Researchers have discovered how proteins produced by oral epithelial cells protect humans from viruses that enter the body through the mouth. They also discovered that oral bacteria can suppress the activity of these cells, making them more vulnerable to infection.
The oral mucosal epithelium acts as a barrier between the underlying tissues and their surroundings. It is made up of two layers: the stratified squamous epithelium on the surface and the deeper lamina propria. The epithelium of keratinized oral mucosa is made up of four layers: stratum basale, stratum spinosum, stratum granulosum, and stratum corneum. The oral epithelial barrier is the result of numerous structural and functional protein interactions, resulting in the ability to respond to a variety of potentially toxic exogenous influences.
Details of how proteins produced by oral epithelial cells protect humans against viruses entering the body through the mouth have been discovered by researchers from the University of Louisville School of Dentistry and their colleagues. They also discovered that oral bacteria can suppress the activity of these cells, making them more vulnerable to infection.
Our research found that certain pathogenic bacterial species, P. gingivalis, which causes periodontal disease, can completely suppress interferon production and significantly increase susceptibility to viral infection. These oral plaque bacteria play an important role in regulating anti-viral responses.
Assistant Professor Juhi Bagaitkar
The oral bacteria Porphyromonas gingivalis reduces the production and effectiveness of interferon lambdas, a family of proteins produced by epithelial cells in the mouth that serve to protect humans from viral infection.
“Our research found that certain pathogenic bacterial species, P. gingivalis, which causes periodontal disease, can completely suppress interferon production and significantly increase susceptibility to viral infection,” said Juhi Bagaitkar, assistant professor in the University of Louisville’s Department of Oral Immunology and Infectious Disease. “These oral plaque bacteria play an important role in regulating anti-viral responses.”
Bagaitkar and Richard Lamont, professor and chair of the UofL Department of Oral Immunology and Infectious Disease, led the study, which was co-authored by first author Carlos J. Rodriguez-Hernandez and other UofL and Washington University in St. Louis researchers. The findings were published in the journal PNAS in December.
Viruses that infect the gastrointestinal tract and lungs, such as SARS-CoV-2, human immunodeficiency virus (HIV), herpes simplex, and cancer-causing viruses, such as human papillomavirus, frequently enter the body through the mouth (HPV).
P. gingivalis, a common oral bacterium that causes periodontitis, has been linked to a variety of other diseases, including Alzheimer’s and rheumatoid arthritis. Immune suppression in patients with periodontitis has been shown in recent clinical studies to increase susceptibility to HIV, herpes simplex, and HPV.
Improved understanding of how interferons provide broad antiviral protection and activate antiviral genes to protect people from viruses, as well as how P. gingivalis compromises that protection, may lead to clinical approaches to increase that protection.
P. gingivalis has been linked to a variety of diseases and conditions, including rheumatoid arthritis, Alzheimer’s disease, and esophageal cancer, according to research at the University of Louisville. Bagaitkar was one of the first junior faculty members whose research was supported by the National Institute of General Medical Sciences’ Center of Biomedical Research Excellence (CoBRE) for research in microorganism disease research.
HCV, HBV, influenza virus, rhinovirus, respiratory syncytial virus (RSV), lymphocytic choriomeningitis virus (LCMV), rotavirus, reovirus, norovirus, and West Nile virus are all important in viral infections (WNV). Many of these IFN antiviral response studies have focused on viruses that infect the liver, respiratory and gastrointestinal mucosa, and, more recently, those that cross the blood–brain barrier (BBB) to cause a neuroinvasive viral infection.
