Respiratory syncytial virus induces pneumonia, cytokine response, airway obstruction, and chronic inflammatory infiltrates associated with long-term airway hyperresponsiveness in mice

Hasan S. Jafri, Susana Chávez-Bueno, Asunción Mejías, Ana M. Gómez, Ana M. Ríos, Shahryar S. Nassi, Munira Yusuf, Payal Kapur, Robert D. Hardy, Jeanine Hatfield, Beverly B. Rogers, Karen Krisher, Octavio Ramilo

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128 Citations (Scopus)

Abstract

Background. Respiratory syncytial virus (RSV) infection is associated with acute morbidity (e.g., pneumonia and airway obstruction [AO]) and long-term complications (e.g., airway hyperresponsiveness [AHR]). We present a comprehensive evaluation of the acute and chronic phases of RSV respiratory tract infection, using a mouse model. Methods. BALB/c mice were inoculated with RSV and monitored for 154 days. RSV loads and cytokines were measured in bronchoalveolar lavage (BAL) samples. Pneumonia severity was assessed using a standard histopathologic score, and pulmonary function was determined by plethysmography. Results. RSV-infected mice exhibited viral replication that peaked on day 4-5 and became undetectable by day 7. These mice developed acute pneumonia (peak days, 4-5) and chronic pulmonary inflammatory infiltrates that lasted up to 154 days after inoculation. BAL concentrations of tumor necrosis factor-α, interleukin (IL)-6, interferon-γ, IL-4, IL-10, KC (an IL-8 homologue), MIG (CXCL9), RANTES, macrophage inflammatory protein-1α, and eotaxin were significantly higher in RSV-infected mice than in control mice. RSV-infected mice developed acute AO during the first week of infection that persisted for 42 days. RSV-infected mice also showed significant AHR in response to methacholine up to 154 days. Conclusion. This model provides a means to investigate the immunopathogenesis of RSV infection and its association with reactive airway disease.

Original languageEnglish (US)
Pages (from-to)1856-1865
Number of pages10
JournalJournal of Infectious Diseases
Volume189
Issue number10
DOIs
StatePublished - May 15 2004

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Respiratory Syncytial Viruses
Airway Obstruction
Pneumonia
Cytokines
Respiratory Syncytial Virus Infections
Bronchoalveolar Lavage
Macrophage Inflammatory Proteins
Chemokine CCL5
Lung
Plethysmography
Methacholine Chloride
Interleukin-8
Respiratory Tract Infections
Interleukin-4
Interleukin-10
Interferons
Interleukin-6
Tumor Necrosis Factor-alpha
Morbidity
Infection

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Immunology

Cite this

Respiratory syncytial virus induces pneumonia, cytokine response, airway obstruction, and chronic inflammatory infiltrates associated with long-term airway hyperresponsiveness in mice. / Jafri, Hasan S.; Chávez-Bueno, Susana; Mejías, Asunción; Gómez, Ana M.; Ríos, Ana M.; Nassi, Shahryar S.; Yusuf, Munira; Kapur, Payal; Hardy, Robert D.; Hatfield, Jeanine; Rogers, Beverly B.; Krisher, Karen; Ramilo, Octavio.

In: Journal of Infectious Diseases, Vol. 189, No. 10, 15.05.2004, p. 1856-1865.

