Allergic Rhinitis in Rats Is Associated with an Inflammatory Response of the Hippocampus.
Shasha YangJing WuQinxiu ZhangXinrong LiDaien LiuBin ZengZhiqing LiuHaoran KangZhendong ZhongPublished in: Behavioural neurology (2018)
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.
Keyphrases
- allergic rhinitis
- cerebral ischemia
- inflammatory response
- public health
- prefrontal cortex
- cognitive impairment
- poor prognosis
- oxidative stress
- rheumatoid arthritis
- subarachnoid hemorrhage
- mental health
- traumatic brain injury
- lipopolysaccharide induced
- brain injury
- drinking water
- cell proliferation
- functional connectivity
- neuropathic pain
- signaling pathway
- small molecule
- lps induced
- resting state
- spinal cord
- spinal cord injury