In sarcoidosis, nodules of inflammatory cells (called granulomas) can form in the lungs, lymph nodes or other organs. The condition can resolve on its own, but for some patients, chronic symptoms – especially with lung nodules – can result in respiratory failure and death. While there is no definitive cause of sarcoidosis, several infectious agents have been implicated. Recent evidence favors a role for mycobacteria (a class that includes the tuberculosis bacterium) and propionibacteria (skin bacteria linked to acne).
Kyra Oswald-Richter, Ph.D., research assistant professor of Pathology, Microbiology and Immunology, and colleagues analyzed the immune responses of airway cells from patients with sarcoidosis to proteins from these bacterial species. They found that while cells from sarcoidosis patients reacted to both propionibacterial and mycobacterial proteins, only the responses to mycobacterial proteins differed from controls. The researchers also identified molecular signals for mycobacteria in sarcoidosis granulomas, but no signals for propionibacteria.
The results, reported in the October Journal of Clinical Immunology, strengthen the role of infectious agents in sarcoidosis and suggest further investigation into these agents is warranted.
The research was supported by grants from the National Heart, Lung and Blood Institute (HL083839), the National Institute of Allergy and Infectious Diseases (AI065744), the National Center for Research Resources/National Center for Advancing Translational Sciences (RR000095, RR024975), the National Institute of General Medical Sciences (GM058008), and the National Cancer Institute (CA068485) of the National Institutes of Health, and the Eliassen Foundation.
