ABSTRACT
Allergic rhinitis (AR), an IgE-mediated response, is characterized by a Th2-type immunological pattern together with mast cells activation. Acupuncture, with the use of implanted catgut, is a traditional therapy that has been widely applied for the treatment of AR. However, the exact mechanism of the immunomodulatory effects of catgut implantation at acupoint (CIAA) remains unclear, in part due to the lack of a suitable laboratory animal model. We developed and optimized a rat model of ovalbumin- (OVA-) induced allergic inflammation, characterized by increased IL-4, sIgE, and SP and reciprocal decrease of IFN-γ. In the present study, we have further used this model to address the immunomodulatory effects of CIAA stimulation at Yingxiang (LI20) and Zusanli (ST36) acupoints and to elucidate the mechanisms involved in the regulation of SP, sIgE, IL-4, IFN-γ, TLR2, and TLR4. After AR model was established via OVA challenge, the rats were randomized as follows: control, model, sham-operated, 1-week CIAA (C1), 2-week CIAA (C2), and Budesonide nasal spray. The C1 and C2 groups were subjected to the bilateral acupoint Yingxiang (LI20) and Zusanli (ST36), respectively. Multiple analyses and quantifications were performed, which revealed that due to the persistent stimulus to acupoints by embedding catgut, the C2 group improved AR symptoms, compared to the C1 group. We conclude that CIAA at the Yingxiang (LI20) and Zusanli (ST36) acupoints effectively reduces allergic symptoms and inflammatory parameters in the rat model of AR. Thus, CIAA treatment is potentially an alternative therapeutic modality in AR.
ABSTRACT
Allergic rhinitis (AR) is a major concern in personal and public health, which negatively affects emotions and behavior, leading to cognitive deficits, memory decline, poor school performance, anxiety, and depression. Several cellular and molecular mediators are released in the inflammatory process of AR and activate common neuroimmune mechanisms, involving emotionally relevant circuits and the induction of anxiety. Responsiveness of the hypothalamic-pituitary-adrenal (HPA) axis to allergic processes have been reported, which may also include responsiveness of the hippocampus, cortex, and other brain regions. Here, we have used an optimized rat model of AR to explore whether the disease has a relationship with inflammatory responses in the hippocampus. AR was established in adult rats by ovalbumin sensitization, and the expression of various inflammatory substances in the hippocampus was measured by specific assays. Comparison between experimental and various control groups of animals revealed an association of AR with significant upregulation of substance P, microglia surface antigen (CD11b), glial fibrillary acid protein (GFAP), tumor necrosis factor-α (TNF-α), and interleukin 6 (IL-6) in the hippocampus. Thus, we hypothesize that the AR challenge may activate these inflammatory mediators in the hippocampus, which in turn contribute to the abnormal behavior and neurological deficits associated with AR.
