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• W3200546210 abstract "Bronchial thermoplasty (BT) is an endoscopic procedure that aims at reducing the hypertrophied asthmatic airway smooth muscle (ASM), and thereby preventing excessive bronchoconstriction, by treating the airways with heat. Three clinical trials showed that BT significantly decreased the numbers of severe asthma exacerbations, hospital emergency visits, and hospital admissions and also improved quality of life. These benefits persisted for 10 years or more.1Chaudhuri R. Rubin A. Sumino K. Lapa E Silva J.R. Niven R. Siddiqui S. et al.Safety and effectiveness of bronchial thermoplasty after 10 years in patients with persistent asthma (BT10+): a follow-up of three randomised controlled.Lancet Respir Med. 2021; 5: 457-466Abstract Full Text Full Text PDF Scopus (30) Google Scholar Histologic examination of the bronchial wall showed that BT not only decreased ASM area2Haj Salem I. Gras G. Joubert P. Boulet L.P. Plante S. Biardel S. et al.Persistent reduction of mucin production following bronchial thermoplasty in severe asthma.Am J Respir Crit Care Med. 2019; 1994: 536-538Crossref Scopus (16) Google Scholar but also induced substantial changes in the airway inflammatory and remodeling features typical of asthmatic airways (Fig 1). Some of these changes, such as reduction of the ASM area and thickening of the basement membrane, are long-lasting and may be explained by BT effects on specific bronchial structural cells and repair processes.2Haj Salem I. Gras G. Joubert P. Boulet L.P. Plante S. Biardel S. et al.Persistent reduction of mucin production following bronchial thermoplasty in severe asthma.Am J Respir Crit Care Med. 2019; 1994: 536-538Crossref Scopus (16) Google Scholar In the current issue of the Journal of Allergy and Clinical Immunology, 3 articles further investigate the effects of BT on airways.3Fang L. Li J. Papakonstantinou E. Karakioulaki M. Sun Q. Schumann D. Tamm M. Stolz D. et al.Secreted heat shock proteins control airway remodeling: evidence from bronchial thermoplasty.J Allergy Clin Immunol. 2021; 148: 1249-1261Abstract Full Text Full Text PDF Scopus (6) Google Scholar, 4Ravi A. Goorsenberg A.W. Dijkhuis A. Dierdorp B.S. Dekker T. van Weeghel M. et al.Metabolic differences between bronchial epithelium from healthy individuals and patients with asthma and the effect of bronchial thermoplasty.J Allergy Clin Immunol. 2021; 148: 1236-1248Abstract Full Text Full Text PDF PubMed Scopus (9) Google Scholar, 5Ladjemi M.Z. Di Candia L. Heddebaut N. Techoueyres C. Airaud E. Soussan D. et al.Clinical and histopathologic predictors of therapeutic response to bronchial thermoplasty in severe refractory asthma.J Allergy Clin Immunol. 2021; 148: 1227-1235Abstract Full Text Full Text PDF Scopus (4) Google Scholar Fang et al previously reported that BT induces a significant reduction of heat shock protein 60 (HSP60) level in bronchoalveolar lavage fluid and showed that in vitro, HSP60 upregulates the expression of mitochondria regulator protein arginine methyltransferase-1 (PRMT1).6Sun Q. Fang L. Roth M. Tang X. Papakonstantinou E. Zhai W. et al.Bronchial thermoplasty decreases airway remodelling by blocking epithelium-derived heat shock protein 60 (HSP60) secretion and protein arginine methyltransferase 1 (PRMT1) in fibroblasts.Eur Respir J. 2019; 541900300Crossref PubMed Scopus (21) Google Scholar In the current issue of the Journal of Allergy and Clinical Immunology, Fang et al pursued their studies of HSPs and evaluated the effect of heat on epithelial cells derived HSPs.3Fang L. Li J. Papakonstantinou E. Karakioulaki M. Sun Q. Schumann D. Tamm M. Stolz D. et al.Secreted heat shock proteins control airway remodeling: evidence from bronchial thermoplasty.J Allergy Clin Immunol. 