Semaphorin 7A is expressed on airway eosinophils and upregulated by IL-5 family cytokines

Stephane Esnault, Elizabeth A. Kelly, Mats W. Johansson, Lin Ying Liu, Shih Tsung Han, Moneeb Akhtar, Nathan Sandbo, Deane F. Mosher, Loren C. Denlinger, Sameer K. Mathur, James S. Malter, Nizar N. Jarjour

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Semaphorin 7A (sema7a) plays a major role in TGF-β1-induced lung fibrosis. Based on the accumulating evidence that eosinophils contribute to fibrosis/remodeling in the airway, we hypothesized that airway eosinophils may be a significant source of sema7a. In vivo, sema7a was expressed on the surface of circulating eosinophils and upregulated on bronchoalveolar lavage eosinophils obtained after segmental bronchoprovocation with allergen. Based on mRNA levels in unfractionated and isolated bronchoalveolar cells, eosinophils are the predominant source of sema7a. In vitro, among the members of the IL-5-family cytokines, sema7a protein on the surface of blood eosinophils was increased more by IL-3 than by GM-CSF or IL-5. Cytokine-induced expression of cell surface sema7a required translation of newly synthesized protein. Finally, a recombinant sema7a induced alpha-smooth muscle actin production in human bronchial fibroblasts. semaphorin 7A is a potentially important modulator of eosinophil profibrotic functions in the airway remodeling of patients with chronic asthma.

Original languageEnglish (US)
Pages (from-to)90-100
Number of pages11
JournalClinical Immunology
Volume150
Issue number1
DOIs
StatePublished - Jan 2014

Fingerprint

Semaphorins
Interleukin-5
Eosinophils
Cytokines
Airway Remodeling
Fibrosis
Interleukin-3
Bronchoalveolar Lavage
Granulocyte-Macrophage Colony-Stimulating Factor
Allergens
Smooth Muscle
Actins
Membrane Proteins
Asthma
Fibroblasts
Lung
Messenger RNA

Keywords

  • Eosinophil
  • Fibrosis
  • IL-3
  • Semaphorin 7A
  • Translation

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Esnault, S., Kelly, E. A., Johansson, M. W., Liu, L. Y., Han, S. T., Akhtar, M., ... Jarjour, N. N. (2014). Semaphorin 7A is expressed on airway eosinophils and upregulated by IL-5 family cytokines. Clinical Immunology, 150(1), 90-100. https://doi.org/10.1016/j.clim.2013.11.009

Semaphorin 7A is expressed on airway eosinophils and upregulated by IL-5 family cytokines. / Esnault, Stephane; Kelly, Elizabeth A.; Johansson, Mats W.; Liu, Lin Ying; Han, Shih Tsung; Akhtar, Moneeb; Sandbo, Nathan; Mosher, Deane F.; Denlinger, Loren C.; Mathur, Sameer K.; Malter, James S.; Jarjour, Nizar N.

In: Clinical Immunology, Vol. 150, No. 1, 01.2014, p. 90-100.

Research output: Contribution to journalArticle

Esnault, S, Kelly, EA, Johansson, MW, Liu, LY, Han, ST, Akhtar, M, Sandbo, N, Mosher, DF, Denlinger, LC, Mathur, SK, Malter, JS & Jarjour, NN 2014, 'Semaphorin 7A is expressed on airway eosinophils and upregulated by IL-5 family cytokines', Clinical Immunology, vol. 150, no. 1, pp. 90-100. https://doi.org/10.1016/j.clim.2013.11.009
Esnault, Stephane ; Kelly, Elizabeth A. ; Johansson, Mats W. ; Liu, Lin Ying ; Han, Shih Tsung ; Akhtar, Moneeb ; Sandbo, Nathan ; Mosher, Deane F. ; Denlinger, Loren C. ; Mathur, Sameer K. ; Malter, James S. ; Jarjour, Nizar N. / Semaphorin 7A is expressed on airway eosinophils and upregulated by IL-5 family cytokines. In: Clinical Immunology. 2014 ; Vol. 150, No. 1. pp. 90-100.
@article{44c790e0ce6f4e8b9f975af1c63658ca,
title = "Semaphorin 7A is expressed on airway eosinophils and upregulated by IL-5 family cytokines",
abstract = "Semaphorin 7A (sema7a) plays a major role in TGF-β1-induced lung fibrosis. Based on the accumulating evidence that eosinophils contribute to fibrosis/remodeling in the airway, we hypothesized that airway eosinophils may be a significant source of sema7a. In vivo, sema7a was expressed on the surface of circulating eosinophils and upregulated on bronchoalveolar lavage eosinophils obtained after segmental bronchoprovocation with allergen. Based on mRNA levels in unfractionated and isolated bronchoalveolar cells, eosinophils are the predominant source of sema7a. In vitro, among the members of the IL-5-family cytokines, sema7a protein on the surface of blood eosinophils was increased more by IL-3 than by GM-CSF or IL-5. Cytokine-induced expression of cell surface sema7a required translation of newly synthesized protein. Finally, a recombinant sema7a induced alpha-smooth muscle actin production in human bronchial fibroblasts. semaphorin 7A is a potentially important modulator of eosinophil profibrotic functions in the airway remodeling of patients with chronic asthma.",
keywords = "Eosinophil, Fibrosis, IL-3, Semaphorin 7A, Translation",
author = "Stephane Esnault and Kelly, {Elizabeth A.} and Johansson, {Mats W.} and Liu, {Lin Ying} and Han, {Shih Tsung} and Moneeb Akhtar and Nathan Sandbo and Mosher, {Deane F.} and Denlinger, {Loren C.} and Mathur, {Sameer K.} and Malter, {James S.} and Jarjour, {Nizar N.}",
year = "2014",
month = "1",
doi = "10.1016/j.clim.2013.11.009",
language = "English (US)",
volume = "150",
pages = "90--100",
journal = "Clinical Immunology",
issn = "1521-6616",
publisher = "Academic Press Inc.",
number = "1",

