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Inflammation induced changes in adipocytes
Title
Inflammation induced changes in adipocytes
Creator
Kim, Kihwan
Date
2019
Description
The significant features of Crohn’s Disease include creeping fat that covers more than 50% of both small and large intestine surfaces and high...
Show moreThe significant features of Crohn’s Disease include creeping fat that covers more than 50% of both small and large intestine surfaces and high level of inflammatory cytokines such as TNF-alpha and IL-6. However, the relationship between these two factors of Crohn’s Disease is still unknown. Therefore, verifying the relationship could contribute to understanding the cause of Crohn’s Disease. In this study, preadipocytes were used because they have a potential to grow as adipocytes which are developed as creeping fat. The objective of this study was to observe proliferation, differentiation, and chemotaxis of preadipocytes in inflammatory microenvironment. It was found that only TNF-alpha stimulates preadipocyte proliferation whereas IL-6 does not. However, both TNF-alpha and IL-6 inhibit differentiation of preadipocytes. Furthermore, preadipocytes did not have chemotactic responses towards both cytokines. Therefore this study concludes that these inflammatory microenvironments induce the preadipocytes proliferation in Crohn’s. However, they inhibit adipogenesis and recruitment of the preadipocytes in Crohn’s.
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DEVELOPING FUSION BACTERIOCINS FOR ERADICATING PSEUDOMONAS AERUGINOSA BIOFILMS
Title
DEVELOPING FUSION BACTERIOCINS FOR ERADICATING PSEUDOMONAS AERUGINOSA BIOFILMS
Creator
An, Sungjun
Date
2022
Description
The opportunistic pathogen Pseudomonas aeruginosa is a leading cause of morbidity and mortality in cystic fibrosis patients and...
Show moreThe opportunistic pathogen Pseudomonas aeruginosa is a leading cause of morbidity and mortality in cystic fibrosis patients and immunocompromised individuals. Due to its remarkable ability to resist antibiotics, eradicating P. aeruginosa has become increasingly difficult. As previously reported, we have successfully engineered a colicin-secretion system that kills target biofilm cells rapidly and selectively in multispecies biofilms as well as demonstrated the potential of using live microorganisms engineered to produce antimicrobial colicin protein to treat biofilm-associated infections. In this study,we constructed a fusion colicin-pyocin that could target P. aeruginosa by DNase activity of colicin E2. The newly engineered bacteriocin-secretion system upon the shift in target, maintained biofilm inhibition capacity. Both during biofilm formation and after its development, the system was able to suppress the P. aeruginosa biofilm. This result opened up the possibility that it could be used for novel live biotherapeutics. A further study was conducted to overcome the challenge of requiring an exogenous inducer. We applied the concept of Quorum-Sensing signal that recognize autoinducer as a trigger of fusion colicin-pyocin producing genetic circuit so that it automates the production and secretion of fusion colicin-pyocin as soon as the genetic circuit senses the target population growing. This study demonstrated that combining the domains of colicin and pyocin could broaden the genetic circuit target range, maintaining strain specificity, while employing the QS system could remove the fundamental problem of diffusion or degradation of extra compounds as they approach engineered cells.
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