TY - JOUR
T1 - Corticosteroid treatment attenuates anxiety and mPFC-amygdala circuit dysfunction in allergic asthma
AU - Dehdar, Kolsoum
AU - Mooziri, Morteza
AU - Samii Moghaddam, Ali
AU - Salimi, Morteza
AU - Nazari, Milad
AU - Dehghan, Samaneh
AU - Jamaati, Hamidreza
AU - Salimi, Alireza
AU - Raoufy, Mohammad Reza
N1 - Publisher Copyright:
© 2023 Elsevier Inc.
PY - 2023/2
Y1 - 2023/2
N2 - Aims: Allergic asthma is associated with anxiety-related behaviors, leading to poor quality of life. Previous studies mainly described the neuropathophysiology of asthma-induced anxiety. However, the effects of corticosteroids, the most common anti-inflammatory agents for asthma treatment, on the neurophysiological foundations of allergic asthma-induced anxiety are unexplored. Main methods: Here, we evaluated lung and brain inflammation as well as anxiety in an animal model of allergic asthma pretreated with inhaled fluticasone propionate. Furthermore, to define the neurophysiological bases of these conditions, we studied the medial prefrontal cortex (mPFC)-amygdala circuit, which is previously shown to accompany asthma-induced anxiety. Key findings: Our data showed that allergen induces anxiety, mPFC and amygdala inflammation, as well as disruptions in the local and long-range oscillatory activities within the mPFC-amygdala circuit. Interestingly, we observed a roughly consistent trend of changes with inhaled fluticasone pretreatment. Namely, the asthma-induced behavioral, inflammatory, and neurophysiological changes were partly, but not totally, prevented by inhaled fluticasone pretreatment. Significance: We suggest that early treatment of asthmatic patients with inhaled corticosteroids improves mPFC-amygdala circuit function by attenuating neuroinflammation leading to reduced anxiety. These findings could lead clinical guidelines of asthma to consider the neuropsychiatric disorders of patients in treatment recommendations.
AB - Aims: Allergic asthma is associated with anxiety-related behaviors, leading to poor quality of life. Previous studies mainly described the neuropathophysiology of asthma-induced anxiety. However, the effects of corticosteroids, the most common anti-inflammatory agents for asthma treatment, on the neurophysiological foundations of allergic asthma-induced anxiety are unexplored. Main methods: Here, we evaluated lung and brain inflammation as well as anxiety in an animal model of allergic asthma pretreated with inhaled fluticasone propionate. Furthermore, to define the neurophysiological bases of these conditions, we studied the medial prefrontal cortex (mPFC)-amygdala circuit, which is previously shown to accompany asthma-induced anxiety. Key findings: Our data showed that allergen induces anxiety, mPFC and amygdala inflammation, as well as disruptions in the local and long-range oscillatory activities within the mPFC-amygdala circuit. Interestingly, we observed a roughly consistent trend of changes with inhaled fluticasone pretreatment. Namely, the asthma-induced behavioral, inflammatory, and neurophysiological changes were partly, but not totally, prevented by inhaled fluticasone pretreatment. Significance: We suggest that early treatment of asthmatic patients with inhaled corticosteroids improves mPFC-amygdala circuit function by attenuating neuroinflammation leading to reduced anxiety. These findings could lead clinical guidelines of asthma to consider the neuropsychiatric disorders of patients in treatment recommendations.
KW - Amygdala
KW - Anxiety
KW - Asthma
KW - Corticosteroid
KW - mPFC
UR - http://www.scopus.com/inward/record.url?scp=85145854799&partnerID=8YFLogxK
U2 - 10.1016/j.lfs.2023.121373
DO - 10.1016/j.lfs.2023.121373
M3 - Journal article
C2 - 36621536
AN - SCOPUS:85145854799
SN - 0024-3205
VL - 315
JO - Life Sciences
JF - Life Sciences
M1 - 121373
ER -