Dead Lactobacillus plantarum Stimulates and Skews Immune Responses toward T helper 1 and 17 Polarizations in RAW 264.7 Cells and Mouse Splenocytes
- Authors
- Lee, Hyun Ah; Kim, Hyunung; Lee, Kwang-Won; Park, Kun-Young
- Issue Date
- 3월-2016
- Publisher
- KOREAN SOC MICROBIOLOGY & BIOTECHNOLOGY
- Keywords
- Dead nano-sized Lactobacillus plantarum; nitric oxide; RAW 264.7 macrophages; splenocyte; Th1/Th2/Th17 cytokines
- Citation
- JOURNAL OF MICROBIOLOGY AND BIOTECHNOLOGY, v.26, no.3, pp.469 - 476
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- JOURNAL OF MICROBIOLOGY AND BIOTECHNOLOGY
- Volume
- 26
- Number
- 3
- Start Page
- 469
- End Page
- 476
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/89431
- DOI
- 10.4014/jmb.1511.11001
- ISSN
- 1017-7825
- Abstract
- This study was undertaken to evaluate the immunomodulatory effect of dead nano-sized Lactobacillus plantarum (nLp) in RAW 264.7 cells and murine primary splenocytes. nLp is a dead, shrunken, processed form of L. plantarum nF1 isolated from kimchi (a traditional Korean fermented cabbage) and is less than 1 mum in size. It was found that nLp treatment stimulated nitric oxide (NO) production more in RAW 264.7 macrophages than pure live L. plantarum (pLp), and that the stimulatory properties were probably largely derived from its cell wall. In addition, nLp induced murine splenocyte proliferation more so than pLp; in particular, a high dose of nLp (1.0 x 10(11) CFU/ml) stimulated proliferation as much as lipopolysaccharide at 2 mug/ml. Moreover, according to our cytokine profile results in splenocytes, nLp treatment promoted Th1 (TNF-alpha, IL-12 p70) responses rather than Th2 (IL-4, IL-5) responses and also increased Th17 (IL-6, IL-17A) responses. Thus, nLp stimulated NO release in RAW 264.7 cells and induced splenocyte proliferation more so than pLp and stimulated Th1 and Th17 cytokine production. These findings suggested that dead nLp has potential use as a functional food ingredient to improve the immune response, and especially as a means of inducing Th1/Th17 immune responses.
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