Alterations of the murine gut microbiome in allergic airway disease are independent of surfactant protein D

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Alterations of the murine gut microbiome in allergic airway disease are independent of surfactant protein D. / Barfod, Kenneth Klingenberg; Roggenbuck, Michael; Al-Shuweli, Suzan; Fakih, Dalia; Sørensen, Søren Johannes; Sørensen, Grith Lykke.

In: Heliyon, Vol. 3, No. 3, e00262, 03.2017.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Barfod, KK, Roggenbuck, M, Al-Shuweli, S, Fakih, D, Sørensen, SJ & Sørensen, GL 2017, 'Alterations of the murine gut microbiome in allergic airway disease are independent of surfactant protein D', Heliyon, vol. 3, no. 3, e00262. https://doi.org/10.1016/j.heliyon.2017.e00262

APA

Barfod, K. K., Roggenbuck, M., Al-Shuweli, S., Fakih, D., Sørensen, S. J., & Sørensen, G. L. (2017). Alterations of the murine gut microbiome in allergic airway disease are independent of surfactant protein D. Heliyon, 3(3), [e00262]. https://doi.org/10.1016/j.heliyon.2017.e00262

Vancouver

Barfod KK, Roggenbuck M, Al-Shuweli S, Fakih D, Sørensen SJ, Sørensen GL. Alterations of the murine gut microbiome in allergic airway disease are independent of surfactant protein D. Heliyon. 2017 Mar;3(3). e00262. https://doi.org/10.1016/j.heliyon.2017.e00262

Author

Barfod, Kenneth Klingenberg ; Roggenbuck, Michael ; Al-Shuweli, Suzan ; Fakih, Dalia ; Sørensen, Søren Johannes ; Sørensen, Grith Lykke. / Alterations of the murine gut microbiome in allergic airway disease are independent of surfactant protein D. In: Heliyon. 2017 ; Vol. 3, No. 3.

Bibtex

@article{437ce9e795d44d00871baf2c9acb1abe,
title = "Alterations of the murine gut microbiome in allergic airway disease are independent of surfactant protein D",
abstract = "Background SP-D is an important host defense lectin in innate immunity and SP-D deficient mice show several abnormal immune effects and are susceptible to allergen-induced airway disease. At the same time, host microbiome interactions play an important role in the development of allergic airway disease, and alterations to gut microbiota have been linked to airway disease through the gut-lung axis. Currently, it is unknown if the genotype (Sftpd-/- or Sftpd+/+) of the standard SP-D mouse model can affect the host microbiota to such an degree that it would overcome the cohousing effect on microbiota and interfere with the interpretation of immunological data from the model. Generally, little is known about the effect of the SP-D protein in itself and in combination with airway disease on the microbiota. In this study, we tested the hypothesis that microbiome composition would change with the lack of SP-D protein and presence of allergic airway disease in the widely used SP-D-deficient mouse model. Results We describe here for the first time the lung and gut microbiota of the SP-D mouse model with OVA induced allergic airway disease. After the challenge animals were killed and fecal samples were taken from the caecum and lungs were subjected to bronchoalveolar lavage for comparison of gut and lung microbiota by Illumina 16S rRNA gene sequencing. A significant community shift was observed in gut microbiota after challenge with OVA. However, the microbial communities were not significantly different between SP-D deficient and wild type mice from the same cages in either na{\"i}ve or OVA treated animals. Wild type animals did however show the largest variation between mice. Conclusions Our results show that the composition of the microbiota is not influenced by the SP-D deficient genotype under na{\"i}ve or OVA induced airway disease. However, OVA sensitization and pulmonary challenge did alter the gut microbiota, supporting a bidirectional lung-gut crosstalk. Future mechanistic investigations of the influence of induced allergic airway disease on gut microbiota are warranted.",
keywords = "Immunology, Microbiology",
author = "Barfod, {Kenneth Klingenberg} and Michael Roggenbuck and Suzan Al-Shuweli and Dalia Fakih and S{\o}rensen, {S{\o}ren Johannes} and S{\o}rensen, {Grith Lykke}",
year = "2017",
month = mar,
doi = "10.1016/j.heliyon.2017.e00262",
language = "English",
volume = "3",
journal = "Heliyon",
issn = "2405-8440",
publisher = "Elsevier",
number = "3",