2021; 148: 1249-1261Abstract Full Text Full Text PDF Scopus (6) Google Scholar First, they observed an increase in HSP70 and HSP90 levels in endobronchial biopsy specimens 1 month after BT. Then, they mimicked BT in vitro by exposing epithelial and ASM cells to heat gradients. They also treated the cells with recombinant exogenous HSPs. In epithelial cells, these in vitro treatments increased their proliferation, decreased their apoptosis, and activated both the AKT/mTOR signaling and the C/EBP-β/PRMT1 pathway. In contrast, these in vitro treatments were proapoptotic and antiproliferative in ASM cells, which might explain at least in part the decrease of ASM observed in BT-treated patients. The work by Fang et al was based on earlier transcriptomic and proteomic data that suggested a role of HSPs' regulation as a potential molecular mechanism involved in the structural changes observed after BT.3Fang L. Li J. Papakonstantinou E. Karakioulaki M. Sun Q. Schumann D. Tamm M. Stolz D. et al.Secreted heat shock proteins control airway remodeling: evidence from bronchial thermoplasty.J Allergy Clin Immunol. 2021; 148: 1249-1261Abstract Full Text Full Text PDF Scopus (6) Google Scholar As these changes in HSPs were observed 1 month after BT, whether this mechanism is permanent and sufficient to explain the long-term effects of BT is unknown. Further studies are needed to confirm the lasting effects of these HSPs and their links with pathways involved in ASM ablation and matrix deposition. Ravi et al4Ravi A. Goorsenberg A.W. Dijkhuis A. Dierdorp B.S. Dekker T. van Weeghel M. et al.Metabolic differences between bronchial epithelium from healthy individuals and patients with asthma and the effect of bronchial thermoplasty.J Allergy Clin Immunol. 2021; 148: 1236-1248Abstract Full Text Full Text PDF PubMed Scopus (9) Google Scholar performed RNA sequencing studies on epithelial cells obtained from BT-treated and untreated control airways of patients with severe asthma. At 6 months after BT treatment, transcriptome analysis of epithelial cells obtained from a treated lobe showed an increase in OXPHOS and a reduction in fatty acid metabolism genes compared with in cells obtained from the untreated right middle lobe, suggesting that BT normalized the metabolic activity of airway epithelium. A previous report evaluating RNA sequencing on bronchial brushing samples obtained from patients with severe asthma treated with a tyrosine kinase inhibitor (imatinib) showed increased OXPHOS gene expression and inhibition of platelet-derived growth factor, a growth factor known to regulate smooth muscle proliferation.7Foer D. Baek S. Cahill K.N. Israel E. Cui J. Weiss S.T. et al.Individual gene expression signatures in severe asthmatics identify responders and non-responders to imatinib.Am J Resp Crit Care. 2019; 199: A1065Google Scholar Whether BT targets platelet-derived growth factor pathways is also unknown. Ravi et al4Ravi A. Goorsenberg A.W. Dijkhuis A. Dierdorp B.S. Dekker T. van Weeghel M. et al.Metabolic differences between bronchial epithelium from healthy individuals and patients with asthma and the effect of bronchial thermoplasty.J Allergy Clin Immunol. 2021; 148: 1236-1248Abstract Full Text Full Text PDF PubMed Scopus (9) Google Scholar used epithelial cells of untreated middle lobe as controls. There is no consensus regarding whether BT can affect the untreated middle lobe. A histologic study by Pretolani et al indicated that BT treatment could diffuse to the untreated area8Pretolani M. Dombret M.C. Thabut G. Knap D. Hamidi F. Debray M.P. et al.Reduction of airway smooth muscle mass by bronchial thermoplasty in patients with severe asthma.Am J Resp Crit Care. 2014; 190: 1452-1454Crossref PubMed Scopus (129) Google Scholar; however, this observation has not been confirmed by other studies. In their article, Ravi el al4Ravi A. Goorsenberg A.W. Dijkhuis A. Dierdorp B.S. Dekker T. van Weeghel M. et al.Metabolic differences between bronchial epithelium from healthy individuals and patients with asthma and the effect of bronchial thermoplasty.J Allergy Clin Immunol. 