Lactobacillus casei strain Shirota suppresses serum immunoglobulin E and immunoglobulin G1 responses and systemic anaphylaxis in a food allergy model
Article first published online: 21 NOV 2002
Clinical & Experimental Allergy
Volume 32, Issue 4, pages 563–570, April 2002
How to Cite
Shida, K., Takahashi, R., Iwadate, E., Takamizawa, K., Yasui, H., Sato, T., Habu, S., Hachimura, S. and Kaminogawa, S. (2002), Lactobacillus casei strain Shirota suppresses serum immunoglobulin E and immunoglobulin G1 responses and systemic anaphylaxis in a food allergy model. Clinical & Experimental Allergy, 32: 563–570. doi: 10.1046/j.0954-7894.2002.01354.x
- Issue published online: 21 NOV 2002
- Article first published online: 21 NOV 2002
- Submitted 18 April 2001; revised 2 July 2001; accepted 29 October 2001
- lactic acid bacterium;
- Lactobacillus casei strain Shirota;
- food allergy;
- TCR transgenic mouse;
Background Our previous study using allergen-sensitized murine splenocyte cultures has shown that Lactobacillus casei strain Shirota (LcS), a lactic acid bacterium widely used as a starter for fermented milk products, suppresses IgE production through promoting a dominant Th1-type response mediated by IL-12 induction.
Objective We tried to evaluate the ability of LcS to suppress both IgE response and allergic reactions in vivo using a food allergy model with ovalbumin-specific T cell receptor transgenic (OVA-TCR-Tg) mice.
Methods The ability of heat-killed LcS to induce IL-12 in serum was tested. OVA-TCR-Tg mice were fed a diet containing OVA for 4 weeks and injected with LcS intraperitoneally three times in the first week of this period. Cytokine and antibody secretion by splenocytes, and serum IgE and IgG1 responses were examined. The inhibitory effect of LcS on systemic anaphylaxis induced by intravenous challenge of OVA-fed OVA-TCR-Tg mice with OVA was also tested.
Results Intraperitoneal injection of LcS induced an IL-12 response in the serum of OVA-TCR-Tg mice. In the food allergy model, LcS administration skewed the pattern of cytokine production by splenocytes toward Th1 dominance, and suppressed IgE and IgG1 secretion by splenocytes. The ability of LcS to modulate cytokine production was blocked by anti-IL-12 antibody treatment. LcS also inhibited serum OVA-specific IgE and IgG1 responses and diminished systemic anaphylaxis.
Conclusion LcS administration suppresses IgE and IgG1 responses and systemic allergic reactions in a food allergy model, suggesting a possible use of this lactic acid bacterium in preventing food allergy.