The role of interleukin-23 in the early development of emphysema in HIV1+ smokers

Igor Z. Barjaktarevic, Ronald Crystal, Robert J. Kaner

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Rationale. Matrix metalloproteinase-9 (MMP-9) expression is upregulated in alveolar macrophages (AM) of HIV1+ smokers who develop emphysema. Knowing that lung epithelial lining fluid (ELF) of HIV1+ smokers contains increased levels of inflammatory cytokines compared to HIV1- smokers, we hypothesized that upregulation of lung cytokines in HIV1+ smokers may be functionally related to increased MMP-9 expression. Methods. Cytokine arrays evaluated cytokine protein levels in ELF obtained from 5 groups of individuals: HIV1- healthy nonsmokers, HIV1- healthy smokers, HIV1- smokers with low diffusing capacity (DLCO), HIV1+ nonsmokers, and HIV1+ smokers with low DLCO. Results. Increased levels of the Th17 related cytokine IL-23 were found in HIV1- smokers with low DLCO and HIV1+ smokers and nonsmokers. Relative IL-23 gene expression was increased in AM of HIV1+ individuals, with greater expression in AM of HIV1+ smokers with low DLCO. Infection with HIV1 in vitro induced IL-23 expression in normal AM. IL-23 stimulation of AM/lymphocyte cocultures in vitro induced upregulation of MMP-9. Lung T lymphocytes express receptor IL-23R and interact with AM in order to upregulate MMP-9. Conclusion. This mechanism may contribute to the increased tissue destruction in the lungs of HIV1+ smokers and suggests that Th17 related inflammation may play a role.

Original languageEnglish
Article number3463104
JournalJournal of Immunology Research
Volume2016
DOIs
Publication statusPublished - 1 Jan 2016
Externally publishedYes

Fingerprint

Interleukin-23
Emphysema
Alveolar Macrophages
Matrix Metalloproteinase 9
Cytokines
Lung
Up-Regulation
Coculture Techniques
Lymphocytes
Inflammation
T-Lymphocytes
Gene Expression
Infection
Proteins

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

The role of interleukin-23 in the early development of emphysema in HIV1+ smokers. / Barjaktarevic, Igor Z.; Crystal, Ronald; Kaner, Robert J.

In: Journal of Immunology Research, Vol. 2016, 3463104, 01.01.2016.

Research output: Contribution to journalArticle

@article{35e523645e334f99a3c296c3528feb5e,
title = "The role of interleukin-23 in the early development of emphysema in HIV1+ smokers",
abstract = "Rationale. Matrix metalloproteinase-9 (MMP-9) expression is upregulated in alveolar macrophages (AM) of HIV1+ smokers who develop emphysema. Knowing that lung epithelial lining fluid (ELF) of HIV1+ smokers contains increased levels of inflammatory cytokines compared to HIV1- smokers, we hypothesized that upregulation of lung cytokines in HIV1+ smokers may be functionally related to increased MMP-9 expression. Methods. Cytokine arrays evaluated cytokine protein levels in ELF obtained from 5 groups of individuals: HIV1- healthy nonsmokers, HIV1- healthy smokers, HIV1- smokers with low diffusing capacity (DLCO), HIV1+ nonsmokers, and HIV1+ smokers with low DLCO. Results. Increased levels of the Th17 related cytokine IL-23 were found in HIV1- smokers with low DLCO and HIV1+ smokers and nonsmokers. Relative IL-23 gene expression was increased in AM of HIV1+ individuals, with greater expression in AM of HIV1+ smokers with low DLCO. Infection with HIV1 in vitro induced IL-23 expression in normal AM. IL-23 stimulation of AM/lymphocyte cocultures in vitro induced upregulation of MMP-9. Lung T lymphocytes express receptor IL-23R and interact with AM in order to upregulate MMP-9. Conclusion. This mechanism may contribute to the increased tissue destruction in the lungs of HIV1+ smokers and suggests that Th17 related inflammation may play a role.",
author = "Barjaktarevic, {Igor Z.} and Ronald Crystal and Kaner, {Robert J.}",
year = "2016",
month = "1",
day = "1",
doi = "10.1155/2016/3463104",
language = "English",
volume = "2016",
journal = "Journal of Immunology Research",
issn = "2314-8861",
publisher = "Hindawi Publishing Corporation",

}

TY - JOUR

T1 - The role of interleukin-23 in the early development of emphysema in HIV1+ smokers

AU - Barjaktarevic, Igor Z.

