The role of SP-D in human colonic inflammatory bowel disease and in murine DSS induced colitis

Research output: Contribution to conference without publisher/journalConference abstract for conferenceResearchpeer-review

Abstract

Background: Inflammatory bowel diseases (IBD) are disorders of the gastrointestinal tract. Surfactant protein D (SP-D) is expressed in the intestinal epithelium and is essential for innate host defence and regulation of inflammatory responses. Genetic variations of SP-D are associated with clinical IBD but SP-D effects in disease development are unknown. We hypothesized that SP-D ameliorates IBD inflammation. Methods: Surgical specimens from IBD patients including Crohn’s disease (CD) (n=9) and ulcerative colitis (UC) (n=18) were scored for expression of SP-D and inflammatory activity. C57BL6 Sftpd+/+ and Sftpd-/- littermate mice were subjected to drinking water (control), 1.5% DSS for 7 days or 1% DSS for 7 days followed by 3 days of water. Weight loss and stool were monitored daily. Colonic levels of inflammatory markers (TNF-α, IFN-γ, CCL-2 and IL-6) were measured by ELISA. H&E-stained tissue was scored for histologic damage. Immunohistochemical stainings were used to quantify the mucosal thickness, epithelial apoptosis, crypt cell proliferation and infiltration of inflammatory cells. Results: Surgical specimens from IBD patients showed a significant positive correlation between immunoscore for SP-D and inflammatory activity (R2 = 0.92, p = <0.0001). DSS induced significant inflammation with weight loss, bloody diarrhoea, increased inflammatory markers and tissue destruction. These changes were unaffected by SP-D genotype/deficiency except for increased TNF-α in sftpd-/- mice during the restitution phase. Conclusion: Although anti-inflammatory effects of SP-D were limited in DSS-induced inflammation in mice, a positive correlation between inflammatory activity and immunoscore for SP-D in IBD patients supports an anti-inflammatory role of SP-D in clinical disease.
Original languageEnglish
Publication date2017
Number of pages1
Publication statusPublished - 2017
Event44th Annual Meeting of the Scandinavian Society of Immunology - Stockholm, Sweden
Duration: 17. Oct 201720. Oct 2017
Conference number: 44

Conference

Conference44th Annual Meeting of the Scandinavian Society of Immunology
Number44
CountrySweden
CityStockholm
Period17/10/201720/10/2017

Cite this

Nexøe, A. B., Pilecki, B., Leicht von Huth, S., Møller, J. B., Husby, S., Arnholdt Pedersen, A., ... Sørensen, G. L. (2017). The role of SP-D in human colonic inflammatory bowel disease and in murine DSS induced colitis. Abstract from 44th Annual Meeting of the Scandinavian Society of Immunology, Stockholm, Sweden.
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title = "The role of SP-D in human colonic inflammatory bowel disease and in murine DSS induced colitis",
abstract = "Background: Inflammatory bowel diseases (IBD) are disorders of the gastrointestinal tract. Surfactant protein D (SP-D) is expressed in the intestinal epithelium and is essential for innate host defence and regulation of inflammatory responses. Genetic variations of SP-D are associated with clinical IBD but SP-D effects in disease development are unknown. We hypothesized that SP-D ameliorates IBD inflammation. Methods: Surgical specimens from IBD patients including Crohn’s disease (CD) (n=9) and ulcerative colitis (UC) (n=18) were scored for expression of SP-D and inflammatory activity. C57BL6 Sftpd+/+ and Sftpd-/- littermate mice were subjected to drinking water (control), 1.5{\%} DSS for 7 days or 1{\%} DSS for 7 days followed by 3 days of water. Weight loss and stool were monitored daily. Colonic levels of inflammatory markers (TNF-α, IFN-γ, CCL-2 and IL-6) were measured by ELISA. H&E-stained tissue was scored for histologic damage. Immunohistochemical stainings were used to quantify the mucosal thickness, epithelial apoptosis, crypt cell proliferation and infiltration of inflammatory cells. Results: Surgical specimens from IBD patients showed a significant positive correlation between immunoscore for SP-D and inflammatory activity (R2 = 0.92, p = <0.0001). DSS induced significant inflammation with weight loss, bloody diarrhoea, increased inflammatory markers and tissue destruction. These changes were unaffected by SP-D genotype/deficiency except for increased TNF-α in sftpd-/- mice during the restitution phase. Conclusion: Although anti-inflammatory effects of SP-D were limited in DSS-induced inflammation in mice, a positive correlation between inflammatory activity and immunoscore for SP-D in IBD patients supports an anti-inflammatory role of SP-D in clinical disease.",
author = "Nex{\o}e, {Anders Bathum} and Bartosz Pilecki and {Leicht von Huth}, Sebastian and M{\o}ller, {Jesper Bonnet} and Steffen Husby and {Arnholdt Pedersen}, Andreas and S{\"o}nke Detlefsen and Niels Marcussen and Uffe Holmskov and S{\o}rensen, {Grith Lykke}",
year = "2017",
language = "English",
note = "null ; Conference date: 17-10-2017 Through 20-10-2017",

}

Nexøe, AB, Pilecki, B, Leicht von Huth, S, Møller, JB, Husby, S, Arnholdt Pedersen, A, Detlefsen, S, Marcussen, N, Holmskov, U & Sørensen, GL 2017, 'The role of SP-D in human colonic inflammatory bowel disease and in murine DSS induced colitis', 44th Annual Meeting of the Scandinavian Society of Immunology, Stockholm, Sweden, 17/10/2017 - 20/10/2017.