2021; 148: 1236-1248Abstract Full Text Full Text PDF PubMed Scopus (9) Google Scholar observed significant differences in OXPHOS gene expression and lipid profile between BT-treated lobes and the untreated middle lobe, suggesting that BT may not affect the untreated lobe to the same extent. Ladjemi et al5Ladjemi M.Z. Di Candia L. Heddebaut N. Techoueyres C. Airaud E. Soussan D. et al.Clinical and histopathologic predictors of therapeutic response to bronchial thermoplasty in severe refractory asthma.J Allergy Clin Immunol. 2021; 148: 1227-1235Abstract Full Text Full Text PDF Scopus (4) Google Scholar evaluated 23 subjects with severe asthma who presented with a high number of annual severe exacerbations (∼10) and a relative blood eosinophilia despite a high daily dose of oral corticosteroids. Their bronchial biopsy specimens demonstrated increased expression of epithelial expression of MUC5AC; elevated numbers of eosinophils and cells positive for IL-13, IL-17, and IL-33 in the mucosa; and elevated numbers of intramuscular mast cells. After BT, the number of exacerbations decreased dramatically (99%) in 15 of the 23 patients (designated as responders) and less so (66%) in the other 8 patients (designated as partial responders). At baseline, the responders had a higher blood eosinophil count, incidence of atopy, and level of total serum IgE than the partial responders did. In the responders, BT significantly decreased the blood eosinophil count and the daily dose of oral prednisone; increased the epithelial expression of MUC5AC and the epithelial expression of IFN-α/β; and decreased the numbers of IL-13– and IL-33–positive cells, mucosal eosinophils, and mucosal and intramuscular mast cells. ASM area and subepithelial basement membrane thickening were similarly reduced in both groups. This study of subjects presenting with a very labile asthma with persistent bronchial eosinophilic inflammation despite high doses of oral corticosteroids demonstrates the capacity of BT to modulate IL-13–driven airway asthmatic inflammation. The fact that 14 of the 15 responders did not improve with omalizumab suggests that the persistence of eosinophilic inflammation during treatment with high doses of oral corticosteroids was not predominantly modulated by allergy but was instead likely modulated by an IL-13/CCL16 pathway.9Larose M. Chakir Archambault A.S. Joubert P. Provost V. Laviolette M. et al.Correlation between CCL26 production by human bronchial epithelial cells and airway eosinophils: involvement in severe eosinophilic asthma.J Allergy Clin Immunol. 2015; 136: 904-913Abstract Full Text Full Text PDF PubMed Scopus (53) Google Scholar Moreover, the AIR2 5-year follow-up study of 162 subjects with severe persistent asthma found no difference in the outcome based on the subjects’ self-reported allergy status.10Wechsler M.E. Laviolette M. Rubin A.S. Fiterman J. Lapa e Silva J.R. Shah P.L. et al.Bronchial thermoplasty: long-term safety and effectiveness in patients with severe persistent asthma.J Allergy Clin Immunol. 2013; 132: 1295-1302Abstract Full Text Full Text PDF PubMed Google Scholar Consequently, in addition to treatment with BT, these subjects with labile and eosinophilic severe asthma are likely good candidates for mAb treatment targeting eosinophil recruitment, as suggested by the Ladjemi et al.5Ladjemi M.Z. Di Candia L. Heddebaut N. Techoueyres C. Airaud E. Soussan D. et al.Clinical and histopathologic predictors of therapeutic response to bronchial thermoplasty in severe refractory asthma.J Allergy Clin Immunol. 