Respiratory syncytial virus infection increases chlorine-induced airway hyperresponsiveness
Exposure to chlorine (Cl2) damages airway and alveolar epithelia resulting in acute lung injury and reactive airway hyperresponsiveness (AHR) to methacholine. However, little is known about the effect of preexisting respiratory disease on Cl2-induced lung injury. By using a murine respiratory syncytial virus (RSV) infection model, we found that preexisting RSV infection increases Cl2 (187 ppm for 30 min)-induced lung inflammation and airway AHR at 24 h after exposure (5 days after infection). RSV infection and Cl2 exposure synergistically induced oxygen desaturation and neutrophil infiltration and increased MCP-1, MIP-1β, IL-10, IFN-γ, and RANTES concentrations in the bronchoalveolar lavage fluid (BALF). In contrast, levels of type 2 cytokines (i.e., IL-4, IL-5, IL-9, and IL-13) were not significantly affected by either RSV infection or Cl2 exposure. Cl2 exposure, but not RSV infection, induced AHR to methacholine challenge as measured by flexiVent. Moreover, preexisting RSV infection amplified BALF levels of hyaluronan (HA) and AHR. The Cl2-induced AHR was mitigated by treatment with inter-α-trypsin inhibitor antibody, which inhibits HA signaling, suggesting a mechanism of HA-mediated AHR from exacerbated oxidative injury. Our results show for the first time that preexisting RSV infection predisposes the lung to Cl2-induced injury. These data emphasize the necessity for further research on the effects of Cl2 in vulnerable populations and the development of appropriate treatments..
Medienart: |
Artikel |
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Erscheinungsjahr: |
2015 |
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Erschienen: |
2015 |
Enthalten in: |
Zur Gesamtaufnahme - volume:309 |
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Enthalten in: |
American journal of physiology / Lung cellular and molecular physiology - 309(2015), 3, Seite L205 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Song, Weifeng [VerfasserIn] |
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Links: |
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doi: |
10.1152/ajplung.00159.2015 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
OLC1968378324 |
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520 | |a Exposure to chlorine (Cl2) damages airway and alveolar epithelia resulting in acute lung injury and reactive airway hyperresponsiveness (AHR) to methacholine. However, little is known about the effect of preexisting respiratory disease on Cl2-induced lung injury. By using a murine respiratory syncytial virus (RSV) infection model, we found that preexisting RSV infection increases Cl2 (187 ppm for 30 min)-induced lung inflammation and airway AHR at 24 h after exposure (5 days after infection). RSV infection and Cl2 exposure synergistically induced oxygen desaturation and neutrophil infiltration and increased MCP-1, MIP-1β, IL-10, IFN-γ, and RANTES concentrations in the bronchoalveolar lavage fluid (BALF). In contrast, levels of type 2 cytokines (i.e., IL-4, IL-5, IL-9, and IL-13) were not significantly affected by either RSV infection or Cl2 exposure. Cl2 exposure, but not RSV infection, induced AHR to methacholine challenge as measured by flexiVent. Moreover, preexisting RSV infection amplified BALF levels of hyaluronan (HA) and AHR. The Cl2-induced AHR was mitigated by treatment with inter-α-trypsin inhibitor antibody, which inhibits HA signaling, suggesting a mechanism of HA-mediated AHR from exacerbated oxidative injury. Our results show for the first time that preexisting RSV infection predisposes the lung to Cl2-induced injury. These data emphasize the necessity for further research on the effects of Cl2 in vulnerable populations and the development of appropriate treatments. | ||
540 | |a Nutzungsrecht: Copyright © 2015 the American Physiological Society. | ||
540 | |a © COPYRIGHT 2015 American Physiological Society | ||
650 | 4 | |a Respiratory Hypersensitivity - virology | |
650 | 4 | |a Chemokines - metabolism | |
650 | 4 | |a Acute Lung Injury - virology | |
650 | 4 | |a Air Pollutants - toxicity | |
650 | 4 | |a Chlorine - toxicity | |
650 | 4 | |a Respiratory Syncytial Virus Infections - immunology | |
650 | 4 | |a Hyaluronic Acid - metabolism | |
650 | 4 | |a Acute Lung Injury - chemically induced | |
650 | 4 | |a Acute Lung Injury - immunology | |
650 | 4 | |a Respiratory Hypersensitivity - chemically induced | |
650 | 4 | |a Respiratory Hypersensitivity - immunology | |
650 | 4 | |a Lung diseases | |
650 | 4 | |a Hyaluronic acid | |
650 | 4 | |a Virus diseases | |
650 | 4 | |a Health aspects | |
650 | 4 | |a Respiratory syncytial virus | |
650 | 4 | |a Inflammatory diseases | |
650 | 4 | |a Physiology | |
650 | 4 | |a Viral infections | |
650 | 4 | |a Chlorine | |
650 | 4 | |a Cytokines | |
650 | 4 | |a Signal transduction | |
700 | 1 | |a Yu, Zhihong |4 oth | |
700 | 1 | |a Doran, Stephen F |4 oth | |
700 | 1 | |a Ambalavanan, Namasivayam |4 oth | |
700 | 1 | |a Steele, Chad |4 oth | |
700 | 1 | |a Garantziotis, Stavros |4 oth | |
700 | 1 | |a Matalon, Sadis |4 oth | |
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856 | 4 | 2 | |u http://www.ncbi.nlm.nih.gov/pubmed/26071553 |
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