Research output: Contribution to journalArticle

Jafri, HS, Chávez-Bueno, S, Mejías, A, Gómez, AM, Ríos, AM, Nassi, SS, Yusuf, M, Kapur, P, Hardy, RD, Hatfield, J, Rogers, BB, Krisher, K & Ramilo, O 2004, 'Respiratory syncytial virus induces pneumonia, cytokine response, airway obstruction, and chronic inflammatory infiltrates associated with long-term airway hyperresponsiveness in mice', Journal of Infectious Diseases, vol. 189, no. 10, pp. 1856-1865. https://doi.org/10.1086/386372
Jafri, Hasan S. ; Chávez-Bueno, Susana ; Mejías, Asunción ; Gómez, Ana M. ; Ríos, Ana M. ; Nassi, Shahryar S. ; Yusuf, Munira ; Kapur, Payal ; Hardy, Robert D. ; Hatfield, Jeanine ; Rogers, Beverly B. ; Krisher, Karen ; Ramilo, Octavio. / Respiratory syncytial virus induces pneumonia, cytokine response, airway obstruction, and chronic inflammatory infiltrates associated with long-term airway hyperresponsiveness in mice. In: Journal of Infectious Diseases. 2004 ; Vol. 189, No. 10. pp. 1856-1865.
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abstract = "Background. Respiratory syncytial virus (RSV) infection is associated with acute morbidity (e.g., pneumonia and airway obstruction [AO]) and long-term complications (e.g., airway hyperresponsiveness [AHR]). We present a comprehensive evaluation of the acute and chronic phases of RSV respiratory tract infection, using a mouse model. Methods. BALB/c mice were inoculated with RSV and monitored for 154 days. RSV loads and cytokines were measured in bronchoalveolar lavage (BAL) samples. Pneumonia severity was assessed using a standard histopathologic score, and pulmonary function was determined by plethysmography. Results. RSV-infected mice exhibited viral replication that peaked on day 4-5 and became undetectable by day 7. These mice developed acute pneumonia (peak days, 4-5) and chronic pulmonary inflammatory infiltrates that lasted up to 154 days after inoculation. BAL concentrations of tumor necrosis factor-α, interleukin (IL)-6, interferon-γ, IL-4, IL-10, KC (an IL-8 homologue), MIG (CXCL9), RANTES, macrophage inflammatory protein-1α, and eotaxin were significantly higher in RSV-infected mice than in control mice. RSV-infected mice developed acute AO during the first week of infection that persisted for 42 days. RSV-infected mice also showed significant AHR in response to methacholine up to 154 days. Conclusion. This model provides a means to investigate the immunopathogenesis of RSV infection and its association with reactive airway disease.",
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AU - Jafri, Hasan S.

AU - Chávez-Bueno, Susana

AU - Mejías, Asunción

AU - Gómez, Ana M.

AU - Ríos, Ana M.

AU - Nassi, Shahryar S.

AU - Yusuf, Munira

AU - Kapur, Payal

AU - Hardy, Robert D.

AU - Hatfield, Jeanine

AU - Rogers, Beverly B.

AU - Krisher, Karen

AU - Ramilo, Octavio

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N2 - Background. Respiratory syncytial virus (RSV) infection is associated with acute morbidity (e.g., pneumonia and airway obstruction [AO]) and long-term complications (e.g., airway hyperresponsiveness [AHR]). We present a comprehensive evaluation of the acute and chronic phases of RSV respiratory tract infection, using a mouse model. Methods. BALB/c mice were inoculated with RSV and monitored for 154 days. RSV loads and cytokines were measured in bronchoalveolar lavage (BAL) samples. Pneumonia severity was assessed using a standard histopathologic score, and pulmonary function was determined by plethysmography. Results. RSV-infected mice exhibited viral replication that peaked on day 4-5 and became undetectable by day 7. These mice developed acute pneumonia (peak days, 4-5) and chronic pulmonary inflammatory infiltrates that lasted up to 154 days after inoculation. BAL concentrations of tumor necrosis factor-α, interleukin (IL)-6, interferon-γ, IL-4, IL-10, KC (an IL-8 homologue), MIG (CXCL9), RANTES, macrophage inflammatory protein-1α, and eotaxin were significantly higher in RSV-infected mice than in control mice. RSV-infected mice developed acute AO during the first week of infection that persisted for 42 days. RSV-infected mice also showed significant AHR in response to methacholine up to 154 days. Conclusion. This model provides a means to investigate the immunopathogenesis of RSV infection and its association with reactive airway disease.

AB - Background. Respiratory syncytial virus (RSV) infection is associated with acute morbidity (e.g., pneumonia and airway obstruction [AO]) and long-term complications (e.g., airway hyperresponsiveness [AHR]). We present a comprehensive evaluation of the acute and chronic phases of RSV respiratory tract infection, using a mouse model. Methods. BALB/c mice were inoculated with RSV and monitored for 154 days. RSV loads and cytokines were measured in bronchoalveolar lavage (BAL) samples. Pneumonia severity was assessed using a standard histopathologic score, and pulmonary function was determined by plethysmography. Results. RSV-infected mice exhibited viral replication that peaked on day 4-5 and became undetectable by day 7. These mice developed acute pneumonia (peak days, 4-5) and chronic pulmonary inflammatory infiltrates that lasted up to 154 days after inoculation. BAL concentrations of tumor necrosis factor-α, interleukin (IL)-6, interferon-γ, IL-4, IL-10, KC (an IL-8 homologue), MIG (CXCL9), RANTES, macrophage inflammatory protein-1α, and eotaxin were significantly higher in RSV-infected mice than in control mice. RSV-infected mice developed acute AO during the first week of infection that persisted for 42 days. RSV-infected mice also showed significant AHR in response to methacholine up to 154 days. Conclusion. This model provides a means to investigate the immunopathogenesis of RSV infection and its association with reactive airway disease.

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