Role of LITAF in LPS stimulated local and systemic response
Date
2006
DOI
Authors
Tai, Te-Yu
Version
OA Version
Citation
Abstract
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.
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Thesis (MSD)--Boston University, Henry M. Goldman School of Dental Medicine, 2006 (Periodontology and Oral Biology).
Includes bibliographical references: leaves 42-50.
Thesis (MSD)--Boston University, Henry M. Goldman School of Dental Medicine, 2006 (Periodontology and Oral Biology).
Includes bibliographical references: leaves 42-50.
License
This work is protected by copyright. Downloading is restricted to the BU community. If you are the author of this work and would like to make it publicly available, please contact open-help@bu.edu.