Detection of rhinovirus RNA in lower airway cells during experimentally induced infection.

Gern, James E.; Galagan, Dawn M.; Jarjour, Nizar N.; Dick, Elliot C.; Busse, William W.

doi:10.1164/ajrccm.155.3.9117003

Cited by 259 publications

(177 citation statements)

References 18 publications

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“…Rhinovirus RNA has recently been detected in bronchial lavage cells taken during experimentally induced colds, suggesting that rhinovirus can promote local inflammation by direct infection of the lower airways (13). Indeed, rhinoviruses are capable of prolonged, noncytolytic infection of respiratory epithelial cells and induce production of proinflammatory cy-tokines such as IL-6, 1 IL-8, and granulocyte-macrophage colony-stimulating factor (14 -17).…”

mentioning

confidence: 99%

Rhinovirus Infection Induces Expression of Its Own Receptor Intercellular Adhesion Molecule 1 (ICAM-1) via Increased NF-κB-mediated Transcription

Papi

Johnston

1999

Journal of Biological Chemistry

318

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Virus infections, the majority of which are rhinovirus infections, are the major cause of asthma exacerbations. Treatment is unsatisfactory, and the pathogenesis unclear. Lower airway lymphocyte and eosinophil recruitment and activation are strongly implicated, but the mechanisms regulating these processes are unknown. Intercellular adhesion molecule-1 (ICAM-1) has a central role in inflammatory cell recruitment to the airways in asthma and is the cellular receptor for 90% of rhinoviruses. We hypothesized that rhinovirus infection of lower airway epithelium might induce ICAM-1 expression, promoting both inflammatory cell infiltration and rhinovirus infection. We therefore investigated the effect of rhinovirus infection on respiratory epithelial cell ICAM-1 expression and regulation to identify new targets for treatment of virus-induced asthma exacerbations. We observed that rhinovirus infection of primary bronchial epithelial cells and the A549 respiratory epithelial cell line increased ICAM-1 cell surface expression over 12-and 3-fold, respectively. We then investigated the mechanisms of this induction in A549 cells and observed rhinovirus-induction of ICAM-1 promoter activity and ICAM-1 mRNA transcription. Rhinovirus induction of ICAM-1 promoter activity was critically dependent upon up-regulation of NF-B proteins binding to the ؊187/؊178 NF-B binding site on the ICAM-1 promoter. The principal components of the rhinovirus-induced binding proteins were NF-B p65 homo-or heterodimers. These studies identify ICAM-1 and NF-B as new targets for the development of therapeutic interventions for virus-induced asthma exacerbations.

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confidence: 99%

Rhinovirus Infection Induces Expression of Its Own Receptor Intercellular Adhesion Molecule 1 (ICAM-1) via Increased NF-κB-mediated Transcription

Papi

Johnston

1999

Journal of Biological Chemistry

318

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“…One possibility is that airway cytokines produced by the upper airway during infection can produce lower airway inflammation [7]. However, a study has reported that rhinovirus ribonucleic acid (RNA) can be detected in the lower airway by PCR after experimental nasal rhinovirus inoculation, suggesting that rhinovirus can directly infect the lower airway [8].…”

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confidence: 99%

Detection of rhinovirus in induced sputum at exacerbation of chronic obstructive pulmonary disease

