Effects of agricultural organic dusts on human lung-resident mesenchymal stem (Stromal) cell function

Tara M. Nordgren, Kristina L Bailey, Art J. Heires, Dawn Katafiasz, Debra Romberger

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Agricultural organic dust exposures trigger harmful airway inflammation, and workers experiencing repetitive dust exposures are at increased risk for lung disease. Mesenchymal stem/stromal cells (MSCs) regulate wound repair processes in the lung, and may contribute to either proresolution or -fibrotic lung responses. It is unknown how organic dust exposures alter lung-resident MSC activation and proinflammatory versus prorepair programs in the lung. To address this gap in knowledge, we isolated human lung-resident MSC from lung tissue. Cells were stimulated with aqueous extracts of organic dusts (DE) derived from swine confinement facilities and were assessed for changes in proliferative and migratory capacities, and production of proinflammatory and prorepair mediators. Through these investigations, we found that DE induces significant release of proinflammatory mediators TNF-α, IL-6, IL-8, and matrix metalloproteases, while also inducing the production of prorepair mediators amphiregulin, FGF-10, and resolvin D1. In addition, DE significantly reduced the growth and migratory capacities of lung-resident MSC. Together, these investigations indicate lung-resident MSC activation and wound repair activities are altered by organic dust exposures. These findings warrant future investigations to assess how organic dusts affect lung-resident mesenchymal stem/stromal cell function and impact airway inflammation, injury, and repair during agricultural aerosol exposures.

Original languageEnglish (US)
Pages (from-to)635-644
Number of pages10
JournalToxicological Sciences
Volume162
Issue number2
DOIs
StatePublished - Apr 1 2018

Fingerprint

Stem cells
Dust
Mesenchymal Stromal Cells
Lung
Repair
Chemical activation
Pulmonary diseases
Metalloproteases
Aerosols
Interleukin-8
Interleukin-6
Wounds and Injuries
Tissue
Inflammation
Lung Volume Measurements
Lung Diseases
Swine

Keywords

  • Agriculture
  • Lung inflammation
  • Mesenchymal stem cell
  • Organic dust

ASJC Scopus subject areas

  • Toxicology

Cite this

Effects of agricultural organic dusts on human lung-resident mesenchymal stem (Stromal) cell function. / Nordgren, Tara M.; Bailey, Kristina L; Heires, Art J.; Katafiasz, Dawn; Romberger, Debra.

In: Toxicological Sciences, Vol. 162, No. 2, 01.04.2018, p. 635-644.

Research output: Contribution to journalArticle

@article{810d868661764f1f91e2ae33bc05a449,
title = "Effects of agricultural organic dusts on human lung-resident mesenchymal stem (Stromal) cell function",
abstract = "Agricultural organic dust exposures trigger harmful airway inflammation, and workers experiencing repetitive dust exposures are at increased risk for lung disease. Mesenchymal stem/stromal cells (MSCs) regulate wound repair processes in the lung, and may contribute to either proresolution or -fibrotic lung responses. It is unknown how organic dust exposures alter lung-resident MSC activation and proinflammatory versus prorepair programs in the lung. To address this gap in knowledge, we isolated human lung-resident MSC from lung tissue. Cells were stimulated with aqueous extracts of organic dusts (DE) derived from swine confinement facilities and were assessed for changes in proliferative and migratory capacities, and production of proinflammatory and prorepair mediators. Through these investigations, we found that DE induces significant release of proinflammatory mediators TNF-α, IL-6, IL-8, and matrix metalloproteases, while also inducing the production of prorepair mediators amphiregulin, FGF-10, and resolvin D1. In addition, DE significantly reduced the growth and migratory capacities of lung-resident MSC. Together, these investigations indicate lung-resident MSC activation and wound repair activities are altered by organic dust exposures. These findings warrant future investigations to assess how organic dusts affect lung-resident mesenchymal stem/stromal cell function and impact airway inflammation, injury, and repair during agricultural aerosol exposures.",
keywords = "Agriculture, Lung inflammation, Mesenchymal stem cell, Organic dust",
author = "Nordgren, {Tara M.} and Bailey, {Kristina L} and Heires, {Art J.} and Dawn Katafiasz and Debra Romberger",
year = "2018",
month = "4",
day = "1",
doi = "10.1093/toxsci/kfx286",
language = "English (US)",
volume = "162",
pages = "635--644",
journal = "Toxicological Sciences",
issn = "1096-6080",
publisher = "Oxford University Press",
number = "2",