}

RIS

TY - JOUR

T1 - Alterations of the murine gut microbiome in allergic airway disease are independent of surfactant protein D

AU - Barfod, Kenneth Klingenberg

AU - Roggenbuck, Michael

AU - Al-Shuweli, Suzan

AU - Fakih, Dalia

AU - Sørensen, Søren Johannes

AU - Sørensen, Grith Lykke

PY - 2017/3

Y1 - 2017/3

N2 - Background SP-D is an important host defense lectin in innate immunity and SP-D deficient mice show several abnormal immune effects and are susceptible to allergen-induced airway disease. At the same time, host microbiome interactions play an important role in the development of allergic airway disease, and alterations to gut microbiota have been linked to airway disease through the gut-lung axis. Currently, it is unknown if the genotype (Sftpd-/- or Sftpd+/+) of the standard SP-D mouse model can affect the host microbiota to such an degree that it would overcome the cohousing effect on microbiota and interfere with the interpretation of immunological data from the model. Generally, little is known about the effect of the SP-D protein in itself and in combination with airway disease on the microbiota. In this study, we tested the hypothesis that microbiome composition would change with the lack of SP-D protein and presence of allergic airway disease in the widely used SP-D-deficient mouse model. Results We describe here for the first time the lung and gut microbiota of the SP-D mouse model with OVA induced allergic airway disease. After the challenge animals were killed and fecal samples were taken from the caecum and lungs were subjected to bronchoalveolar lavage for comparison of gut and lung microbiota by Illumina 16S rRNA gene sequencing. A significant community shift was observed in gut microbiota after challenge with OVA. However, the microbial communities were not significantly different between SP-D deficient and wild type mice from the same cages in either naïve or OVA treated animals. Wild type animals did however show the largest variation between mice. Conclusions Our results show that the composition of the microbiota is not influenced by the SP-D deficient genotype under naïve or OVA induced airway disease. However, OVA sensitization and pulmonary challenge did alter the gut microbiota, supporting a bidirectional lung-gut crosstalk. Future mechanistic investigations of the influence of induced allergic airway disease on gut microbiota are warranted.

AB - Background SP-D is an important host defense lectin in innate immunity and SP-D deficient mice show several abnormal immune effects and are susceptible to allergen-induced airway disease. At the same time, host microbiome interactions play an important role in the development of allergic airway disease, and alterations to gut microbiota have been linked to airway disease through the gut-lung axis. Currently, it is unknown if the genotype (Sftpd-/- or Sftpd+/+) of the standard SP-D mouse model can affect the host microbiota to such an degree that it would overcome the cohousing effect on microbiota and interfere with the interpretation of immunological data from the model. Generally, little is known about the effect of the SP-D protein in itself and in combination with airway disease on the microbiota. In this study, we tested the hypothesis that microbiome composition would change with the lack of SP-D protein and presence of allergic airway disease in the widely used SP-D-deficient mouse model. Results We describe here for the first time the lung and gut microbiota of the SP-D mouse model with OVA induced allergic airway disease. After the challenge animals were killed and fecal samples were taken from the caecum and lungs were subjected to bronchoalveolar lavage for comparison of gut and lung microbiota by Illumina 16S rRNA gene sequencing. A significant community shift was observed in gut microbiota after challenge with OVA. However, the microbial communities were not significantly different between SP-D deficient and wild type mice from the same cages in either naïve or OVA treated animals. Wild type animals did however show the largest variation between mice. Conclusions Our results show that the composition of the microbiota is not influenced by the SP-D deficient genotype under naïve or OVA induced airway disease. However, OVA sensitization and pulmonary challenge did alter the gut microbiota, supporting a bidirectional lung-gut crosstalk. Future mechanistic investigations of the influence of induced allergic airway disease on gut microbiota are warranted.

KW - Immunology

KW - Microbiology

UR - http://www.scopus.com/inward/record.url?scp=85016632483&partnerID=8YFLogxK

U2 - 10.1016/j.heliyon.2017.e00262

DO - 10.1016/j.heliyon.2017.e00262

M3 - Journal article

C2 - 28367508

AN - SCOPUS:85016632483

VL - 3

JO - Heliyon

JF - Heliyon

SN - 2405-8440

IS - 3

M1 - e00262

ER -

ID: 181449594