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Published on: November 4, 2015
Augmented adherence and internalization of group A Streptococcus pyogenes to influenza A virus infected MDCK cells
Mohamed M Hafez1, Kouka S E Abdel-Wahab, Daad F I El-Fouhil
1Department of Microbiology and Immunology, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt. amn1971@lycos.com
Abstract:
Respiratory tract infections are one of the leading causes of morbidity and mortality. There is considerable epidemiologic evidence that infection with respiratory viruses increases the incidence and severity of secondary bacterial complications. However, very limited number of studies were concerned with the mechanism behind such synergy. In this context, our study aimed to explore the interaction between Group A Streptococcus pyogenes (GAS) and Influenza A virus (IAV). Our results revealed that the GAS adherence and internalization into Madin-Darby canine kidney (MDCK) cells markedly increased after IAV infection. When M6 protein defective mutant of GAS was used, the virus enhanced adherence and internalization was nearly abolished indicating the involvement of M protein binding sites on the MDCK cell surface. Interestingly, the modulation of some O-linked glycolproteins as well as sialic acid, mucin and fibrinogen-like residues on the surface of MDCK cells contributed to augmented bacterial adherence and/or internalization. In the same way, qRT-PCR experiments showed an overexpression of the membrane associated mucin (MUC1) on the surface of the MDCK cells after IAV infection. Altogether, the present study revealed that IAV infection augments the adherence and internalization of GAS to MDCK cells via modulation of membrane associated O-linked glycoproteins, fibrinogen, sialic acid residues and the mucin, MUC1 on the surface of MDCK cell.
Insights
Influenza A virus infection enhances Group A Streptococcus adherence and internalization into respiratory cells. This interaction is mediated by viral effects on bacterial M protein binding sites and host cell surface molecules like MUC1.
Area of Science:
- Microbiology
- Virology
- Immunology
Background:
- Respiratory tract infections cause significant morbidity and mortality.
- Viral infections often lead to secondary bacterial complications, but mechanisms are poorly understood.
Purpose of the Study:
- To investigate the interaction between Influenza A virus (IAV) and Group A Streptococcus pyogenes (GAS).
- To elucidate the cellular mechanisms underlying enhanced bacterial adherence and invasion following viral infection.
Main Methods:
- Utilized Madin-Darby canine kidney (MDCK) cell models.
- Employed M6 protein defective GAS mutants.
- Conducted quantitative reverse transcription PCR (qRT-PCR) for gene expression analysis.
Main Results:
- IAV infection significantly increased GAS adherence and internalization in MDCK cells.
- M protein of GAS is crucial for virus-enhanced bacterial uptake.
- IAV infection modulated MDCK cell surface O-linked glycoproteins, sialic acid, mucin, and fibrinogen-like residues, promoting bacterial interaction.
- Overexpression of membrane-associated mucin (MUC1) was observed on MDCK cells post-IAV infection.
Conclusions:
- IAV infection promotes GAS adherence and internalization into respiratory epithelial cells.
- The mechanism involves alterations in host cell surface molecules, including MUC1, sialic acid, and glycoproteins, facilitating bacterial binding and entry.
- GAS M protein plays a key role in this synergistic interaction.
