Effect of low doses of lipopolysaccharide prior to ozone exposure on bronchoalveolar lavage. Differences between wild type and surfactant protein A-deficient mice

Rizwanul Haque, Todd M. Umstead, Kwangmi Ahn, David Phelps, Joanna Floros

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7 Citations (Scopus)

Abstract

Background: Several aspects of the inflammatory response to a single insult, i.e., exposure to 2 ppm of ozone (O3) for 3 h or 6 h, are less pronounced in surfactant protein A deficient (SP-A -/-) mice (KO) than in wild type mice (WT). It was hypothesized that a mild insult, specifically low doses of lipopolysaccharide (LPS), would adversely affect host defense and differentially potentiate O3-induced injury in WT and KO mice. Methods: WT and KO mice were treated with different doses of LPS or LPS (2 ng) + O3 (2 ppm) or filtered air (FA) for 3 h, then sacrificed 4 h following exposure (O3, FA) or 20 h after LPS treatment alone. Several endpoints of inflammation were measured in bronchoalveolar lavage (BAL). Results: 1) At 20 h after LPS treatment alone, both WT and KO mice exhibited signs of inflammation, but with differences in the macrophage inflammatory protein 2 (MIP-2) response pattern, total cells (at 0.5 ng LPS) and basal levels of oxidized protein and phospholipids; 2) After LPS + O3, KO compared to WT showed decrease in polymorphonuclear leukocytes (PMNs) and MIP-2 and increase in phospholipids, and after LPS + FA an increase in total cells; 3) WT after LPS + FA showed an increase in SP-A with no further increase after LPS + O3, and an increase in oxidized SP-A dimer following O3 or LPS + O3. Conclusions: LPS treatment has negative effects on inflammation endpoints in mouse BAL long after exposure and renders KO mice less capable of responding to a second insult. LPS and O3 affect SP-A, quantitatively and qualitatively, respectively.

Original languageEnglish (US)
Pages (from-to)143-155
Number of pages13
JournalPneumon
Volume22
Issue number2
StatePublished - Oct 21 2009

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Pulmonary Surfactant-Associated Protein A
Ozone
Bronchoalveolar Lavage
Lipopolysaccharides
Air
Chemokine CXCL2
Inflammation
Phospholipids

All Science Journal Classification (ASJC) codes

  • Pulmonary and Respiratory Medicine

Cite this

@article{b1f0c83114634a2eafbaaec9f62a45ff,
title = "Effect of low doses of lipopolysaccharide prior to ozone exposure on bronchoalveolar lavage. Differences between wild type and surfactant protein A-deficient mice",
abstract = "Background: Several aspects of the inflammatory response to a single insult, i.e., exposure to 2 ppm of ozone (O3) for 3 h or 6 h, are less pronounced in surfactant protein A deficient (SP-A -/-) mice (KO) than in wild type mice (WT). It was hypothesized that a mild insult, specifically low doses of lipopolysaccharide (LPS), would adversely affect host defense and differentially potentiate O3-induced injury in WT and KO mice. Methods: WT and KO mice were treated with different doses of LPS or LPS (2 ng) + O3 (2 ppm) or filtered air (FA) for 3 h, then sacrificed 4 h following exposure (O3, FA) or 20 h after LPS treatment alone. Several endpoints of inflammation were measured in bronchoalveolar lavage (BAL). Results: 1) At 20 h after LPS treatment alone, both WT and KO mice exhibited signs of inflammation, but with differences in the macrophage inflammatory protein 2 (MIP-2) response pattern, total cells (at 0.5 ng LPS) and basal levels of oxidized protein and phospholipids; 2) After LPS + O3, KO compared to WT showed decrease in polymorphonuclear leukocytes (PMNs) and MIP-2 and increase in phospholipids, and after LPS + FA an increase in total cells; 3) WT after LPS + FA showed an increase in SP-A with no further increase after LPS + O3, and an increase in oxidized SP-A dimer following O3 or LPS + O3. Conclusions: LPS treatment has negative effects on inflammation endpoints in mouse BAL long after exposure and renders KO mice less capable of responding to a second insult. LPS and O3 affect SP-A, quantitatively and qualitatively, respectively.",
author = "Rizwanul Haque and Umstead, {Todd M.} and Kwangmi Ahn and David Phelps and Joanna Floros",
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Effect of low doses of lipopolysaccharide prior to ozone exposure on bronchoalveolar lavage. Differences between wild type and surfactant protein A-deficient mice. / Haque, Rizwanul; Umstead, Todd M.; Ahn, Kwangmi; Phelps, David; Floros, Joanna.

