Role of LITAF in LPS-induced tissue and cellular response
Date
2006
DOI
Authors
Cheng, Karen
Version
OA Version
Citation
Abstract
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 expression of TNF[alpha]. TNF[alpha] is an important mediator in the innate inflammatory response. 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. The purpose of this study is to elucidate the relationship between LITAF and LPS-induced tissue and cellular response.
In our experiment, twelve wild type (WT) mice and twelve LITAF +/- mice were inoculated subcutaneously with 10 superscipt 10 CFU/mL P. gingivalis A7436 at the calvaria. Quantitative histological analysis of inflammatory cells and fibroblasts showed that LITAF +/- animals had elevated local inflammatory response and tissue destruction in comparison to the WT animals. Also, the resolution of inflammation was delayed for the LITAF +/- animals.
Another part of this study concluded that LITAF +/- animals experienced delay onset of sepsis-related lethality. The results suggested that animals with decreased expression of LITAF can still produce LPS-induced local toxicity. That is, decreased expression of LITAF, and in turn, TNF-a contributes to increased local but decreased systemic symptoms.
Conclusion: Our study revealed that bacterial challenge in animals with partial suppression of LITAF resulted in altered inflammatory reaction. This is likely to be a result of decreased expression of TNF[alpha], and TNF[alpha] has an essential homeostatic role in limiting the extent and duration of inflammatory processes as well as LPS-induced toxicities. 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, Goldman School of Dental Medicine, 2006 (Periodontology and Oral Biology).
Includes bibliographical references: leaves 58-68.
Thesis (MSD)--Boston University, Goldman School of Dental Medicine, 2006 (Periodontology and Oral Biology).
Includes bibliographical references: leaves 58-68.
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.