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    LITAF mediation of increased TNF-α secretion from inflamed colonic lamina propria macrophages.

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    License
    http://creativecommons.org/licenses/by/4.0/
    Date Issued
    2011
    Publisher Version
    10.1371/journal.pone.0025849
    Author(s)
    Bushell, Kristen N.
    Leeman, Susan E.
    Gillespie, Earl
    Gower, Adam C.
    Reed, Karen L.
    Stucchi, Arthur F.
    Becker, James M.
    Amar, Salomon
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    Permanent Link
    https://hdl.handle.net/2144/40661
    Version
    Published version
    Citation (published version)
    Kristen N. Bushell, Susan E. Leeman, Earl Gillespie, Adam C. Gower, Karen L. Reed, Arthur F. Stucchi, James M. Becker, Salomon Amar. 2011. "LITAF mediation of increased TNF-α secretion from inflamed colonic lamina propria macrophages.." PLoS One, Volume 6, Issue 9, https://doi.org/10.1371/journal.pone.0025849
    Abstract
    Dysregulation of TNF-α in lamina propria macrophages (LPM) is a feature of inflammatory bowel diseases (IBD). LPS-Induced-TNF-Alpha-Factor (LITAF) is a transcription factor that mediates TNF-α expression. To determine whether LITAF participates in the mediation of TNF-α expression in acutely inflamed colonic tissues, we first established the TNBS-induced colonic inflammation model in C57BL/6 mice. LPM were harvested from non-inflamed and inflamed colonic tissue and inflammatory parameters TNF-α and LITAF mRNA and protein levels were measured ex-vivo. LPM from TNBS-treated mice secreted significantly more TNF-α at basal state and in response to LPS than LPM from untreated mice (p<0.05). LITAF mRNA and protein levels were elevated in LPM from TNBS compared with untreated animals and LPS further increased LITAF protein levels in LPM from inflamed tissue (P<0.05). To further confirm the role of LITAF in acutely inflamed colonic tissues, TNBS-induced colonic inflammation was produced in LITAF macrophage specific knockout mice (LITAF mac -/- mice) and compared to wild type (WT) C57BL/6. Twenty four hours following TNBS administration, colonic tissue from LITAF mac -/- mice had less MPO activity and reduced colonic TNF-α mRNA then WT C57BL/6 mice (p<0.05). LPM harvested from LITAF mac -/- secreted significantly less TNF-α in response to LPS than wild type (WT) C57BL/6 (p<0.05). This study provides evidence that LITAF contributes to the regulation of TNF-α in LPM harvested following acute inflammation or LPS treatment paving the way for future work focusing on LITAF inhibitors in the treatment of TNF-α-mediated inflammatory conditions.
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