Potent effects of, and mechanisms for, modification of crosstalk between macrophages and adipocytes by lactobacilli
Version of Record online: 29 NOV 2012
© 2012 The Societies and Wiley Publishing Asia Pty Ltd
Microbiology and Immunology
Volume 56, Issue 12, pages 847–854, December 2012
How to Cite
Miyazawa, K., He, F., Yoda, K. and Hiramatsu, M. (2012), Potent effects of, and mechanisms for, modification of crosstalk between macrophages and adipocytes by lactobacilli. Microbiology and Immunology, 56: 847–854. doi: 10.1111/j.1348-0421.2012.00512.x
- Issue online: 29 NOV 2012
- Version of Record online: 29 NOV 2012
- Accepted manuscript online: 27 SEP 2012 12:51PM EST
- Received 12 April 2012; revised 29 August 2012; accepted 30 August 2012.
- J774.1 cells;
- 3T3-L1 cells
The murine macrophage-like cell line J774.1 was treated with heat-killed cells of Lactobacillus GG (LGG) and L. gasseri TMC0356 (TMC 0356). Interleukin (IL)-6, IL-12, and tumor necrosis factor-α were profiled from the J774.1 cells using enzyme-linked immunosorbent assay methods. The conditioned medium from cultured J774.1 cells was transferred to the preadipocyte cell line 3T3-L1 (which is a mouse embryonic fibroblast-adipose-like cell line). Growth and differentiation of 3T3-L1 cells were monitored by analyzing lipid accumulation and expression of peroxisome proliferator-activated receptor (PPAR)-γ mRNA. The medium conditioned by 3T3-L1 cells was added to J774.1 cells and the cytokines in the supernatant analyzed. Compared with that of cells exposed to a PBS-conditioned medium, lipid accumulation in 3T3-L1 cells was significantly suppressed in a dose-dependent manner by each medium that had been conditioned with LGG and TMC0356. PPAR-γ mRNA expression in 3T3-L1 cells was also significantly downregulated (P < 0.01, P < 0.05, respectively). The conditioned medium of 3T3-L1 adipose phenotype significantly stimulated production of IL-6 and IL-12 in J774.1 cells treated with LGG and TMC0356. These results suggest that lactobacilli may suppress differentiation of preadipocytes through macrophage activation and alter the immune responses of macrophages to adipose cells.