Adherence of Type IStreptococcus pneumoniaeto Tracheal Epithelium of Mice Infected with Influenza A/PR8 Virus^1–3

Abstract

Bacterial adherence to virus-infected respiratory tract cells may be one of the several mechanisms whereby virus predisposes to bacterial pneumonia. To evaluate the effect of influenza virus infection on pneumococcus adhesion, 39 mice were infected with PR8/A influenza virus. The adherence of radiolabeled pneumococcus to mice tracheal cells was determined 2, 4, and 6 days after viral inoculation. The pneumococcal adhesion to infected tracheas was significantly enhanced on Day 6 (p less than 0.001). Scanning and transmission electron microscopy revealed that by the fourth and sixth days after virus inoculation, the ciliated and the secretory cells of the tracheal epithelium had desquamated and the mucosa were coated with a continuous layer of basal cells. In a few cases, a desquamation of the basal layer was observed and the exposed basement membrane appeared as a pole of attraction for bacteria. Pneumococci were never seen attached to control tracheas. In contrast, they were observed adhered to the microvilli of the basal cells and, to a greater extent, to the exposed basement membrane.

In vitro adherence of Streptococcus pneumoniae to oropharyngeal cells: Enhanced activity and colonization of the upper respiratory tract in patients with recurrent respiratory infections.

“…Raman et al (1983) observed that cells from smokers bind more S. pneumoniae than those from nonsmokers. Plotkowski et al (1986) showed that prior influenza virus infection enhanced the adherence of S. pneumoniae to the tracheal epithelium of mice. Though Selinger and Reed (1979) proposed that the ability of S. pneumoniae to adhere to oropharyngeal cells might not be associated with virulency, Andersson et al (1981), have suggested that adherence of S. pneumoniae to oropharyngeal cells is an important step in the pathogenesis of otitis media, since this organism adhered avidly to pharyngeal cells from otitis media patients in an in vitro assay.…”

IL-10 Is an Important Mediator of the Enhanced Susceptibility to Pneumococcal Pneumonia after Influenza Infection

“…Influenza infection is known to increase adherence of and subsequent colonization with bacterial respiratory pathogens. Bacteria may adhere to the basal membrane after disruption of the airway epithelial layer by the cytopathic effect of the virus (8). It has also been suggested that the increased adherence is due to up-regulation of receptors involved in the attachment of these bacteria (9).…”

Viral infection of the lung: Host response and sequelae

“…142 IAV replication in the respiratory epithelium leads to impairment of mucosalciliary clearance and increased bacterial colonization. 143,144 Secondary infections primarily coincide with resolution of inflammation and the onset of reparative responses rather than early viral replication, 142,145,146 indicating host responses also have a significant effect on the susceptibility to bacterial superinfection. In experimental models the release of type I interferons and IFN-during viral clearance from the lung negatively affects the ability of lung-infiltrating neutrophils and macrophages, respectively, to control bacterial infection.…”