AU - Crystal, Ronald

AU - Kaner, Robert J.

PY - 2016/1/1

Y1 - 2016/1/1

N2 - Rationale. Matrix metalloproteinase-9 (MMP-9) expression is upregulated in alveolar macrophages (AM) of HIV1+ smokers who develop emphysema. Knowing that lung epithelial lining fluid (ELF) of HIV1+ smokers contains increased levels of inflammatory cytokines compared to HIV1- smokers, we hypothesized that upregulation of lung cytokines in HIV1+ smokers may be functionally related to increased MMP-9 expression. Methods. Cytokine arrays evaluated cytokine protein levels in ELF obtained from 5 groups of individuals: HIV1- healthy nonsmokers, HIV1- healthy smokers, HIV1- smokers with low diffusing capacity (DLCO), HIV1+ nonsmokers, and HIV1+ smokers with low DLCO. Results. Increased levels of the Th17 related cytokine IL-23 were found in HIV1- smokers with low DLCO and HIV1+ smokers and nonsmokers. Relative IL-23 gene expression was increased in AM of HIV1+ individuals, with greater expression in AM of HIV1+ smokers with low DLCO. Infection with HIV1 in vitro induced IL-23 expression in normal AM. IL-23 stimulation of AM/lymphocyte cocultures in vitro induced upregulation of MMP-9. Lung T lymphocytes express receptor IL-23R and interact with AM in order to upregulate MMP-9. Conclusion. This mechanism may contribute to the increased tissue destruction in the lungs of HIV1+ smokers and suggests that Th17 related inflammation may play a role.

AB - Rationale. Matrix metalloproteinase-9 (MMP-9) expression is upregulated in alveolar macrophages (AM) of HIV1+ smokers who develop emphysema. Knowing that lung epithelial lining fluid (ELF) of HIV1+ smokers contains increased levels of inflammatory cytokines compared to HIV1- smokers, we hypothesized that upregulation of lung cytokines in HIV1+ smokers may be functionally related to increased MMP-9 expression. Methods. Cytokine arrays evaluated cytokine protein levels in ELF obtained from 5 groups of individuals: HIV1- healthy nonsmokers, HIV1- healthy smokers, HIV1- smokers with low diffusing capacity (DLCO), HIV1+ nonsmokers, and HIV1+ smokers with low DLCO. Results. Increased levels of the Th17 related cytokine IL-23 were found in HIV1- smokers with low DLCO and HIV1+ smokers and nonsmokers. Relative IL-23 gene expression was increased in AM of HIV1+ individuals, with greater expression in AM of HIV1+ smokers with low DLCO. Infection with HIV1 in vitro induced IL-23 expression in normal AM. IL-23 stimulation of AM/lymphocyte cocultures in vitro induced upregulation of MMP-9. Lung T lymphocytes express receptor IL-23R and interact with AM in order to upregulate MMP-9. Conclusion. This mechanism may contribute to the increased tissue destruction in the lungs of HIV1+ smokers and suggests that Th17 related inflammation may play a role.

UR - http://www.scopus.com/inward/record.url?scp=84982794816&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84982794816&partnerID=8YFLogxK

U2 - 10.1155/2016/3463104

DO - 10.1155/2016/3463104

M3 - Article

VL - 2016

JO - Journal of Immunology Research

JF - Journal of Immunology Research

SN - 2314-8861

M1 - 3463104

ER -