Suppression of Inflammation by Recombinant Salmonella typhimurium Harboring CCL22 MicroRNA
- Authors
- Yoon, Won Suck; Ryu, Seung Rel; Lee, Seung Seok; Chae, Yang Seok; Kim, Eun Jae; Choi, Ji Hyun; Oh, Sejin; Park, Se Ho; Choung, Ji Tae; Yoo, Young; Park, Yong Keun
- Issue Date
- 3월-2012
- Publisher
- MARY ANN LIEBERT, INC
- Keywords
- INDUCED ATOPIC-DERMATITIS; ANTIGEN-EXPRESSION; T-CELLS; MICE; CHEMOKINES; MDC/CCL22; VACCINES; CD4(+); CCL17; SKIN
- Citation
- DNA AND CELL BIOLOGY, v.31, no.3, pp.289 - 296
- Indexed
- SCIE
SCOPUS
- Journal Title
- DNA AND CELL BIOLOGY
- Volume
- 31
- Number
- 3
- Start Page
- 289
- End Page
- 296
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/105442
- DOI
- 10.1089/dna.2010.1118
- ISSN
- 1044-5498
- Abstract
- Atopic dermatitis (AD) is an inflammatory, chronically relapsing, puritic skin disorder. These syndromes result from multifactorial inheritance, with interaction between genetic and environmental factors. In particular, the macrophage-derived chemokine CCL22 is directly implicated in skin inflammatory reactions and its levels are significantly elevated in serum and correlated with disease severity in AD. We tested the suppression of the CCL22 gene by microRNA (miRNA) and observed the effects in mice with inflammation similar to AD. We used Salmonella as a vector to deliver miRNA. The recombinant strain of Salmonella typhimurium expressing CCL22 miRNA (ST-miRCCL22) was prepared for in vivo knockdown of CCL22. ST-miRCCL22 was orally inoculated into mice and the CCL22 gene suppressed with CCL22 miRNA in the activated lymphocytes. IgE and interleukin-4 were inhibited and interferon-g was induced after treatments with ST-miRCCL22 and CCL22 was suppressed. Further, Th17 cells were suppressed in the atopic mice treated with ST-miRCCL22. These results suggested that suppression of the CCL22 gene using Salmonella induced anti-inflammatory effects.
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- Appears in
Collections - College of Medicine > Department of Medical Science > 1. Journal Articles
- Graduate School > Department of Life Sciences > 1. Journal Articles
- College of Life Sciences and Biotechnology > Division of Life Sciences > 1. Journal Articles
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