Role of LITAF in LPS-induced tissue and cellular response
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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.
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, Goldman School of Dental Medicine, 2006 (Periodontology and Oral Biology).Includes bibliographical references: leaves 58-68.
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