Influenza A Virus-Infected Hosts Boost an Invasive Type of<i>Streptococcus pyogenes</i>Infection in Mice

Okamoto, Shigefumi; Kawabata, Shigetada; Nakagawa, Ichirô; Okuno, Yoshinobu; Goto, Toshiyuki; Sano, Kohei; Hamada, Shigeyuki

doi:10.1128/jvi.77.7.4104-4112.2003

Cited by 95 publications

(106 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It is unlikely that either the RSV-induced cytopathic effect on the epithelium or expression of viral glycoproteins or upregulation of host proteins on the cellular surface contribute to the RSV-enhanced pneumococcal bacteremia when RSV and pneumococci are inoculated simultaneously. Okamoto et al found that the direct interaction between influenza A virus and group A streptococci induced a lethal respiratory infection in a murine model (23,24). Similar findings with respect to a lethal synergism between influenza virus and pneumococci were obtained by Mc.…”

Section: Discussionsupporting

confidence: 66%

Direct Binding of Respiratory Syncytial Virus to Pneumococci: A Phenomenon That Enhances Both Pneumococcal Adherence to Human Epithelial Cells and Pneumococcal Invasiveness in a Murine Model

et al. 2005

View full text Add to dashboard Cite

In a previous study we showed that pneumococcal adherence to epithelial cells was enhanced by a preceding respiratory syncytial virus (RSV) infection. RSV-glycoproteins, expressed on the infected cell surface, may play a role in this enhanced pneumococcal binding, by acting as bacterial receptors. In the current study, it was attempted to analyze the capacity of pneumococci to interact directly with RSV virions. By flowcytometry, a direct interaction between RSV and pneumococci could be detected. Heparin, an inhibitor of RSV infectivity that interacts with RSV protein-G, blocked RSV-pneumococcal binding, indicating that the latter interaction is indeed mediated by protein-G. RSV-pneumococcal complexes showed enhanced adherence to uninfected human epithelial cells, compared with pneumococcal adherence without bound RSV, and this enhancement was also blocked by heparin. In addition, the significance of these findings in vitro was explored in vivo in a murine model. Both mice that were pretreated with RSV at day 4 before pneumococcal challenge and mice infected with both agents simultaneously showed significantly higher levels of bacteraemia than controls. Simultaneous infection with both agents enhanced the development of pneumococcal bacteraemia most strongly. It was hypothesized that direct viral binding is another mechanism by which RSV can induce enhanced pneumococcal binding to epithelial cells, a phenomenon that is translated in vivo by a higher invasiveness of pneumococci when administered simultaneously with RSV to mice. Apparently, RSV acts in this process as a direct coupling particle between bacteria and uninfected epithelial cells, thereby increasing colonization by and enhancing invasiveness of pneumococci. Clinical and epidemiologic data suggest that respiratory syncytial virus (RSV) infections in humans can be complicated by bacterial superinfection e.g., with Streptococcus pneumoniae, leading to increased morbidity (1-5). Mechanisms underlying bacterial superinfection include virus-induced local destruction of the epithelium, compromising the host's physiologic barrier, and virus-induced modulation of the immune response (6,7).In addition, enhanced bacterial adherence to virus-infected cells is considered an important factor increasing the risk of bacterial superinfection (8 -11). In a previous study in vitro, we obtained evidence for such a mechanism. A preceding RSV infection of human respiratory tract epithelium led to significantly enhanced adherence of S. pneumoniae (12).The basis of RSV-enhanced pneumococcal adherence is not known. RSV infection both leads to expression of viral glycoproteins and up-regulation of cellular molecules on the hostcell membrane. Both could possibly serve as bacterial receptors, as has been described for Neisseria meningitidis: viral glycoprotein G as well as cellular molecules, like CD 14 and CD18, are involved in enhanced binding of N. meningitidis to RSV-infected cells (13,14

show abstract

Section: Discussionsupporting

confidence: 66%

Direct Binding of Respiratory Syncytial Virus to Pneumococci: A Phenomenon That Enhances Both Pneumococcal Adherence to Human Epithelial Cells and Pneumococcal Invasiveness in a Murine Model

et al. 2005

View full text Add to dashboard Cite

show abstract

“…The RSV attachment glycoprotein (G) protein, present on the surface of either RSV virions or infected cells, can serve as a binding structure for non-typeable H. influenzae (Avadhanula et al, 2007), S. pneumoniae (Avadhanula et al, 2007;Hament et al, 2005) and Pseudomonas aeruginosa (Van Ewijk et al, 2007). Similarly, integration of influenza virus haemagglutinin into the cell membrane of infected cells facilitates attachment and invasive disease of group A streptococci in mice (Okamoto et al, 2003). On top of this, the binding of fibrinogen to cells infected with influenza A, and the modulation of several surface molecules in influenzainfected cells is thought to aid the binding and invasion of group A streptococci (Hafez et al, 2010;Sanford et al, 1982).…”

Section: Receptor Expressionmentioning

confidence: 99%

Viral–bacterial interactions in the respiratory tract

Bellinghausen

Rohde

Savelkoul

et al. 2016

Journal of General Virology

View full text Add to dashboard Cite

“…Though RV infection is notable for the lack of cytotoxicity relative to other respiratory viruses, such as RSV and influenza (14,30,31), RV has been shown to induce apoptosis by activating caspase 3 and caspase 9 and poly(ADP-ribose) polymerase activation in nonpolarized airway epithelial cells (32). To examine whether RV causes apoptosis in primary airway epithelial cells differentiated into mucociliary phenotype and in polarized 16HBE14o-cells, we infected these cultures with RV39 (MOI of 1) or sham, as described above, and determined the population of apoptotic cells by staining with annexin V and propidium iodide followed by flow cytometric analysis.…”

Section: Apoptosis Does Not Contribute To Rv-induced Reductions In R Tmentioning

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

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.

show abstract

Influenza A Virus-Infected Hosts Boost an Invasive Type ofStreptococcus pyogenesInfection in Mice

Cited by 95 publications

References 39 publications

Direct Binding of Respiratory Syncytial Virus to Pneumococci: A Phenomenon That Enhances Both Pneumococcal Adherence to Human Epithelial Cells and Pneumococcal Invasiveness in a Murine Model

Direct Binding of Respiratory Syncytial Virus to Pneumococci: A Phenomenon That Enhances Both Pneumococcal Adherence to Human Epithelial Cells and Pneumococcal Invasiveness in a Murine Model

Viral–bacterial interactions in the respiratory tract

Rhinovirus Disrupts the Barrier Function of Polarized Airway Epithelial Cells

Contact Info

Product

Resources

About