Bacterial Adherence to Virus-Infected Cells: A Cell Culture Model of Bacterial Superinfection

Sanford, Barbara A.; Shelokov, Alexis; Ramsay, Mary A.

doi:10.1093/infdis/137.2.176

Cited by 108 publications

(60 citation statements)

References 13 publications

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“…Our observations identify two new mechanisms by which certain viruses may promote adherence of secondary pathogens to nonphagocytic cells. These mechanisms, like the previously described adherence both of bacteria to viral antigens themselves (24) and of protein Acontaining cocci to fixed antiviral antibody (25), require further study to ascertain their clinical significance.…”

Section: Resultsmentioning

confidence: 80%

Antibody-mediated bacterial adhesion to cytomegalovirus-induced Fc receptors. Potential relationship to secondary infections complicating herpesvirus infections.

Mackowiak¹,

Marling-Cason²,

Smith³

et al. 1984

J. Clin. Invest.

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Abstract. Cytomegalovirus (CMV) and other viruses within the herpes group have recently been shown to induce Fc receptors in infected monolayers. We have examined the possibility that such receptors might facilitate the adherence of antibody-coated bacteria to CMVinfected cells. To do this, we infected confluent human embryonic lung (HEL) cell monolayers with CMV (strain AD 169) and then used a double radiolabel assay to measure adherence of Escherichia colt 06 to both infected and control monolayers. We examined infected monolayers 48 h after viral seeding, at which time 30-60% of the cells exhibited characteristic cytopathic changes. We compared the adherence of untreated E. coli 06 with the adherence of E. coli 06 that had been preincubated for 1 h at 370C with either nonimmune or anti-E. coli 06 antiserum. Pretreatment of the E. coli 06 with specific antiserum significantly enhanced its adherence to CMVinfected, but not to control, monolayers (P < 0.01 by the Mann-Whitney U test). We did not see such enhancement when we used anti-E. coli 06 antiserum to treat a nontypable E. colt. The augmented adherence of antibodycoated E. colt 06 to CMV-infected monolayers was abrogated by pretreating the monolayers with nonimmune serum or purified Fc fragments, but not by pretreating with IgA, IgM, or 1 mM trypan blue. Preincubating HEL cell monolayers with 100 U/ml human leukocyte interferon for 72 h at 370C did not affect the adherence of antibody-coated E. coli 06 to the monolayers.

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Section: Resultsmentioning

confidence: 80%

Antibody-mediated bacterial adhesion to cytomegalovirus-induced Fc receptors. Potential relationship to secondary infections complicating herpesvirus infections.

Mackowiak¹,

Marling-Cason²,

Smith³

et al. 1984

J. Clin. Invest.

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“…Various in vitro and in vivo studies have focused on the increased bacterial adherence after a preceding viral infection (25,26). Certain strains of S. pneumoniae were found to adhere in greater numbers to A549 cells infected with adenovirus compared with uninfected A549 cells (22).…”

Section: Discussionmentioning

confidence: 99%

Enhanced Adherence of Streptococcus pneumoniae to Human Epithelial Cells Infected with Respiratory Syncytial Virus

et al. 2004

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In the present study, we analyzed the effect of a preceding respiratory syncytial virus (RSV) infection of human respiratory epithelial cells on the adherence of Streptococcus pneumoniae tested by means of a cytometric fluorescence assay. Adherence of clinically relevant pneumococcal serotypes 3, 9, 14, 18, 19, and 23 was studied using uninfected and RSV-infected monolayers. To this end, monolayers of both human nasopharyngeal cells (HEp-2) and pneumocyte type II cells (A549) were infected with RSV serotype A. Adherence to uninfected epithelial cells varied between pneumococcal serotypes. After RSV infection of the monolayers, all serotypes showed a strongly (2-to 10-fold) and significantly increased adherence when compared with adherence to uninfected monolayers. Enhanced adherence was observed with both cell lines. By fluorescence and scanning electron microscopy, we observed redistribution of pneumococcal adherence over the epithelial surface due to RSV infection, with dense bacterial accumulations near to epithelial syncytia. Streptococcus pneumoniae and RSV belong to the most important pathogens of upper and lower respiratory tract infections in young children (1, 2). There is accumulating evidence for a positive relationship between infections with S. pneumoniae and RSV, especially in the pathogenesis of otitis media, pneumonia, and meningitis (3-8). Epidemiologically, the peak incidences of RSV infections and invasive infections due to S. pneumoniae coincide (9). In a large study on the etiology of community-acquired bacterial pneumonia, a preceding viral infection could be detected by serology in 39% of the children (10). The combination of RSV and S. pneumoniae was seen most frequently in children below age 5 y.The most prevalent pneumococcal serotypes causing invasive pneumococcal disease in children include serotypes 9, 14, 18, 19, and 23. Pneumococcal sepsis in adults is often caused by serotype 3 (11-14).Enhanced pneumococcal adherence, secondary to a preceding RSV infection of the respiratory tract epithelium, is considered one of the mechanisms facilitating bacterial infection (15,16).The aim of the present study was to examine the influence of prior RSV infection on pneumococcal adherence to confluently grown epithelial cells using an assay based on adherence of fluorescent pneumococci. The influence of RSV-preinfection on pneumococcal superinfection with serotypes 3, 9, 14, 18, 19, and 23 was evaluated. MATERIAL AND METHODS Bacteria.Clinical pneumococcal isolates, serotypes 3, 9, 14, 18, 19, and 23, were kindly provided by Dr. C. Neeleman, Intensive Care Department of the University Hospital of Nijmegen, The Netherlands, and stored at Ϫ70°C in micro-banks (Pro-Lab Diagnostics, Austin, TX, U.S.AϾ). Before testing, an aliquot of stored bacteria was transferred from a micro-bank bead to blood-agar plates and was incubated overnight at 37°C in a CO 2 incubator. The next day, the bacteria were inoculated in Todd-Hewitt broth (Difco, Detroit, MI, U.S.A.), supple-

