Bacterial endotoxin primes the human alveolar macrophage for subsequent stimulation by silica but silica does not prime for stimulation by bacterial endotoxin

Laurence Demers, Lesley J. Gaydos, John L. Stauffer, Douglas C. Kuhn

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

It has been suggested that prior exposure to mineral dust may attenuate the ability of the alveolar macrophage (AM) to respond to subsequent provocative stimuli, thus compromising the host defense mechanism. On the contrary, prior exposure of the AM with lipo-polysacharride (LPS) has been shown to sensitize the AM for subsequent stimuli, thereby enhancing the reactivity of the AM. Since AM-derived eicosanoids serve as important mediators of the lung’s response to AM activation, we evaluated the relative effects of LPS and silica dust on the production of several key eicosanoids when these activating agents were administered in sequence. Prior exposure of AM to LPS, followed by exposure to silica dust, led to an enhanced production of thromboxane A2 (TXA2) and leukotriene B4 (LTB4) when results were compared to AM stimulated with silica alone. In contrast, prior exposure of AM to silica dust reduced the ability of AM to respond to LPS, since levels of PGE2 and TXA2 produced by silica-primed AM subsequently exposed to LPS were lower than those produced by AM exposed to LPS alone. The results of these studies suggest that underlying bacterial infection in the lung may exacerbate the inflammatory effects of silica dust, while chronic occupational exposure to silica may reduce the ability of the AM to respond to bacterial invasion of the lung.

Original languageEnglish (US)
Number of pages1
JournalApplied Occupational and Environmental Hygiene
Volume11
Issue number7
DOIs
StatePublished - Jan 1 1996

Fingerprint

Alveolar Macrophages
Endotoxins
Silicon Dioxide
Dust
Thromboxane A2
Eicosanoids
Lung
Leukotriene B4
Macrophage Activation
Occupational Exposure
Bacterial Infections
Dinoprostone
Minerals

All Science Journal Classification (ASJC) codes

  • Public Health, Environmental and Occupational Health

Cite this

@article{6c8c26107b584eaf959ecb5f459f5dff,
title = "Bacterial endotoxin primes the human alveolar macrophage for subsequent stimulation by silica but silica does not prime for stimulation by bacterial endotoxin",
abstract = "It has been suggested that prior exposure to mineral dust may attenuate the ability of the alveolar macrophage (AM) to respond to subsequent provocative stimuli, thus compromising the host defense mechanism. On the contrary, prior exposure of the AM with lipo-polysacharride (LPS) has been shown to sensitize the AM for subsequent stimuli, thereby enhancing the reactivity of the AM. Since AM-derived eicosanoids serve as important mediators of the lung’s response to AM activation, we evaluated the relative effects of LPS and silica dust on the production of several key eicosanoids when these activating agents were administered in sequence. Prior exposure of AM to LPS, followed by exposure to silica dust, led to an enhanced production of thromboxane A2 (TXA2) and leukotriene B4 (LTB4) when results were compared to AM stimulated with silica alone. In contrast, prior exposure of AM to silica dust reduced the ability of AM to respond to LPS, since levels of PGE2 and TXA2 produced by silica-primed AM subsequently exposed to LPS were lower than those produced by AM exposed to LPS alone. The results of these studies suggest that underlying bacterial infection in the lung may exacerbate the inflammatory effects of silica dust, while chronic occupational exposure to silica may reduce the ability of the AM to respond to bacterial invasion of the lung.",
author = "Laurence Demers and Gaydos, {Lesley J.} and Stauffer, {John L.} and Kuhn, {Douglas C.}",
year = "1996",
month = "1",
day = "1",
doi = "10.1080/1047322X.1996.10389988",
language = "English (US)",
volume = "11",
journal = "Applied Occupational and Environmental Hygiene",
issn = "1047-322X",
publisher = "Taylor and Francis Ltd.",
number = "7",

}

Bacterial endotoxin primes the human alveolar macrophage for subsequent stimulation by silica but silica does not prime for stimulation by bacterial endotoxin. / Demers, Laurence; Gaydos, Lesley J.; Stauffer, John L.; Kuhn, Douglas C.

In: Applied Occupational and Environmental Hygiene, Vol. 11, No. 7, 01.01.1996.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Bacterial endotoxin primes the human alveolar macrophage for subsequent stimulation by silica but silica does not prime for stimulation by bacterial endotoxin

AU - Demers, Laurence

AU - Gaydos, Lesley J.

AU - Stauffer, John L.

AU - Kuhn, Douglas C.

PY - 1996/1/1

Y1 - 1996/1/1

N2 - It has been suggested that prior exposure to mineral dust may attenuate the ability of the alveolar macrophage (AM) to respond to subsequent provocative stimuli, thus compromising the host defense mechanism. On the contrary, prior exposure of the AM with lipo-polysacharride (LPS) has been shown to sensitize the AM for subsequent stimuli, thereby enhancing the reactivity of the AM. Since AM-derived eicosanoids serve as important mediators of the lung’s response to AM activation, we evaluated the relative effects of LPS and silica dust on the production of several key eicosanoids when these activating agents were administered in sequence. Prior exposure of AM to LPS, followed by exposure to silica dust, led to an enhanced production of thromboxane A2 (TXA2) and leukotriene B4 (LTB4) when results were compared to AM stimulated with silica alone. In contrast, prior exposure of AM to silica dust reduced the ability of AM to respond to LPS, since levels of PGE2 and TXA2 produced by silica-primed AM subsequently exposed to LPS were lower than those produced by AM exposed to LPS alone. The results of these studies suggest that underlying bacterial infection in the lung may exacerbate the inflammatory effects of silica dust, while chronic occupational exposure to silica may reduce the ability of the AM to respond to bacterial invasion of the lung.

AB - It has been suggested that prior exposure to mineral dust may attenuate the ability of the alveolar macrophage (AM) to respond to subsequent provocative stimuli, thus compromising the host defense mechanism. On the contrary, prior exposure of the AM with lipo-polysacharride (LPS) has been shown to sensitize the AM for subsequent stimuli, thereby enhancing the reactivity of the AM. Since AM-derived eicosanoids serve as important mediators of the lung’s response to AM activation, we evaluated the relative effects of LPS and silica dust on the production of several key eicosanoids when these activating agents were administered in sequence. Prior exposure of AM to LPS, followed by exposure to silica dust, led to an enhanced production of thromboxane A2 (TXA2) and leukotriene B4 (LTB4) when results were compared to AM stimulated with silica alone. In contrast, prior exposure of AM to silica dust reduced the ability of AM to respond to LPS, since levels of PGE2 and TXA2 produced by silica-primed AM subsequently exposed to LPS were lower than those produced by AM exposed to LPS alone. The results of these studies suggest that underlying bacterial infection in the lung may exacerbate the inflammatory effects of silica dust, while chronic occupational exposure to silica may reduce the ability of the AM to respond to bacterial invasion of the lung.

UR - http://www.scopus.com/inward/record.url?scp=0029788791&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029788791&partnerID=8YFLogxK

U2 - 10.1080/1047322X.1996.10389988

DO - 10.1080/1047322X.1996.10389988

M3 - Article

VL - 11

JO - Applied Occupational and Environmental Hygiene

JF - Applied Occupational and Environmental Hygiene

SN - 1047-322X

IS - 7

ER -