Hyperresponsiveness to Extracellular Acidification-Mediated Contraction in Isolated Bronchial Smooth Muscles of Murine Experimental Asthma

Recent advances in acid sensing by G protein coupled receptors

“…Expression of TDAG8 and OGR1 was increased in a murine model of allergic asthma in bronchial smooth muscle cells. Intriguingly, this study also found that human bronchial smooth muscle cells only express TDAG8 and OGR1 whilst murine bronchial smooth muscle cells also express GPR4 [ 10 ]. Furthermore, TDAG8 was shown to be upregulated in lung fibroblasts from patients with idiopathic pulmonary fibrosis compared to healthy individuals, whilst OGR1 was downregulated in these cells, and GPR4 was not detected in primary human lung fibroblasts [ 65 ], hence mirroring expression patterns of bronchial smooth muscle cells.…”

“…OGR1 has been implicated in allergen-induced hyper-responsiveness and idiopathic pulmonary fibrosis [ 3 , 10 , 56 , 57 ] and was reported to be pro-inflammatory [ 29 , 56 ]. It is expressed in lung fibroblasts [ 3 , 56 ] and bronchial smooth muscle cells [ 10 , 29 ].…”

“…OGR1 has been implicated in allergen-induced hyper-responsiveness and idiopathic pulmonary fibrosis [ 3 , 10 , 56 , 57 ] and was reported to be pro-inflammatory [ 29 , 56 ]. It is expressed in lung fibroblasts [ 3 , 56 ] and bronchial smooth muscle cells [ 10 , 29 ]. Whilst OGR1 expression is increased in bronchial smooth muscle cells in an ovalbumin antigen-challenged murine asthma model [ 10 ], it is downregulated in fibroblasts from patients with idiopathic pulmonary fibrosis [ 65 ], which promotes myofibroblast differentiation, suggesting that OGR1 has anti-fibrotic effects in lung fibroblasts [ 56 ].…”

LUNG Year in Review: 2022

“…Clinical studies of COPD examined diagnosis [ 2 ], risk factors [ 3 ], predictors of outcomes [ 4 – 9 ], and therapeutic interventions [ 10 , 11 ], whereas preclinical investigations evaluated chronic cigarette smoke-induced inflammation and airway remodeling [ 12 , 13 ]. Contributions in the field of asthma included physiological studies [ 14 – 18 ], effects of therapeutic interventions [ 19 ], social determinants of clinical outcomes [ 20 ], asthma-associated cough [ 21 , 22 ] and preclinical investigations [ 23 ].…”

“…To that end, LUNG assigned a Deputy Editor for Basic Science Research to spearhead this effort going forward. Publications during the year included studies relevant to cigarette smoke-induced airway injury and COPD [ 12 , 13 ]; asthma [ 23 ]; pulmonary fibrosis [ 42 ]; pulmonary hypertension [ 63 ]; sarcoidosis [ 64 ]; allergic airway inflammation [ 65 ]; immunity [ 66 ]; and, acute lung injury [ 67 ].…”