Acute cytokine responses to inhaled swine confinement building dust
Author: Wang, Zhiping
Date: 1997-12-11
Location: Hörsalen, Arbetslivsinstitutet, Ekelundsvägen 16, Solna
Time: 9.00
Abstract
Inhalation of swine house dust (swine dust) may cause an acute
inflammatory reaction Organic Dust Toxic Syndrome (ODTS). The reaction
does not require sensitisafion and is associated with airway
inflammation, general symptoms, and slight spirometric changes. The
agents and causing this reaction are not known. The purpose of this study
was to investigate the release of pro-inflammatory cytokines in the
airways and peripheral blood following acute exposure to swine dust, the
correlation between markers for microbial contaminants in the dust,
cytokine responses and health effects, and the release of those cytokines
from an epithelial cell line (EP) and from human alveolar macrophages
(AM) stimulated by swine dust and LPS.
Healthy subjects, previously unengaged in farm work were exposed to swine
dust for 3-4 hours. Interleukin(IL)-6,IL-I receptor antagonist(ra)
andtumour necrosis factor(TNF)-a in serum, and IL-Ib in peripheral blood
mononuclear cell(PBMC)were measured prior to and rear to exposure. IL-Ia,
IL-IB, IL-6 and TNF-a were also measured in nasal lavage (NAL) fluid and
bronchoalveolar lavage (BAL) before and after exposure. The time curve
were done for IL-6, TNF-a and IL- IB . The mass of inhaled dust, the
endotoxin concentration and two markers (muramic acid is a marker for
total peptidoglycan content and 3 -(OH)-fatty acid is a marker for total
lipopolysaccharide content.) for microbial exposure were quantified.
Spirometry and a methacholine bronchial challenge were performed before
and 7h after exposure to swine dust. Granulocytes, monocytes, and
Iymphocytes were measured in blood widh flow cytometry. NAL, BAL and PBMC
cells were measured with colour stain. The oral temperature and general
symptoms were recorded.
Exposure to swine dust caused fever, headache, malaise, increased
bronchial responsiveness, and a slight decrease in FEVI and VC. IL-Ira,
IL-6 and TNF-a increased significantly in serum, IL- IB increased
signficantly in PBMC and plasma, IL- I, IL-6 and TNF-a increased
significantly in BAL and NAL fluids.Therewas a marked influx of
inflammatory cells, especially, of granulocytes. In peripheral blood,
TNF-a, IL-6 and IL-IB increased and peaked during 3-5h, 5-7h and 3-7h
respectively, after dhe start of exposure. The leukocytes doubled and
monocytes increased slightly 6-8h after exposure. Endotoxin, muramic
acid, and 3-OH fatty acid correlated signficantly with increase in serum
IL-6. Inhalable dust correlated with increase in serum IL-Ira, and
endotoxin correlated with increase IL-IB in PBMC. Endotoxin and 3-OH
fatty acids also correlated significantly widh the IL-6 increase in BAL.
Bacterial markers showed better correlation widh IL 6 changes than total
dust concentrations. LPS correlated with symptoms and with lung function
changes. Peptidoglycan correlated widh increase in blood granulocytes and
body temperature. Swine dust caused a dose-dependent increase of IL-IB,
IL-6 and TNF-a in AM. No increase of IL- IB or TNF-a, but a clear
increase in IL-6 was found in EP. LPS caused a clear increase in all
three cytokines in AM, but none of cytokines in EP.
In conclusion, acute inhalation of dust contaminated with bacterial
debris increased the concentration of pro-inflammatory cytokines in BAL,
NAL, PBMC and peripheral blood. The changes in cytokines and inflammatory
parameters correlated better with markers of bacterial contaminants than
with total dust. A markers for bacterial peptidoglycan showed better
correlation widh some changes than endotoxin suggesting that several
bacterial constituents may play a role in ODTS. The results in vitro test
suggest dhat swine dust activated a cytokine response in EP and AM. The
EP had more limited cytokine response profile than AM. The swine dust is
a more potent stimulus for cytokine release than LPS in EP. Both cells
can contribute to inflammatory reaction after inhalation swine dust, and
several agents including LPS may play important role in those cytokine
release.
Issue date: 1997-11-20
Publication year: 1997
ISBN: 91-7045-445-0
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