Allergic Rhinitis in Rats Is Associated with an Inflammatory Response of the Hippocampus.

Shasha Yang,Zhendong Zhong,Xinrong Li,Daien Liu,Qinxiu Zhang,Haoran Kang,Jing Wu,Bin Zeng,Zhiqing Liu

doi:10.1155/2018/8750464

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.

Highlights

Allergic rhinitis (AR) is an IgE antibody-mediated immune reaction, in which expansion of the type 2 (TH2) subset of T cells [1, 2] causes typical allergy symptoms, consisting of sneezing, itching, nasal congestion, watery rhinorrhea, and even impaired quality of life (QOL) [3,4,5], affecting sleep, psychomotor functions, and social activities
In order to determine whether the AR model was established in the rat, we resorted to three major kinds of parameter points, namely, AR behavior; objective indicators including serum specific for IgE (sIgE), interleukin 4 (IL-4), and IFN-γ levels; and HE staining
Post hoc analysis revealed that AR behavior scores significantly increased in the model group of rats, compared to the control group (P < 0 01, Figure 1)

Summary

Introduction

Allergic rhinitis (AR) is an IgE antibody-mediated immune reaction, in which expansion of the type 2 (TH2) subset of T cells [1, 2] causes typical allergy symptoms, consisting of sneezing, itching, nasal congestion, watery rhinorrhea, and even impaired quality of life (QOL) [3,4,5], affecting sleep, psychomotor functions, and social activities. Multiple clinical practitioners have reported behavioral complications associated with the progression of AR, which include cognitive deficits, memory decline, poor school performance, attention deficiency and hyperactivity, anxiety, and depression [7,8,9], mainly in childhood and adolescent populations. Recent human studies have hinted at a direct relationship between antigen exposure and alteration in brain function that may precipitate high levels of anxiety and emotional reactivity [10, 11]. Increased anxiety in the open field test and activation of limbic brain regions was reported during the early phase in a mice model of food allergies [14]. In humans, increased brain activity in the prefrontal cortex was observed using functional magnetic resonance during the late phase of an asthma episode [12]

Methods

Results

Conclusion