Seemungal

Harper-Owen²,

Bhowmik³

et al. 2000

Eur Respir J

309

208

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Common colds are associated with exacerbations of chronic obstructive pulmonary disease (COPD). However, the role of the common cold virus (human rhinovirus) in the production of symptoms and lower airway inflammation at COPD exacerbation is unknown.Thirty three patients with moderate-to-severe COPD were seen at baseline, when the number of chest infections in the previous year was noted, and acutely at COPD exacerbation. Within 48 h after the onset of the exacerbation and at baseline, nasal aspirates and induced sputum were taken for rhinovirus reverse transcriptase polymerase chain reaction (RT-PCR) analysis and determination of cytokine levels. Symptoms, recorded on diary cards, were noted and forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) measured.At exacerbation, mean FEV1 and FVC fell significantly from baseline (p<0.001). Ten of 43 exacerbations were associated with rhinovirus infection, detected in induced sputum. In four of these, nasophageal samples contained no detectable rhinovirus. All baseline samples were negative for rhinovirus. The simultaneous presence of increased nasal discharge/nasal congestion (in 26 of the 43 exacerbations) and increased sputum (29 exacerbations) was strongly associated with the presence of rhinovirus (odds ratio 6.15; p=0.036). Total symptom scores were greater for rhinovirus as compared to nonrhinovirus exacerbations (p=0.039). Median baseline sputum interleukin-6 levels rose from 90.2 to 140.3 pg . mL -1 at exacerbation (p=0.005); the change was greater in the presence of rhinovirus infection (p=0.008).Rhinovirus infection can be detected at chronic obstructive pulmonary disease exacerbation. This is associated with elevation of lower airway interleukin-6 levels, which may mediate lower airway symptom expression during chronic obstructive pulmonary disease exacerbations. Eur Respir J 2000; 16: 677±683.

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“…Several studies attest to the ability of RV to infect the lower airways, supporting the notion of RV involvement in COPD exacerbations (9)(10)(11). RV readily infects airway epithelial cells from normal subjects in vitro, inducing the expression of such inflammatory mediators as IL-8, GRO-a, ENA-78, IL-6, and TNF-a (12)(13)(14)(15).…”

mentioning

confidence: 73%

Increased Cytokine Response Of Rhinovirus-Infected Airway Epithelial Cells In Chronic Obstructive Pulmonary Disease

Schneider¹,

Comstock²,

Ganesan³

et al. 2010

C32. Rhinovirus and the Airways

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Rationale: Airway inflammation is a central feature of chronic obstructive pulmonary disease (COPD). COPD exacerbations are often triggered by rhinovirus (RV) infection. Objectives: We hypothesized that airway epithelial cells from patients with COPD maintain a proinflammatory phenotype compared with control subjects, leading to greater RV responses. Methods: Cells were isolated from tracheobronchial tissues of 12 patients with COPD and 10 transplant donors. Eight patients with COPD had severe emphysema, three had mild to moderate emphysema, and one had no emphysema. All had moderate to severe airflow obstruction, and six met criteria for chronic bronchitis or had at least one exacerbation the previous year. Cells were grown at airliquid interface and infected with RV serotype 39. Cytokine and IFN expression was measured by ELISA. Selected genes involved in inflammation, oxidative stress, and proteolysis were assessed by focused gene array and real-time polymerase chain reaction. Measurements and Main Results: Compared with control subjects, cells from patients with COPD demonstrated increased mRNA expression of genes involved in oxidative stress and the response to viral infection, including NOX1, DUOXA2, MMP12, ICAM1, DDX58/RIG-I, STAT1, and STAT2. COPD cells showed elevated baseline and RVstimulated protein levels of IL-6, IL-8/CXCL8, and growth-related oncogene-a/CXCL1. COPD cells demonstrated increased viral titer and copy number after RV infection, despite increased IL-29/IFN-l1, IL-28A/IFN-l2, and IFN-inducible protein-10/CXCL10 protein levels. Finally, RV-infected COPD cultures showed increased mRNA expression of IL28A/IFNl2, IL29/IFNl1, IFIH1/MDA5, DDX58/RIG-I, DUOX1, DUOX2, IRF7, STAT1, and STAT2. Conclusions: Airway epithelial cells from patients with COPD show higher baseline levels of cytokine expression and increased susceptibility to RV infection, despite an increased IFN response.

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Detection of rhinovirus RNA in lower airway cells during experimentally induced infection.

Cited by 259 publications

References 18 publications

Rhinovirus Infection Induces Expression of Its Own Receptor Intercellular Adhesion Molecule 1 (ICAM-1) via Increased NF-κB-mediated Transcription

Rhinovirus Infection Induces Expression of Its Own Receptor Intercellular Adhesion Molecule 1 (ICAM-1) via Increased NF-κB-mediated Transcription

Detection of rhinovirus in induced sputum at exacerbation of chronic obstructive pulmonary disease

Increased Cytokine Response Of Rhinovirus-Infected Airway Epithelial Cells In Chronic Obstructive Pulmonary Disease

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