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

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.

Activation of Dopamine D2 Receptor Alleviates Neuroinflammation and Neuronal Injury in Mice Model of Allergic Rhinitis With Olfactory Dysfunction

“…This study also showed that AR-induced OD was closely related to neuroin ammation of the olfactory bulb. The expression of microglia marker protein CD11b, TNF-α, IL-1β and IL-6 in the olfactory bulbs were signi cantly increased in the AR mice with OD, which is similar to the ndings in the hippocampus [32]. However, the mechanism of allergen-induced damage to the olfactory bulb is not clear.…”

“…Several studies on humans and rodents have shown that the intranasal or nebulized inhalation in allergen-sensitized animals induced avoidance behavior and activated limbic brain areas [8,9,32,33]. OVA or pollen-induced AR rats produced TH2 cytokines in the olfactory bulb and prefrontal cortex but not in the temporal cortex and hypothalamus, and increased brain activity was observed by functional MRI [8].…”

Montelukast use over the past 20 years: monitoring of its effects and safety issues

“…However, the study concluded that antidepressant use, not montelukast use, may be correlated with asthma severity [ 49 ]. A study using an animal allergic rhinitis model reported that allergic rhinitis was associated with the induction of an inflammatory response in the hippocampus and that it may trigger associated neuropsychiatric events [ 50 ]. These findings do not guarantee the safety of montelukast; therefore, clinicians should consider the benefits and risks of montelukast before prescribing it.…”

Distraction of olfactory bulb-medial prefrontal cortex circuit may induce anxiety-like behavior in allergic rhinitis

“…Allergic rhinitis (AR) is a chronic inflammatory disorder of the nasal mucosa, which is characterized by the presence of one or some symptoms, including itchiness, sneezing, rhinorrhea, nasal congestion, and daily alterations in sense of olfaction [1–4]. AR is a highly prevalent chronic disease that affects 400 million people worldwide; and epidemiological studies have reported that 20–30% of adults and 40% of children suffer from AR [5–7].…”