}

TY - JOUR

T1 - Effects of agricultural organic dusts on human lung-resident mesenchymal stem (Stromal) cell function

AU - Nordgren, Tara M.

AU - Bailey, Kristina L

AU - Heires, Art J.

AU - Katafiasz, Dawn

AU - Romberger, Debra

PY - 2018/4/1

Y1 - 2018/4/1

N2 - Agricultural organic dust exposures trigger harmful airway inflammation, and workers experiencing repetitive dust exposures are at increased risk for lung disease. Mesenchymal stem/stromal cells (MSCs) regulate wound repair processes in the lung, and may contribute to either proresolution or -fibrotic lung responses. It is unknown how organic dust exposures alter lung-resident MSC activation and proinflammatory versus prorepair programs in the lung. To address this gap in knowledge, we isolated human lung-resident MSC from lung tissue. Cells were stimulated with aqueous extracts of organic dusts (DE) derived from swine confinement facilities and were assessed for changes in proliferative and migratory capacities, and production of proinflammatory and prorepair mediators. Through these investigations, we found that DE induces significant release of proinflammatory mediators TNF-α, IL-6, IL-8, and matrix metalloproteases, while also inducing the production of prorepair mediators amphiregulin, FGF-10, and resolvin D1. In addition, DE significantly reduced the growth and migratory capacities of lung-resident MSC. Together, these investigations indicate lung-resident MSC activation and wound repair activities are altered by organic dust exposures. These findings warrant future investigations to assess how organic dusts affect lung-resident mesenchymal stem/stromal cell function and impact airway inflammation, injury, and repair during agricultural aerosol exposures.

AB - Agricultural organic dust exposures trigger harmful airway inflammation, and workers experiencing repetitive dust exposures are at increased risk for lung disease. Mesenchymal stem/stromal cells (MSCs) regulate wound repair processes in the lung, and may contribute to either proresolution or -fibrotic lung responses. It is unknown how organic dust exposures alter lung-resident MSC activation and proinflammatory versus prorepair programs in the lung. To address this gap in knowledge, we isolated human lung-resident MSC from lung tissue. Cells were stimulated with aqueous extracts of organic dusts (DE) derived from swine confinement facilities and were assessed for changes in proliferative and migratory capacities, and production of proinflammatory and prorepair mediators. Through these investigations, we found that DE induces significant release of proinflammatory mediators TNF-α, IL-6, IL-8, and matrix metalloproteases, while also inducing the production of prorepair mediators amphiregulin, FGF-10, and resolvin D1. In addition, DE significantly reduced the growth and migratory capacities of lung-resident MSC. Together, these investigations indicate lung-resident MSC activation and wound repair activities are altered by organic dust exposures. These findings warrant future investigations to assess how organic dusts affect lung-resident mesenchymal stem/stromal cell function and impact airway inflammation, injury, and repair during agricultural aerosol exposures.

KW - Agriculture

KW - Lung inflammation

KW - Mesenchymal stem cell

KW - Organic dust

UR - http://www.scopus.com/inward/record.url?scp=85044849575&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85044849575&partnerID=8YFLogxK

U2 - 10.1093/toxsci/kfx286

DO - 10.1093/toxsci/kfx286

M3 - Article

C2 - 29319804

AN - SCOPUS:85044849575

VL - 162

SP - 635

EP - 644

JO - Toxicological Sciences

JF - Toxicological Sciences

SN - 1096-6080

IS - 2

ER -