Infant airway microbiota and topical immune perturbations in the origins of childhood asthma

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Standard

Infant airway microbiota and topical immune perturbations in the origins of childhood asthma. / Thorsen, Jonathan; Rasmussen, Morten A.; Waage, Johannes; Mortensen, Martin; Brejnrod, Asker; Bønnelykke, Klaus; Chawes, Bo L.; Brix, Susanne; Sørensen, Søren J.; Stokholm, Jakob; Bisgaard, Hans.

I: Nature Communications, Bind 10, 5001, 2019.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Thorsen, J, Rasmussen, MA, Waage, J, Mortensen, M, Brejnrod, A, Bønnelykke, K, Chawes, BL, Brix, S, Sørensen, SJ, Stokholm, J & Bisgaard, H 2019, 'Infant airway microbiota and topical immune perturbations in the origins of childhood asthma', Nature Communications, bind 10, 5001. https://doi.org/10.1038/s41467-019-12989-7

APA

Thorsen, J., Rasmussen, M. A., Waage, J., Mortensen, M., Brejnrod, A., Bønnelykke, K., Chawes, B. L., Brix, S., Sørensen, S. J., Stokholm, J., & Bisgaard, H. (2019). Infant airway microbiota and topical immune perturbations in the origins of childhood asthma. Nature Communications, 10, [5001]. https://doi.org/10.1038/s41467-019-12989-7

Vancouver

Thorsen J, Rasmussen MA, Waage J, Mortensen M, Brejnrod A, Bønnelykke K o.a. Infant airway microbiota and topical immune perturbations in the origins of childhood asthma. Nature Communications. 2019;10. 5001. https://doi.org/10.1038/s41467-019-12989-7

Author

Thorsen, Jonathan ; Rasmussen, Morten A. ; Waage, Johannes ; Mortensen, Martin ; Brejnrod, Asker ; Bønnelykke, Klaus ; Chawes, Bo L. ; Brix, Susanne ; Sørensen, Søren J. ; Stokholm, Jakob ; Bisgaard, Hans. / Infant airway microbiota and topical immune perturbations in the origins of childhood asthma. I: Nature Communications. 2019 ; Bind 10.

Bibtex

@article{aeb1333a6e4444c3b9b28ba35ed40a39,
title = "Infant airway microbiota and topical immune perturbations in the origins of childhood asthma",
abstract = "Asthma is believed to arise through early life aberrant immune development in response to environmental exposures that may influence the airway microbiota. Here, we examine the airway microbiota during the first three months of life by 16S rRNA gene amplicon sequencing in the population-based Copenhagen Prospective Studies on Asthma in Childhood 2010 (COPSAC2010) cohort consisting of 700 children monitored for the development of asthma since birth. Microbial diversity and the relative abundances of Veillonella and Prevotella in the airways at age one month are associated with asthma by age 6 years, both individually and with additional taxa in a multivariable model. Higher relative abundance of these bacteria is furthermore associated with an airway immune profile dominated by reduced TNF-α and IL-1β and increased CCL2 and CCL17, which itself is an independent predictor for asthma. These findings suggest a mechanism of microbiota-immune interactions in early infancy that predisposes to childhood asthma.",
author = "Jonathan Thorsen and Rasmussen, {Morten A.} and Johannes Waage and Martin Mortensen and Asker Brejnrod and Klaus B{\o}nnelykke and Chawes, {Bo L.} and Susanne Brix and S{\o}rensen, {S{\o}ren J.} and Jakob Stokholm and Hans Bisgaard",
year = "2019",
doi = "10.1038/s41467-019-12989-7",
language = "English",
volume = "10",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "nature publishing group",

}

RIS

TY - JOUR

T1 - Infant airway microbiota and topical immune perturbations in the origins of childhood asthma

AU - Thorsen, Jonathan

AU - Rasmussen, Morten A.

AU - Waage, Johannes

AU - Mortensen, Martin

AU - Brejnrod, Asker

AU - Bønnelykke, Klaus

AU - Chawes, Bo L.

AU - Brix, Susanne

AU - Sørensen, Søren J.

AU - Stokholm, Jakob

AU - Bisgaard, Hans

PY - 2019

Y1 - 2019

N2 - Asthma is believed to arise through early life aberrant immune development in response to environmental exposures that may influence the airway microbiota. Here, we examine the airway microbiota during the first three months of life by 16S rRNA gene amplicon sequencing in the population-based Copenhagen Prospective Studies on Asthma in Childhood 2010 (COPSAC2010) cohort consisting of 700 children monitored for the development of asthma since birth. Microbial diversity and the relative abundances of Veillonella and Prevotella in the airways at age one month are associated with asthma by age 6 years, both individually and with additional taxa in a multivariable model. Higher relative abundance of these bacteria is furthermore associated with an airway immune profile dominated by reduced TNF-α and IL-1β and increased CCL2 and CCL17, which itself is an independent predictor for asthma. These findings suggest a mechanism of microbiota-immune interactions in early infancy that predisposes to childhood asthma.

AB - Asthma is believed to arise through early life aberrant immune development in response to environmental exposures that may influence the airway microbiota. Here, we examine the airway microbiota during the first three months of life by 16S rRNA gene amplicon sequencing in the population-based Copenhagen Prospective Studies on Asthma in Childhood 2010 (COPSAC2010) cohort consisting of 700 children monitored for the development of asthma since birth. Microbial diversity and the relative abundances of Veillonella and Prevotella in the airways at age one month are associated with asthma by age 6 years, both individually and with additional taxa in a multivariable model. Higher relative abundance of these bacteria is furthermore associated with an airway immune profile dominated by reduced TNF-α and IL-1β and increased CCL2 and CCL17, which itself is an independent predictor for asthma. These findings suggest a mechanism of microbiota-immune interactions in early infancy that predisposes to childhood asthma.

U2 - 10.1038/s41467-019-12989-7

DO - 10.1038/s41467-019-12989-7

M3 - Journal article

C2 - 31676759

AN - SCOPUS:85074341820

VL - 10

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

M1 - 5001

ER -

ID: 230095079