Viral respiratory infections in cystic fibrosis

Ewijk, Bart E. van; Zalm, Marieke M. van der; Wolfs, Tom F. W.; Ent, Cornelis K. van der

doi:10.1016/j.jcf.2005.05.011

Cited by 82 publications

(85 citation statements)

References 40 publications

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“…Viruses detected include rhinovirus (RV), influenza A/B, respiratory syncytial virus (RSV), parainfluenza, adenovirus and human metapneumovirus, with RV being the most common (1)(2)(3)(4)(5)(6)(7). Although the frequency of viral isolation is similar in normal healthy control subjects and patients with CF, the clinical impact of viral infection in patients with CF is higher than in control subjects (5,(8)(9)(10). Patients with virus-associated lower respiratory symptoms had a higher frequency of exacerbations and hospitalizations (5,8,9,(11)(12)(13), increased use of antibiotics at longterm follow-up (2,(4)(5)(6)14), and had a shorter time to next pulmonary exacerbation (14).…”

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confidence: 99%

“…Although the frequency of viral isolation is similar in normal healthy control subjects and patients with CF, the clinical impact of viral infection in patients with CF is higher than in control subjects (5,(8)(9)(10). Patients with virus-associated lower respiratory symptoms had a higher frequency of exacerbations and hospitalizations (5,8,9,(11)(12)(13), increased use of antibiotics at longterm follow-up (2,(4)(5)(6)14), and had a shorter time to next pulmonary exacerbation (14). Viral infections also lead to deterioration in clinical status (3,4,6,8,10,11).…”

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confidence: 99%

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Differential Responses to Rhinovirus- and Influenza-associated Pulmonary Exacerbations in Patients with Cystic Fibrosis

et al. 2014

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Rationale: The mechanism by which viruses cause exacerbations of chronic airway disease and the capacity of patients with cystic fibrosis (CF) to respond to viral infection are not precisely known.Objectives: To determine the antiviral response to infection in patients with CF.Methods: Sputum was collected from patients with CF with respiratory exacerbation. Viruses were detected in multiplex polymerase chain reaction (PCR)-based assays. Gene expression of 84 antiviral response genes was measured, using a focused quantitative PCR gene array. Measurements and Main Results:We examined 36 samples from 23 patients with respiratory exacerbation. Fourteen samples tested virus-positive and 22 virus-negative. When we compared exacerbations associated with rhinovirus (RV, n = 9) and influenza (n = 5) with virus-negative specimens, we found distinct patterns of antiviral gene expression. RV was associated with greater than twofold induction of five genes, including those encoding the monocyte-attracting chemokines CXCL10, CXCL11, and CXCL9. Influenza was associated with overexpression of 20 genes, including those encoding the cytokines tumor necrosis factor and IL-12; the kinases MEK, TBK-1, and STAT-1; the apoptosis proteins caspase-8 and caspase-10; the influenza doublestranded RNA receptor RIG-I and its downstream effector MAVS; and pyrin, an IFN-stimulated protein involved in influenza resistance. Conclusions:We conclude that virus-induced exacerbations of CF are associated with immune responses tailored to specific infections. Influenza induced a more potent response consisting of inflammation, whereas RV infection had a pronounced effect on chemokine expression. As far as we are aware, this study is the first to compare specific responses to different viruses in live patients with chronic airway disease.

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confidence: 99%

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confidence: 99%

Differential Responses to Rhinovirus- and Influenza-associated Pulmonary Exacerbations in Patients with Cystic Fibrosis

et al. 2014

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“…The latter is responsible for a complex allergic syndrome, termed allergic bronchopulmonary aspergillosis (ABPA) (Stevens et al, 2003;Moss, 2010). Besides bacteria and fungi, respiratory viral infections have been associated with a higher decrease in lung function and higher probability of hospitalization in CF patients (Hiatt et al, 1999;van Ewijk et al, 2005). Therefore, the chronic inflammation characteristic of the CF airway disease is linked to persistent infection-and neutrophil-driven tissue damage (Rieber et al, 2014).…”

Section: The Cf Airway Microenvironmentmentioning

confidence: 99%

Neutrophils in cystic fibrosis

Laval

Ralhan

Hartl

2016

Biological Chemistry

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Cystic fibrosis (CF) lung disease is characterized by chronic infection and inflammation. Among inflammatory cells, neutrophils represent the major cell population accumulating in the airways of CF patients. While neutrophils provide the first defensive cellular shield against bacterial and fungal pathogens, in chronic disease conditions such as CF these short-lived immune cells release their toxic granule contents that cause tissue remodeling and irreversible structural damage to the host. A variety of human and murine studies have analyzed neutrophils and their products in the context of CF, yet their precise functional role and therapeutic potential remain controversial and incompletely understood. Here, we summarize the current evidence in this field to shed light on the complex and multi-faceted role of neutrophils in CF lung disease.

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“…In the lung disease cystic fibrosis (CF), viral infections are linked to pulmonary function decline, antibiotic use, prolonged hospitalizations, and increased respiratory symptoms (4). Respiratory syncytial virus (RSV) is one of the most common viral copathogens in CF and is a culprit in disease progression, promoting early respiratory tract morbidity and reductions in lung function (5,6).…”

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confidence: 99%

Respiratory syncytial virus infection enhances Pseudomonas aeruginosa biofilm growth through dysregulation of nutritional immunity

Hendricks

Lashua

Fischer

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

147

162

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Clinical observations link respiratory virus infection and Pseudomonas aeruginosa colonization in chronic lung disease, including cystic fibrosis (CF) and chronic obstructive pulmonary disease. The development of P. aeruginosa into highly antibiotic-resistant biofilm communities promotes airway colonization and accounts for disease progression in patients. Although clinical studies show a strong correlation between CF patients' acquisition of chronic P. aeruginosa infections and respiratory virus infection, little is known about the mechanism by which chronic P. aeruginosa infections are initiated in the host. Using a coculture model to study the formation of bacterial biofilm formation associated with the airway epithelium, we show that respiratory viral infections and the induction of antiviral interferons promote robust secondary P. aeruginosa biofilm formation. We report that the induction of antiviral IFN signaling in response to respiratory syncytial virus (RSV) infection induces bacterial biofilm formation through a mechanism of dysregulated iron homeostasis of the airway epithelium. Moreover, increased apical release of the host iron-binding protein transferrin during RSV infection promotes P. aeruginosa biofilm development in vitro and in vivo. Thus, nutritional immunity pathways that are disrupted during respiratory viral infection create an environment that favors secondary bacterial infection and may provide previously unidentified targets to combat bacterial biofilm formation.respiratory syncytial virus | nutritional immunity | cystic fibrosis | Pseudomonas aeruginosa | biofilm

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Viral respiratory infections in cystic fibrosis

Cited by 82 publications

References 40 publications

Differential Responses to Rhinovirus- and Influenza-associated Pulmonary Exacerbations in Patients with Cystic Fibrosis

Differential Responses to Rhinovirus- and Influenza-associated Pulmonary Exacerbations in Patients with Cystic Fibrosis

Neutrophils in cystic fibrosis

Respiratory syncytial virus infection enhances Pseudomonas aeruginosa biofilm growth through dysregulation of nutritional immunity

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