Rhinoviruses promote internalisation of Staphylococcus aureus into non-fully permissive cultured pneumocytes

Passariello, Claudio; Schippa, Serena; Conti, Cinzia; Russo, Patrizia; Poggiali, Federica; Garaci, Enrico; Palamara, Anna Teresa

doi:10.1016/j.micinf.2005.09.013

Cited by 46 publications

(57 citation statements)

References 44 publications

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“…Glycoproteins elaborated by influenza virus and RSV during replication can integrate into the host cell surface and serve as receptors for bacteria (15)(16)(17). Viruses can also expose or upregulate the expression of native receptors for bacteria on the host cell surface, thereby increasing the bacterial adherence and colonization (18)(19)(20)(21).…”

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

306

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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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

306

312

View full text Add to dashboard Cite

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“…They reported that the adherence of S. aureus was significantly higher in rhinovirus-infected cells compared to uninfected cells. Only recently, various in vitro studies have shown that inflammation due to rhinovirus infection increased cellular patterns that facilitate the adhesion and internalization of S. aureus within host cells [52–56]. …”

Section: Mechanisms Involved In Interactions Between Staphylococcus Amentioning

confidence: 99%

“…The intercellular adhesion molecule 1 (ICAM-1), which is the receptor of the major group of rhinoviruses [60], have been found to be overexpressed during rhinovirus infection [52,61]. Adhesion and internalization of S. aureus to epithelial cells is also mediated by ICAM-1 [52,54].…”

Section: Mechanisms Involved In Interactions Between Staphylococcus Amentioning

confidence: 99%

“…Adhesion and internalization of S. aureus to epithelial cells is also mediated by ICAM-1 [52,54]. Both immortalized pneumocytes (A549 cell line) and primary human nasal epithelial cells have been found to release higher levels of IL-6 and IL-8 when infected by rhinovirus and subsequently overexpressed ICAM-1.…”

Section: Mechanisms Involved In Interactions Between Staphylococcus Amentioning

confidence: 99%

“…Both immortalized pneumocytes (A549 cell line) and primary human nasal epithelial cells have been found to release higher levels of IL-6 and IL-8 when infected by rhinovirus and subsequently overexpressed ICAM-1. The pro-inflammatory effect of IL-6 and IL-8 also induces an overexpression of ICAM-1 in the surrounding uninfected cells, which increases S. aureus uptake by the epithelial cells [52]. The up-regulation of ICAM-1 and pro-inflammatory cytokines in rhinovirus-infected epithelial cells seems to follow the NFκB pathway [61–63].…”

Section: Mechanisms Involved In Interactions Between Staphylococcus Amentioning

confidence: 99%

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Staphylococcus aureus colonization and non-influenza respiratory viruses: Interactions and synergism mechanisms

et al. 2018

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Viral infections of the respiratory tract can be complicated by bacterial superinfection, resulting in a significantly longer duration of illness and even a fatal outcome. In this review, we focused on interactions between S. aureus and non-influenza viruses. Clinical data evidenced that rhinovirus infection may increase the S. aureus carriage load in humans and its spread. In children, respiratory syncytial virus infection is associated with S. aureus carriage. The mechanisms by which some non-influenza respiratory viruses predispose host cells to S. aureus superinfection can be summarized in three categories: i) modifying expression levels of cellular patterns involved in S. aureus adhesion and/or internalization, ii) inducing S. aureus invasion of epithelial cells due to the disruption of tight junctions, and iii) decreasing S. aureus clearance by altering the immune response. The comprehension of pathways involved in S. aureus-respiratory virus interactions may help developing new strategies of preventive and curative therapy.

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