Published on July 16, 2012 at 1:57 AM
While the study, "HVEM signaling at mucosal barriers provides host defense against pathogenic bacteria," focused on E. coli and pneumococcus (also known as Streptococcus pneumoniae), Dr. Kronenberg said the HVEM mechanism is likely involved in protecting the body from many other dangerous bacteria and other microorganisms. In fact, HVEM stands for herpes virus entry mediator, and it is a protein that herpes virus uses to enter cells.
In the study, the researchers used mice genetically engineered not to have HVEM. When these mice were exposed to pneumococcus or a mouse pathogen very similar to E. coli, the HVEM deficiency led to a much greater susceptibility to infection, higher bacterial burdens and significantly compromised the mucosal barrier. "It is striking how similar the responses in the lung and the intestine were," said Dr. Kronenberg. "The mice without HVEM were unable to respond effectively at either site, and the deficit was not only major but also nearly immediate, within two days of exposure to the microorganisms."
"In the present era of ever increasing antibiotic resistance, innovative approaches to treatment of bacterial infections are urgently needed," commented Victor Nizet, M.D., a professor of Pediatrics and Pharmaceutical Sciences at the University of California San Diego. "These importantly include new approaches to strengthen immune resistance to infection, and the discovery by the La Jolla Institute scientists reveals HVEM as a candidate drug target with relevance to multiple pathogens and multiple sites of infection."
Source: La Jolla Institute for Allergy and Immunology