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“…Based on the hypothesis that microbial superinfections frequently accompanied a fatal outcome during the 1918 Spanish influenza epidemic, various attempts have been made to examine the interaction between influenza viruses and some bacteria in animal models (13,16,22,25,27,32,37). It is still unknown, however, which bacterial virulence factor(s) is important for the induction of invasive bacterial-viral superinfection.…”

Section: Discussionmentioning

confidence: 99%

TheStreptococcus pyogenesCapsule Is Required for Adhesion of Bacteria to Virus-Infected Alveolar Epithelial Cells and Lethal Bacterial-Viral Superinfection

et al. 2004

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An apparent worldwide resurgence of invasive group A Streptococcus (GAS) infections remains unexplained. However, we recently demonstrated in mice that when an otherwise nonlethal intranasal GAS infection is preceded by a nonlethal influenza A virus (IAV) infection, induction of lethal invasive GAS infections is often the result. In the present study, we established several isogenic mutants from a GAS isolate and evaluated several virulence factors as candidates responsible for the induction of invasive GAS infections. Disruption of the synthesis of the capsule, Mga, streptolysin O, streptolysin S, or streptococcal pyrogenic exotoxin B of GAS significantly reduced mortality among mice superinfected with IAV and a mutant. In addition, the number of GAS organisms adhering to IAV-infected alveolar epithelial cells was markedly reduced with the capsuledepleted mutant, although this was not the case with the other mutants. Wild-type GAS was found to bind directly to IAV particles, whereas the nonencapsulated mutant showed much less ability to bind. These results suggest that the capsule plays a key role in the invasion of host tissues by GAS following superinfection with IAV and GAS.Streptococcus pyogenes (group A Streptococcus [GAS]) is known to be the cause of such diseases as uncomplicated pharyngitis, impetigo, and acute rheumatic fever (10). In addition, severe invasive GAS infections, leading to a wide range of diverse diseases that include acute respiratory distress syndrome, renal failure, streptococcal toxic shock syndrome, sepsis, and cellulitis, have been reported in North America, Europe, and Japan (4,23,30,35,41). GAS invades the host via the upper respiratory tract or injured skin surfaces (10). Although many invasive GAS isolates are reportedly of the M1 or M3 serotype, which produce streptococcal pyrogenic exotoxin A (10), the reasons for the recent emergence, or reemergence, of invasive GAS infections remain unknown.Statistically, the incidence of GAS infections is highest in winter, when influenza epidemics are common (5,12,28). In that regard, we recently used a mouse model to show that superinfection with influenza A virus (IAV) and GAS applied intranasally causes a lethal GAS infection that affects various tissues and organs of the host (32). In that study, GAS organisms adhered to the surface of IAV-infected alveolar epithelial cells of superinfected mice, although no GAS adhered to epithelial cells of mice infected with GAS alone. Moreover, our electron microscopic observations confirmed that GAS organisms bind directly to IAV particles on the cell surfaces. Taken together, these results suggest that IAV infection plays a key role in the enhanced internalization of GAS by alveolar epithelial cells, resulting in the emergence of sepsis and other invasive GAS diseases. Beyond this, however, little is known about the mechanisms via which invasive IAV-GAS superinfections occur.Ashbaugh et al. (3) established a murine model of human necrotizing fasciitis and concluded that the GAS hyaluronic acid ca...

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Bacterial Adherence to Virus-Infected Cells: A Cell Culture Model of Bacterial Superinfection

Cited by 108 publications

References 13 publications

Antibody-mediated bacterial adhesion to cytomegalovirus-induced Fc receptors. Potential relationship to secondary infections complicating herpesvirus infections.

Antibody-mediated bacterial adhesion to cytomegalovirus-induced Fc receptors. Potential relationship to secondary infections complicating herpesvirus infections.

Enhanced Adherence of Streptococcus pneumoniae to Human Epithelial Cells Infected with Respiratory Syncytial Virus

TheStreptococcus pyogenesCapsule Is Required for Adhesion of Bacteria to Virus-Infected Alveolar Epithelial Cells and Lethal Bacterial-Viral Superinfection

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