Role of LITAF in LPS stimulated local and systemic response
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TNF-alpha can play crucial roles in the adverse development of systemic toxicity and septic shock. Low amounts of TNF-alpha can contribute to host defense by limiting the spread of pathogenic organisms into the circulation. On the contrary, high amounts of TNF-alpha correlate with increased risk of mortality/lethality. Lipopolysaccharides Induced TNF-alpha Factor (LITAF) is a transcription factor which binds to the promoter region of TNF-alpha gene and has been shown to have the ability to up-regulate the production of TNF-alpha. The purpose of this study is to elucidate the relationship between LITAF and LPS-induced TNF-alpha production. In our experiment, twelve wild type mice and twelve LITAF +/- mice were inoculated subcutaneously at the calvaria with 10 superscript 10 CFU/mL P. gingivalis A7436. According to the daily clinical observation and histological observations of injection sites, we found that there was a twenty-four hour delay in the onset of lethality in LITAF +/- mice (Day two for wild type; Day three for LITAF +/-). Moreover, the LITAF +/- animals recruited more inflammatory cells in a well-contained local inflammatory lesion when comparing to wild type animals. It thus appeared that LITAF +/- mice had diminished secretion of TNF-alpha after LPS-challenge, but the onset of lethality was still observed. Conclusion: LITAF+/- animals exhibited increased level of local inflammation with well-contained lesions and delayed onset of lethality. Therefore, our study confirms the role of LITAF, a transcriptional factor, in LPS induced TNF-alpha toxicity and lethality. Further studies, including experiments with LITAF -/- animals will help to comprehensively elucidate the relationship of LITAF and LPS-induced TNF-alpha secretion.
PLEASE NOTE: This work is protected by copyright. Downloading is restricted to the BU community: please click Download and log in with a valid BU account to access. If you are the author of this work and would like to make it publicly available, please contact firstname.lastname@example.org.Thesis (MSD)--Boston University, Henry M. Goldman School of Dental Medicine, 2006 (Periodontology and Oral Biology).Includes bibliographical references: leaves 42-50.
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