The role of SP-D in human colonic inflammatory bowel disease and in murine DSS induced colitis. / Nexøe, Anders Bathum; Pilecki, Bartosz; Leicht von Huth, Sebastian ; Møller, Jesper Bonnet; Husby, Steffen; Arnholdt Pedersen, Andreas ; Detlefsen, Sönke; Marcussen, Niels; Holmskov, Uffe; Sørensen, Grith Lykke.

2017. Abstract from 44th Annual Meeting of the Scandinavian Society of Immunology, Stockholm, Sweden.

Research output: Contribution to conference without publisher/journalConference abstract for conferenceResearchpeer-review

TY - ABST

T1 - The role of SP-D in human colonic inflammatory bowel disease and in murine DSS induced colitis

AU - Nexøe, Anders Bathum

AU - Pilecki, Bartosz

AU - Leicht von Huth, Sebastian

AU - Møller, Jesper Bonnet

AU - Husby, Steffen

AU - Arnholdt Pedersen, Andreas

AU - Detlefsen, Sönke

AU - Marcussen, Niels

AU - Holmskov, Uffe

AU - Sørensen, Grith Lykke

PY - 2017

Y1 - 2017

N2 - Background: Inflammatory bowel diseases (IBD) are disorders of the gastrointestinal tract. Surfactant protein D (SP-D) is expressed in the intestinal epithelium and is essential for innate host defence and regulation of inflammatory responses. Genetic variations of SP-D are associated with clinical IBD but SP-D effects in disease development are unknown. We hypothesized that SP-D ameliorates IBD inflammation. Methods: Surgical specimens from IBD patients including Crohn’s disease (CD) (n=9) and ulcerative colitis (UC) (n=18) were scored for expression of SP-D and inflammatory activity. C57BL6 Sftpd+/+ and Sftpd-/- littermate mice were subjected to drinking water (control), 1.5% DSS for 7 days or 1% DSS for 7 days followed by 3 days of water. Weight loss and stool were monitored daily. Colonic levels of inflammatory markers (TNF-α, IFN-γ, CCL-2 and IL-6) were measured by ELISA. H&E-stained tissue was scored for histologic damage. Immunohistochemical stainings were used to quantify the mucosal thickness, epithelial apoptosis, crypt cell proliferation and infiltration of inflammatory cells. Results: Surgical specimens from IBD patients showed a significant positive correlation between immunoscore for SP-D and inflammatory activity (R2 = 0.92, p = <0.0001). DSS induced significant inflammation with weight loss, bloody diarrhoea, increased inflammatory markers and tissue destruction. These changes were unaffected by SP-D genotype/deficiency except for increased TNF-α in sftpd-/- mice during the restitution phase. Conclusion: Although anti-inflammatory effects of SP-D were limited in DSS-induced inflammation in mice, a positive correlation between inflammatory activity and immunoscore for SP-D in IBD patients supports an anti-inflammatory role of SP-D in clinical disease.

AB - Background: Inflammatory bowel diseases (IBD) are disorders of the gastrointestinal tract. Surfactant protein D (SP-D) is expressed in the intestinal epithelium and is essential for innate host defence and regulation of inflammatory responses. Genetic variations of SP-D are associated with clinical IBD but SP-D effects in disease development are unknown. We hypothesized that SP-D ameliorates IBD inflammation. Methods: Surgical specimens from IBD patients including Crohn’s disease (CD) (n=9) and ulcerative colitis (UC) (n=18) were scored for expression of SP-D and inflammatory activity. C57BL6 Sftpd+/+ and Sftpd-/- littermate mice were subjected to drinking water (control), 1.5% DSS for 7 days or 1% DSS for 7 days followed by 3 days of water. Weight loss and stool were monitored daily. Colonic levels of inflammatory markers (TNF-α, IFN-γ, CCL-2 and IL-6) were measured by ELISA. H&E-stained tissue was scored for histologic damage. Immunohistochemical stainings were used to quantify the mucosal thickness, epithelial apoptosis, crypt cell proliferation and infiltration of inflammatory cells. Results: Surgical specimens from IBD patients showed a significant positive correlation between immunoscore for SP-D and inflammatory activity (R2 = 0.92, p = <0.0001). DSS induced significant inflammation with weight loss, bloody diarrhoea, increased inflammatory markers and tissue destruction. These changes were unaffected by SP-D genotype/deficiency except for increased TNF-α in sftpd-/- mice during the restitution phase. Conclusion: Although anti-inflammatory effects of SP-D were limited in DSS-induced inflammation in mice, a positive correlation between inflammatory activity and immunoscore for SP-D in IBD patients supports an anti-inflammatory role of SP-D in clinical disease.

M3 - Conference abstract for conference

ER -

Nexøe AB, Pilecki B, Leicht von Huth S, Møller JB, Husby S, Arnholdt Pedersen A et al. The role of SP-D in human colonic inflammatory bowel disease and in murine DSS induced colitis. 2017. Abstract from 44th Annual Meeting of the Scandinavian Society of Immunology, Stockholm, Sweden.