title: Inhaled budesonide protects against chronic asthma-induced neuroinflammation in mouse brain.
abstract: Chronic asthma is one of the most common respiratory diseases, characterized by airway inflammation. However, little is known whether asthma-induced airway inflammation might influence the brain. We found that chronic asthma not only resulted in peripheral inflammation, but also induced neuroinflammation which was characterized by microglial activations and increased levels of TNFα and IL-1β in the hippocampus and prefrontal cortex. Simultaneously, we found that there was significant neuronal loss in the asthmatic mouse brain. Inhaled budesonide, the classic therapeutic drug for chronic asthma, could inhibit asthma-induced microglial activation, down-regulate TNFα and IL-1β but up-regulate TGFβ and IL-10 of mouse brain, and thereby attenuate neuronal loss. Further study showed that chronic asthma increased the expressions of TLR4 and p65/NFκB in the brain, which could be reversed by budesonide treatment. Therefore, the present study reveals that inhaled budesonide protects against asthma-induced neuroinflammation in mouse brain, which might be contributed to attenuate neuronal loss.
authors.affiliation: Jiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029, China.
authors.forename: Ming-Xu
authors.initials: MX
authors.lastname: Xia
authors.affiliation: Jiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029, China.
authors.forename: Xu
authors.initials: X
authors.lastname: Ding
authors.affiliation: Jiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Qi
authors.affiliation: Jiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Gu
authors.affiliation: Jiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029, China.
authors.forename: Gang
authors.initials: G
authors.lastname: Hu
authors.affiliation: Jiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029, China. Electronic address: xiulans@njmu.edu.cn.
authors.forename: Xiu-Lan
authors.initials: XL
authors.lastname: Sun
mesh_terms: D000280:Administration, Inhalation; D000704:Analysis of Variance; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage*; D001249:Asthma / Q000139:chemically induced / Q000150:complications*; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D019819:Budesonide / Q000008:administration & dosage*; D039481:CD11b Antigen / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D004660:Encephalitis / Q000209:etiology* / Q000517:prevention & control*; D005260:Female; D051379:Mice; D008807:Mice, Inbred BALB C; D016328:NF-kappa B / Q000378:metabolism; D010047:Ovalbumin; D015398:Signal Transduction / Q000187:drug effects; D051197:Toll-Like Receptor 4 / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D039481:CD11b Antigen; D016207:Cytokines; D016328:NF-kappa B; D051197:Toll-Like Receptor 4; D019819:Budesonide; D010047:Ovalbumin
keywords: Asthma; Budesonide; NFκB; Neuroinflammation; Toll-like receptor 4