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Pregled bibliografske jedinice broj: 1247906

Mendelian randomisation of eosinophils and other cell types in relation to lung function and disease


(SpiroMeta Consortium) Guyatt, Anna; John, Catherine; Williams, Alexander T.; Shrine, Nick; Reeve, Nicola F.; Sayers, Ian; Hall, Ian; Wain, Louise, V; Sheehan, Nuala; Dudbridge, Frank et al.
Mendelian randomisation of eosinophils and other cell types in relation to lung function and disease // Thorax (2022) doi:10.1136/thoraxjnl-2021-217993 (znanstveni, online first)


CROSBI ID: 1247906 Za ispravke kontaktirajte CROSBI podršku putem web obrasca

Naslov
Mendelian randomisation of eosinophils and other cell types in relation to lung function and disease

Autori
Guyatt, Anna ; John, Catherine ; Williams, Alexander T. ; Shrine, Nick ; Reeve, Nicola F. ; Sayers, Ian ; Hall, Ian ; Wain, Louise, V ; Sheehan, Nuala ; Dudbridge, Frank ; Tobin, Martin D. ; ... ; Polašek, Ozren ; ... ; Rudan, Igor ; [et al.]

Kolaboracija
SpiroMeta Consortium

Vrsta, podvrsta
Radovi u časopisima, znanstveni

Izvornik
Thorax (2022)

Status rada
Online first

Ključne riječi
Asthma Epidemiology ; Asthma Genetics ; Asthma Mechanisms ; COPD epidemiology ; COPD exacerbations mechanisms ; Eosinophil Biology ; Respiratory Infection

Sažetak
Rationale Eosinophils are associated with airway inflammation in respiratory disease. Eosinophil production and survival is controlled partly by interleukin-5: anti-interleukin-5 agents reduce asthma and response correlates with baseline eosinophil counts. However, whether raised eosinophils are causally related to chronic obstructive pulmonary disease (COPD) and other respiratory phenotypes is not well understood. Objectives We investigated causality between eosinophils and: lung function, acute exacerbations of COPD, asthma-COPD overlap (ACO), moderate-to-severe asthma and respiratory infections. Methods We performed Mendelian randomisation (MR) using 151 variants from genome- wide association studies of blood eosinophils in UK Biobank/INTERVAL, and respiratory traits in UK Biobank/SpiroMeta, using methods relying on different assumptions for validity. We performed multivariable analyses using eight cell types where there was possible evidence of causation by eosinophils. Measurements and main results Causal estimates derived from individual variants were highly heterogeneous, which may arise from pleiotropy. The average effect of raising eosinophils was to increase risk of ACO (weighted median OR per SD eosinophils, 1.44 (95%CI 1.19 to 1.74)), and moderate-severe asthma (weighted median OR 1.50 (95%CI 1.23 to 1.83)), and to reduce forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) and FEV1 (weighted median estimator, SD FEV1/FVC: -0.054 (95% CI -0.078 to -0.029), effect only prominent in individuals with asthma). Conclusions Broad consistency across MR methods may suggest causation by eosinophils (although of uncertain magnitude), yet heterogeneity necessitates caution: other important mechanisms may be responsible for the impairment of respiratory health by these eosinophil-raising variants. These results could suggest that anti-IL5 agents (designed to lower eosinophils) may be valuable in treating other respiratory conditions, including people with overlapping features of asthma and COPD.

Izvorni jezik
Engleski

Znanstvena područja
Biologija, Temeljne medicinske znanosti, Kliničke medicinske znanosti



POVEZANOST RADA


Ustanove:
Medicinski fakultet, Split

Profili:

Avatar Url Ozren Polašek (autor)

Poveznice na cjeloviti tekst rada:

doi thorax.bmj.com pubmed.ncbi.nlm.nih.gov

Citiraj ovu publikaciju:

(SpiroMeta Consortium) Guyatt, Anna; John, Catherine; Williams, Alexander T.; Shrine, Nick; Reeve, Nicola F.; Sayers, Ian; Hall, Ian; Wain, Louise, V; Sheehan, Nuala; Dudbridge, Frank et al.
Mendelian randomisation of eosinophils and other cell types in relation to lung function and disease // Thorax (2022) doi:10.1136/thoraxjnl-2021-217993 (znanstveni, online first)
(SpiroMeta Consortium) (SpiroMeta Consortium) Guyatt, A., John, C., Williams, A., Shrine, N., Reeve, N., Sayers, I., Hall, I., Wain, Louise, V, Sheehan, N. & Dudbridge, F. (2022) Mendelian randomisation of eosinophils and other cell types in relation to lung function and disease. Prihvaćen za objavljivanje u Thorax. [Preprint] doi:10.1136/thoraxjnl-2021-217993.
@unknown{unknown, author = {Guyatt, Anna and John, Catherine and Williams, Alexander T. and Shrine, Nick and Reeve, Nicola F. and Sayers, Ian and Hall, Ian and Sheehan, Nuala and Dudbridge, Frank and Tobin, Martin D. and Pola\v{s}ek, Ozren and Rudan, Igor}, year = {2022}, DOI = {10.1136/thoraxjnl-2021-217993}, keywords = {Asthma Epidemiology, Asthma Genetics, Asthma Mechanisms, COPD epidemiology, COPD exacerbations mechanisms, Eosinophil Biology, Respiratory Infection}, journal = {Thorax}, doi = {10.1136/thoraxjnl-2021-217993}, title = {Mendelian randomisation of eosinophils and other cell types in relation to lung function and disease}, keyword = {Asthma Epidemiology, Asthma Genetics, Asthma Mechanisms, COPD epidemiology, COPD exacerbations mechanisms, Eosinophil Biology, Respiratory Infection} }
@unknown{unknown, author = {Guyatt, Anna and John, Catherine and Williams, Alexander T. and Shrine, Nick and Reeve, Nicola F. and Sayers, Ian and Hall, Ian and Sheehan, Nuala and Dudbridge, Frank and Tobin, Martin D. and Pola\v{s}ek, Ozren and Rudan, Igor}, year = {2022}, DOI = {10.1136/thoraxjnl-2021-217993}, keywords = {Asthma Epidemiology, Asthma Genetics, Asthma Mechanisms, COPD epidemiology, COPD exacerbations mechanisms, Eosinophil Biology, Respiratory Infection}, journal = {Thorax}, doi = {10.1136/thoraxjnl-2021-217993}, title = {Mendelian randomisation of eosinophils and other cell types in relation to lung function and disease}, keyword = {Asthma Epidemiology, Asthma Genetics, Asthma Mechanisms, COPD epidemiology, COPD exacerbations mechanisms, Eosinophil Biology, Respiratory Infection} }

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