8 production and increased MCP–1 production (p≤0.0196). TGFb2 decreased IL–8 production (p≤0.0127) and had no effect on MCP–1 production. The combination of IL–4 and TGFb2 resulted in a decrease in IL–8 production (p≤0.0062) and an increase in MCP–1 production (p≤0.0024) in response to either TNFa or IL–1b. Results using a combination of TNFa and IL–1b were similar for each case. Conclusions: Production of the proinflammatory chemokines IL–8 and MCP–1 by HTM cells appears to be tightly regulated by immunomodulatory factors known to be present in aqueous humor, such as IL–4 and TGFb2. These factors might be important in controlling initiation and/or development of inflammatory reactions within the trabecular meshwork micro–environment.

Keywords: trabecular meshwork • immunomodulation/immunoregulation • inflammation 
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