Get access

Induction of tolerance after establishment of peanut allergy by the food allergy herbal formula-2 is associated with up-regulation of interferon-γ


Xiu-Min Li, Pediatric Allergy and Immunology, The Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029-6574, USA.


Background Peanut (PN)-anaphylaxis is potentially life threatening. We previously reported that a Chinese herbal medicine preparation, food allergy herbal formula-2 (FAHF-2), prevented peanut allergy (PNA) in mice when administered during sensitization.

Objective To investigate whether FAHF-2 also can prevent anaphylactic reactions when administered to mice with established PNA and, if so, whether protection would persist after cessation of therapy.

Methods C3H/HeJ mice sensitized and boosted over 8 weeks with a standard protocol known to establish PN hypersensitivity received seven weeks of FAHF-2 treatment or water as a sham treatment. Mice were subsequently challenged with PN at week 14 (1-day post-therapy) and week 18 (4-week post-therapy) to evaluate the efficacy and persistence of FAHF-2 treatment by assessing anaphylactic scores, core body temperatures and plasma histamine levels. Serum PN-specific antibody levels and cytokine profiles from splenocytes and mesenteric lymph node (MLN) cells were also determined.

Results All sham-treated mice challenged at weeks 14 and 18 showed anaphylactic symptoms. In contrast, FAHF-2-treated mice showed no sign of anaphylactic reactions. PN-specific IgE levels in FAHF-2-treated mice also were reduced whereas IgG2a levels were increased. Furthermore, MLN cells from FAHF-2-treated mice produced markedly less IL-4 and IL-5, but more IFN-γ, and contained increased numbers of IFN-γ-producing CD8+ cells as compared with sham-treated mice.

Conclusion FAHF-2 treatment established PN tolerance in this model, which persisted for at least 4-week post-treatment. This result was associated with modulation of intestinal T helper type 1 cell (Th1) and Th2 cytokine production, and with increased numbers of mesenteric IFN-γ-producing CD8+ cells.