In: Pneumon, Vol. 22, No. 2, 21.10.2009, p. 143-155.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Effect of low doses of lipopolysaccharide prior to ozone exposure on bronchoalveolar lavage. Differences between wild type and surfactant protein A-deficient mice

AU - Haque, Rizwanul

AU - Umstead, Todd M.

AU - Ahn, Kwangmi

AU - Phelps, David

AU - Floros, Joanna

PY - 2009/10/21

Y1 - 2009/10/21

N2 - Background: Several aspects of the inflammatory response to a single insult, i.e., exposure to 2 ppm of ozone (O3) for 3 h or 6 h, are less pronounced in surfactant protein A deficient (SP-A -/-) mice (KO) than in wild type mice (WT). It was hypothesized that a mild insult, specifically low doses of lipopolysaccharide (LPS), would adversely affect host defense and differentially potentiate O3-induced injury in WT and KO mice. Methods: WT and KO mice were treated with different doses of LPS or LPS (2 ng) + O3 (2 ppm) or filtered air (FA) for 3 h, then sacrificed 4 h following exposure (O3, FA) or 20 h after LPS treatment alone. Several endpoints of inflammation were measured in bronchoalveolar lavage (BAL). Results: 1) At 20 h after LPS treatment alone, both WT and KO mice exhibited signs of inflammation, but with differences in the macrophage inflammatory protein 2 (MIP-2) response pattern, total cells (at 0.5 ng LPS) and basal levels of oxidized protein and phospholipids; 2) After LPS + O3, KO compared to WT showed decrease in polymorphonuclear leukocytes (PMNs) and MIP-2 and increase in phospholipids, and after LPS + FA an increase in total cells; 3) WT after LPS + FA showed an increase in SP-A with no further increase after LPS + O3, and an increase in oxidized SP-A dimer following O3 or LPS + O3. Conclusions: LPS treatment has negative effects on inflammation endpoints in mouse BAL long after exposure and renders KO mice less capable of responding to a second insult. LPS and O3 affect SP-A, quantitatively and qualitatively, respectively.

AB - Background: Several aspects of the inflammatory response to a single insult, i.e., exposure to 2 ppm of ozone (O3) for 3 h or 6 h, are less pronounced in surfactant protein A deficient (SP-A -/-) mice (KO) than in wild type mice (WT). It was hypothesized that a mild insult, specifically low doses of lipopolysaccharide (LPS), would adversely affect host defense and differentially potentiate O3-induced injury in WT and KO mice. Methods: WT and KO mice were treated with different doses of LPS or LPS (2 ng) + O3 (2 ppm) or filtered air (FA) for 3 h, then sacrificed 4 h following exposure (O3, FA) or 20 h after LPS treatment alone. Several endpoints of inflammation were measured in bronchoalveolar lavage (BAL). Results: 1) At 20 h after LPS treatment alone, both WT and KO mice exhibited signs of inflammation, but with differences in the macrophage inflammatory protein 2 (MIP-2) response pattern, total cells (at 0.5 ng LPS) and basal levels of oxidized protein and phospholipids; 2) After LPS + O3, KO compared to WT showed decrease in polymorphonuclear leukocytes (PMNs) and MIP-2 and increase in phospholipids, and after LPS + FA an increase in total cells; 3) WT after LPS + FA showed an increase in SP-A with no further increase after LPS + O3, and an increase in oxidized SP-A dimer following O3 or LPS + O3. Conclusions: LPS treatment has negative effects on inflammation endpoints in mouse BAL long after exposure and renders KO mice less capable of responding to a second insult. LPS and O3 affect SP-A, quantitatively and qualitatively, respectively.

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