Severe viral respiratory infections in infants with cystic fibrosis

Armstrong, David; Grimwood, Keith; Carlin, John B.; Carzino, Rosemary; Hull, Jeremy; Olinsky, Anthony; Phelan, P. D.

doi:10.1002/(sici)1099-0496(199812)26:6<371::aid-ppul1>3.0.co;2-n

Cited by 170 publications

(138 citation statements)

References 33 publications

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“…CF mice react with increased inflammation and decreased viral clearance to RSV infection (19). RSV is known to trigger exacerbations of CF lung disease (37)(38)(39) and to facilitate colonization with P. aeruginosa (40). Both cDCs and pDCs are typically activated and increase in number in response to RSV infection (41,42).…”

Section: Discussionmentioning

confidence: 99%

Low Sphingosine-1–Phosphate Impairs Lung Dendritic Cells in Cystic Fibrosis

Krause

Limberis

et al. 2013

Am J Respir Cell Mol Biol

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Dysfunction of the cystic fibrosis transmembrane regulator (CFTR) leads to chronic inflammation and infection of the respiratory tract. The role of CFTR for cells of the pulmonary immune system is only partly understood. The present study analyzes the phenotype and immune stimulatory capacity of lung dendritic cells (DCs) from CFTR knockout (CF) mice. Total numbers of conventional DCs, plasmacytoid DCs, and CD103-positive DCs were lower in CF mice compared with wild-type (WT) control mice, as was the expression of major histocompatibility complex class II molecules (MHCII), CD40, and CD86. After pulmonary infection with respiratory syncytial virus, DC numbers increased in WT mice but not in CF mice, and the T cellstimulatory capacity of CF DCs was impaired. The culture of CF lung DCs with bronchoalveolar lavage fluid (BALF) from WT mice increased the expression of MHCII, CD40, and CD86. The supplementation of CF BALF with sphingosine-1-phosphate (S1P), a mediator of immune cell migration and activation that is decreased in CF BALF, rescued the reduced expression of MHCII and CD40 in WT lung DCs and human blood DCs. These findings suggest that DCs are impaired in the CF lung, and that altered S1P affects lung DC function. These findings provide a novel link between defective CFTR and pulmonary innate immune dysfunction in CF.

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Section: Discussionmentioning

confidence: 99%

Low Sphingosine-1–Phosphate Impairs Lung Dendritic Cells in Cystic Fibrosis

Krause

Limberis

et al. 2013

Am J Respir Cell Mol Biol

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“…The coinfection of viruses and bacteria have been recognized in several respiratory diseases including pneumonia, otitis media (1-3), chronic obstructive pulmonary disease (COPD) (4-7) and cystic fibrosis (CF) (8)(9)(10)(11). Viruses predispose the host to bacterial infection by various mechanisms including destruction of the respiratory epithelium, modulation of innate defenses, and alteration of cell membranes, which in turn facilitates bacterial adherence.…”

mentioning

confidence: 99%

Rhinovirus Disrupts the Barrier Function of Polarized Airway Epithelial Cells

Sajjan¹,

Wang²,

Zhao³

et al. 2008

Am J Respir Crit Care Med

303

312

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Rationale : Secondary bacterial infection following rhinovirus (RV) infection has been recognized in chronic obstructive pulmonary disease. Objectives: We sought to understand mechanisms by which RV infection facilitates secondary bacterial infection. Methods : Primary human airway epithelial cells grown at air-liquid interface and human bronchial epithelial (16HBE14o-) cells grown as polarized monolayers were infected apically with RV. Transmigration of bacteria (nontypeable Haemophilus influenzae and others) was assessed by colony counting and transmission electron microscopy. Transepithelial resistance (R T ) was measured by using a voltmeter. The distribution of zona occludins (ZO)-1 was determined by immunohistochemistry and immunoblotting. Measurements and Main Results : Epithelial cells infected with RV showed 2-log more bound bacteria than sham-infected cultures, and bacteria were recovered from the basolateral media of RV-but not sham-infected cells. Infection of polarized airway epithelial cell cultures with RV for 24 hours caused a significant decrease in R T without causing cell death or apoptosis. Ultraviolet-treated RV did not decrease R T , suggesting a requirement for viral replication. Reduced R T was associated with increased paracellular permeability, as determined by flux of fluorescein isothiocyanate (FITC)-inulin. Neutralizing antibodies to tumor necrosis factor (TNF)-a, IFN-g and IL-1b reversed corresponding cytokine-induced reductions in R T but not that induced by RV, indicating that the RV effect is independent of these proinflammatory cytokines. Confocal microscopy and immunoblotting revealed the loss of ZO-1 from tight junction complexes in RV-infected cells. Intranasal inoculation of mice with RV1B also caused the loss of ZO-1 from the bronchial epithelium tight junctions in vivo. Conclusions: RV facilitates binding, translocation, and persistence of bacteria by disrupting airway epithelial barrier function.

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“…Early studies looking at respiratory viruses in CF relied on repeated serological testing, either alone (Petersen, Hoiby et al 1981) or in combination with viral cultures for viral detection (Wang, Prober et al 1984;Ramsey, Gore et al 1989;Pribble, Black et al 1990;Armstrong, Grimwood et al 1998;Hiatt, Grace et al 1999). These methods are relatively insensitive and more recent studies have utilised PCR based methodologies (Smyth, Smyth et al 1995;Collinson, Nicholson et al 1996;Punch, Syrmis et al 2004;Olesen, Nielsen et al 2006;).…”

Section: Viral Respiratory Infections In Cfmentioning

confidence: 99%

Viral Respiratory Tract Infections in Cystic Fibrosis

Wat¹

2012

Cystic Fibrosis - Renewed Hopes Through Research

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Severe viral respiratory infections in infants with cystic fibrosis

Cited by 170 publications

References 33 publications

Low Sphingosine-1–Phosphate Impairs Lung Dendritic Cells in Cystic Fibrosis

Low Sphingosine-1–Phosphate Impairs Lung Dendritic Cells in Cystic Fibrosis

Rhinovirus Disrupts the Barrier Function of Polarized Airway Epithelial Cells

Viral Respiratory Tract Infections in Cystic Fibrosis

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