2021; 148: 1227-1235Abstract Full Text Full Text PDF Scopus (4) Google Scholar In this small group of 15 responders, the observed correlations between clinical and histopathologic parameters were possibly due to the concomitant presence of high levels of symptoms and airway inflammation and remodeling at baseline, together with the high magnitude of improvements brought by BT in both clinical and histologic parameters. The previous studies of BT reported many fewer improvements in clinical and histologic parameters and did not report any correlation between them.2Haj Salem I. Gras G. Joubert P. Boulet L.P. Plante S. Biardel S. et al.Persistent reduction of mucin production following bronchial thermoplasty in severe asthma.Am J Respir Crit Care Med. 2019; 1994: 536-538Crossref Scopus (16) Google Scholar,8Pretolani M. Dombret M.C. Thabut G. Knap D. Hamidi F. Debray M.P. et al.Reduction of airway smooth muscle mass by bronchial thermoplasty in patients with severe asthma.Am J Resp Crit Care. 2014; 190: 1452-1454Crossref PubMed Scopus (129) Google Scholar Ladjemi et al5Ladjemi M.Z. Di Candia L. Heddebaut N. Techoueyres C. Airaud E. Soussan D. et al.Clinical and histopathologic predictors of therapeutic response to bronchial thermoplasty in severe refractory asthma.J Allergy Clin Immunol. 2021; 148: 1227-1235Abstract Full Text Full Text PDF Scopus (4) Google Scholar suggest that BT could provide benefit to individuals with asthma presenting with different phenotypes and endotypes, although the histologic and clinical benefits may be greater in young subjects with severe asthma, atopy, and persisting eosinophilic inflammation. However, in such subjects, the intake of oral corticosteroids before and after inclusion in a BT program must be closely monitored. This monitoring will make it possible to ensure that airway inflammation improvements observed after BT are not due to better compliance with corticosteroids during the post-BT follow-up, notably in the responder patients. Moreover, it is also important to evaluate whether the difference in blood eosinophil counts observed between the responder patients and partial responder patients at the beginning of the study was not due to better compliance with prednisone in the latter group before inclusion in the study. In summary, these reports further support the idea that as a 1-time treatment, BT can significantly reverse some asthma-induced airway inflammatory processes and many remodeling processes, particularly through its effects on epithelial cells. In many ways, it seems to “reprogram” airway homeostasis in a durable fashion, providing sustained and significant clinical benefits. However, links between the histologic and clinical improvements need to be further investigated. Moreover, the proposed changes in airway inflammation parameters and the indication for BT in patients with severe eosinophilic asthma remain to be confirmed. Secreted heat shock proteins control airway remodeling: Evidence from bronchial thermoplastyJournal of Allergy and Clinical ImmunologyVol. 148Issue 5PreviewIncreased airway smooth muscle mass is a key pathology in asthma. Bronchial thermoplasty is a treatment for severe asthma based on selective heating of the airways that aims to reduce the mass of airway smooth muscle cells (ASMCs), and thereby bronchoconstriction. However, short heat exposure is insufficient to explain the long-lasting effect, and heat shock proteins (HSPs) have been suggested to play a role. Full-Text PDF Clinical and histopathologic predictors of therapeutic response to bronchial thermoplasty in severe refractory asthmaJournal of Allergy and Clinical ImmunologyVol. 148Issue 5PreviewPhenotypes and endotypes predicting optimal response to bronchial thermoplasty (BT) in patients with severe asthma remain elusive. Full-Text PDF Metabolic differences between bronchial epithelium from healthy individuals and patients with asthma and the effect of bronchial thermoplastyJournal of Allergy and Clinical ImmunologyVol. 148Issue 5PreviewAsthma is a heterogeneous disease with differences in onset, severity, and inflammation. Bronchial epithelial cells (BECs) contribute to asthma pathophysiology. Full-Text PDF Open Access" @default.
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• W3200546210 title "Bronchial thermoplasty: The heat that reprograms the airways?" @default.
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