}

TY - JOUR

T1 - Semaphorin 7A is expressed on airway eosinophils and upregulated by IL-5 family cytokines

AU - Esnault, Stephane

AU - Kelly, Elizabeth A.

AU - Johansson, Mats W.

AU - Liu, Lin Ying

AU - Han, Shih Tsung

AU - Akhtar, Moneeb

AU - Sandbo, Nathan

AU - Mosher, Deane F.

AU - Denlinger, Loren C.

AU - Mathur, Sameer K.

AU - Malter, James S.

AU - Jarjour, Nizar N.

PY - 2014/1

Y1 - 2014/1

N2 - Semaphorin 7A (sema7a) plays a major role in TGF-β1-induced lung fibrosis. Based on the accumulating evidence that eosinophils contribute to fibrosis/remodeling in the airway, we hypothesized that airway eosinophils may be a significant source of sema7a. In vivo, sema7a was expressed on the surface of circulating eosinophils and upregulated on bronchoalveolar lavage eosinophils obtained after segmental bronchoprovocation with allergen. Based on mRNA levels in unfractionated and isolated bronchoalveolar cells, eosinophils are the predominant source of sema7a. In vitro, among the members of the IL-5-family cytokines, sema7a protein on the surface of blood eosinophils was increased more by IL-3 than by GM-CSF or IL-5. Cytokine-induced expression of cell surface sema7a required translation of newly synthesized protein. Finally, a recombinant sema7a induced alpha-smooth muscle actin production in human bronchial fibroblasts. semaphorin 7A is a potentially important modulator of eosinophil profibrotic functions in the airway remodeling of patients with chronic asthma.

AB - Semaphorin 7A (sema7a) plays a major role in TGF-β1-induced lung fibrosis. Based on the accumulating evidence that eosinophils contribute to fibrosis/remodeling in the airway, we hypothesized that airway eosinophils may be a significant source of sema7a. In vivo, sema7a was expressed on the surface of circulating eosinophils and upregulated on bronchoalveolar lavage eosinophils obtained after segmental bronchoprovocation with allergen. Based on mRNA levels in unfractionated and isolated bronchoalveolar cells, eosinophils are the predominant source of sema7a. In vitro, among the members of the IL-5-family cytokines, sema7a protein on the surface of blood eosinophils was increased more by IL-3 than by GM-CSF or IL-5. Cytokine-induced expression of cell surface sema7a required translation of newly synthesized protein. Finally, a recombinant sema7a induced alpha-smooth muscle actin production in human bronchial fibroblasts. semaphorin 7A is a potentially important modulator of eosinophil profibrotic functions in the airway remodeling of patients with chronic asthma.

KW - Eosinophil

KW - Fibrosis

KW - IL-3

KW - Semaphorin 7A

KW - Translation

UR - http://www.scopus.com/inward/record.url?scp=84890081267&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84890081267&partnerID=8YFLogxK

U2 - 10.1016/j.clim.2013.11.009

DO - 10.1016/j.clim.2013.11.009

M3 - Article

VL - 150

SP - 90

EP - 100

JO - Clinical Immunology

JF - Clinical Immunology

SN - 1521-6616

IS - 1

ER -