(Boston) — Researchers from the Boston University School of Medicine (BUSM) have demonstrated that commensal species of the genus Neisseriae are low inducers of human airway epithelial cell responses as compared to the pathogenic species. Specifically, the study indicates that a Neisserial outer membrane component appears to play a differential role in the host inflammatory responses via interaction with a receptor on the surface of human airway epithelial cells.
Paola Massari, an assistant professor in the section of infectious diseases at BUSM, is lead author of this study, which is published in the Dec. 2010 issue of the journal Infection and Immunity.
The team focused their research on Neisseria lactamica, a gram negative organism comprising both commensal and pathogenic bacteria. Neisseria meningitidis, the causative agent of meningococcal meningitis, as well as Neisseria lactamica, colonize the human nasopharynx, but only Neisseria meningitidis is pathogenic.
“We set out to understand the relationship between commensal Neisseriae organisms and the human hosts,” said Massari. “Although Neisseriae organisms express mostly identical surface antigens and structures, they appear to induce different responses when they interact with the host.”
To examine how the bacteria interact with human nasopharyngeal cells, Massari and her research team honed in on a bacterial surface component, the PorB porin, present in all Neisseriae organisms. After purifying the PorB, they found that the protein from the commensal bacteria induced lower levels of human airway epithelial cell activation compared to PorB purified from the pathogenic organisms.
Next, the team demonstrated that PorB from N. lactamica and PorB from N. meningitidis appear to interact with the host cell surface receptor, Toll-like receptor 2 (TLR2), in a differential manner, thus leading to different inflammatory responses in human airway epithelial cells.
“This study confirms that TLR2 signaling is essential for the activation of human airway epithelial cells,” said Massari. “This is likely one of the mechanisms by which the body limits inflammation in response to colonization with harmless commensal bacteria, thus avoiding exacerbation of inflammatory responses and local chronic local inflammation.
About Boston University School of Medicine
Originally established in 1848 as the New England Female Medical College, and incorporated into Boston University in 1873, Boston University School of Medicine today is a leading academic medical center with an enrollment of more than 700 medical students and more than 800 masters and PhD students. Its 1,246 full and part-time faculty members generated more than $335 million in funding in the 2009-2010 academic year for research in amyloidosis, arthritis, cardiovascular disease, cancer, infectious disease, pulmonary disease and dermatology among others. The School is affiliated with Boston Medical Center, its principal teaching hospital, the Boston and Bedford Veterans Administration Medical Centers and 16 other regional hospitals as well as the Boston HealthNet.