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Staphylococcus aureus is a major pathogen in humans. The nasal vestibule is considered as the main reservoir of S. aureus. However, even though the nasal cavity may also be colonized by S. aureus, the relationships between the two sites are still unclear. We conducted a prospective study in humans to assess the S. aureus colonization profiles in the vestibule and nasal cavity, and to investigate the presence of intracellular S. aureus in the two sites. Patients undergoing ear, nose, and throat surgery were swabbed during endoscopy to determine S. aureus nasal load, genotype, and presence of intracellular S. aureus. Among per-operative samples from 90 patients, the prevalence of S. aureus carriage was 32.2% and 33.3% in the vestibule and the nasal cavity, respectively. The mean S. aureus load was 4.10 and 4.25 log 10 CFU/swab for the nasal vestibule and nasal cavity, respectively (P > 0.05). Genotyping of S. aureus revealed that all nasal strains isolated from a given individual belong to the same clonal complex and spa-type. An intracellular carriage was observed in 5.6% of the patients, all of whom exhibited a S. aureus vestibule load higher than 3 log 10 CFU/swab. An intracellular niche was observed in the vestibule as well as in the nasal cavity. In conclusion, the nasal cavity was also found to be a major site of S. aureus carriage in humans and should draw attention when studying host-pathogen interactions related to the risk of infection associated with colonization., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Background: Staphylococcus aureus is able to invade mammalian cells during infection and was recently observed inside nasal mucosa of healthy carriers., Objectives: To determine the intracellular activity of antimicrobial compounds used for decolonization procedures using a cell model mimicking S. aureus nasal epithelium invasion., Patients and Methods: HaCaT cells and human nasal epithelial cells (HNECs) recovered from nasal swabs of S. aureus carriers were visualized by confocal laser scanning microscopy to detect intracellular S. aureus cells. An HaCaT cell model, mimicking S. aureus internalization observed ex vivo in HNECs, was used to assess the intracellular activity against S. aureus of 21 antimicrobial compounds used for nasal decolonization, including mupirocin and chlorhexidine., Results: HaCaT cells and HNECs were found to internalize S. aureus with the same focal pattern. Most antimicrobial compounds tested on HaCaT cells were shown to have weak activity against intracellular S. aureus. Some systemic antimicrobials, including fusidic acid, clindamycin, linezolid, minocycline, ciprofloxacin, moxifloxacin, rifampicin and levofloxacin, reduced S. aureus intracellular loads by 0.43-1.66 log cfu/106 cells compared with the control (P < 0.001). By contrast, mupirocin and chlorhexidine reduced the S. aureus intracellular load by 0.19 and 0.23 log cfu/106 cells, respectively., Conclusions: These data indicate that most of the antimicrobial compounds used for nasal decolonization, including mupirocin and chlorhexidine, exhibit weak activity against intracellular S. aureus using the HaCaT cell model. This work emphasizes the need to better understand the role of the S. aureus intracellular reservoir during nasal colonization in order to improve decolonization procedures.

The in vitro propagation of human rhinoviruses (RVs) is difficult because only few continuous human cell lines are permissive to these agents. We propose an innovative model of epithelial cell infection using a non-transformed continuous keratinocyte line from human origin (HaCaT cells). After infection with RV-A13, RV-A16 or RV-A19, HaCaT cells produced infectious particles without showing any observable cytopathic effect and overexpressed ICAM-1 (intercellular adhesion molecule 1), the major entry receptor of RVs. Furthermore, the treatment of HaCaT cells with 10 µM clarithromycin reduced the viral titer by 93% and 60% during the first and second days following viral infection, respectively, probably by down-regulating ICAM-1 expression. This original model of epithelial cell infection by RV could be useful to study chronic viral infection and bacterium-virus interactions at the cell level. These results also suggest that clarithromycin may be evaluated for treating in vivo infections associating RV to a susceptible bacterium., (Copyright © 2018. Published by Elsevier Inc.)

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.