Identification of mast cell progenitor cells in the airways of individuals with allergic asthma

Murphy, Ryan; Chow, Yu‐Hua; Lü, Ying; Al‐Shaikhly, Taha; Petroni, Daniel; Black, Michele; Hamerman, Jessica A.; Lacy‐Hulbert, Adam; Piliponsky, Adrian M.; Hallstrand, Teal S.

doi:10.1111/all.15498

Cited by 1 publication

(2 citation statements)

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Section: Discussionmentioning

confidence: 99%

“… 50 Reductions in AHR with imatinib were noted without an associated effect on eosinophil counts in blood or bronchiolar lavage fluid or in FeNO level, and there was a negative correlation between peripheral blood eosinophil counts and changes in AHR; these findings suggest a mechanism targeting both T2 and non-T2 pathways in mast cells. 50 Mast cells serve as a source of T2 cytokines 51 and a shift in mast cells to the airway epithelium has been associated with both T2 gene expression in the airways and indirect AHR in the form of exercise-induced bronchoconstriction (EIB), a form of AHR that correlates with mannitol induced AHR. 11 However, non-T2 mast cell-derived products are also implicated in AHR as some patients with EIB do not have high T2 gene expression.…”

Section: Discussionmentioning

confidence: 99%

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Effect of Biologic Therapies on Airway Hyperresponsiveness and Allergic Response: A Systematic Literature Review

Spahn¹,

Brightling²,

O’Byrne³

et al. 2023

JAA

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Background: Airway hyperresponsiveness (AHR) is a key feature of asthma. Biologic therapies used to treat asthma target specific components of the inflammatory pathway, and their effects on AHR can provide valuable information about the underlying disease pathophysiology. This review summarizes the available evidence regarding the effects of biologics on allergen-specific and nonallergen-specific airway responses in patients with asthma. Methods: We conducted a systematic review in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines, including risk-of-bias assessment. PubMed and Ovid were searched for studies published between January 1997 and December 2021. Eligible studies were randomized, placebo-controlled trials that assessed the effects of biologics on AHR, early allergic response (EAR) and/or late allergic response (LAR) in patients with asthma. Results: Thirty studies were identified for inclusion. Bronchoprovocation testing was allergen-specific in 18 studies and non-allergenspecific in 12 studies. Omalizumab reduced AHR to methacholine, acetylcholine or adenosine monophosphate (3/9 studies), and reduced EAR (4/5 studies) and LAR (2/3 studies). Mepolizumab had no effect on AHR (3/3 studies), EAR or LAR (1/1 study). Tezepelumab reduced AHR to methacholine or mannitol (3/3 studies), and reduced EAR and LAR (1/1 study). Pitrakinra reduced LAR, with no effect on AHR (1/1 study). Etanercept reduced AHR to methacholine (1/2 studies). No effects were observed for lebrikizumab, tocilizumab, efalizumab, IMA-638 and anti-OX40 ligand on AHR, EAR or LAR; benralizumab on LAR; tralokinumab on AHR; and Ro-24-7472 on AHR or LAR (all 1/1 study each). No dupilumab or reslizumab studies were identified. Conclusion: Omalizumab and tezepelumab reduced EAR and LAR to allergens. Tezepelumab consistently reduced AHR to methacholine or mannitol. These findings provide insights into AHR mechanisms and the precise effects of asthma biologics. Furthermore, findings suggest that tezepelumab broadly targets allergen-specific and non-allergic forms of AHR, and the underlying cells and mediators involved in asthma.

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Section: Discussionmentioning

confidence: 99%