Dietary Intake of Various Lactic Acid Bacteria Suppresses Type 2 Helper T Cell Production in Antigen-Primed Mice Splenocyte

  • Lee, Hui-Young (Department of Laboratory Animal Medicine, College of Veterinary Medicine, Seoul National University) ;
  • Park, Jong-Hwan (Department of Laboratory Animal Medicine, College of Veterinary Medicine, Seoul National University) ;
  • Seok, Seung-Hyeok (Department of Laboratory Animal Medicine, College of Veterinary Medicine, Seoul National University) ;
  • Cho, Sun-A. (Department of Laboratory Animal Medicine, College of Veterinary Medicine, Seoul National University) ;
  • Baek, Min-Won (Department of Laboratory Animal Medicine, College of Veterinary Medicine, Seoul National University) ;
  • Kim, Dong-Jae (Department of Laboratory Animal Medicine, College of Veterinary Medicine, Seoul National University) ;
  • Lee, Yeon-Hee (Department of Biology, Seoul Womens University) ;
  • Park, Jae-Hak (Department of Laboratory Animal Medicine, College of Veterinary Medicine, Seoul National University)
  • 발행 : 2004.02.01

Abstract

Lactic acid bacteria (LABs) have been proposed as a potential oral allergy-therapeutic means of modulating immune phenotype expression in vivo, via promoting or reducing cytokine production. This study investigated the ability of LABs to suppress allergic response via modulating cytokine production in mice splenocytes. BALB/c mice were intraperitoneally primed with ovalbumin together with alum adjuvant to invoke antigen-specific Th1/Th2 cytokine-secreting cell populations in splenocytes. Spleen cells from mice fed with Lactobacillus confusus PL9001 (KCCM-10245), L. fermentum PL9005 (KCCM-10250), L. plantarum PL9011 (KCCM-10358), and Bifidobacterium infantis PL9506 (KCCM-10406) suppressed the levels of Th2 cell cytokines such as IL-4 and IL-5 during antigen sensitization. In addition, all mice fed with LABs induced secretion of Th1 cell cytokines such as IL-2 in splenocytes. These results suggested that LABs are anti-allergic agents, in view of their Th1/anti-Th2 immunoregulation.

Keywords

References

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