Chronic Sinusitis Patients Have Enhanced Immune Responses to Fungi

The researchers, led by Hirohito Kita, M.D., of the Mayo Clinic in Rochester, MN, compared blood samples taken from 18 people diagnosed with chronic sinusitis with blood samples from 15 healthy volunteers. Nasal secretions from the two groups were also examined for the presence of fungal proteins and inflammation-causing immune system molecules.

Airborne microscopic fungi spores abound indoors and out. People may inhale a million or more fungal spores each day, notes Dr. Kita. The mere presence of such fungi in the airways, however, is not enough to cause sinusitis because these spores can be found in the upper respiratory tracts of both sinusitis sufferers and non-sufferers. Indeed, in this study, levels of fungal proteins in nasal secretions were similar in both groups.

The Mayo Clinic scientists looked for evidence that people with sinusitis respond abnormally to these harmless fungi. The investigators exposed immune cells derived from the blood samples to extracts of four common airborne fungi: Alternaria, Aspergillus, Penicillium and Cladosporium. The cells of chronic sinusitis sufferers released significant amounts of three immune-modulating chemicals, called cytokines, specifically interferon-gamma, interleukin-5 (IL-5) and IL-13. In contrast, cells from healthy volunteers released very little interferon-gamma and no IL-5 or IL-13. The most dramatic responses occurred after exposure to Alternaria.

Importantly, says Dr. Kita, the released cytokines represent both major classes of cytokines — interferon-gamma is in the Th1 group and IL-5 and IL-13 are in the Th2 class. This is notable because scientists have thought that allergic reactions involve only Th2 cytokines, Dr. Kita explains. (While chronic sinusitis is not considered to be an allergic disease, people with the condition also often have asthma and allergic rhinitis, giving scientists reason to suspect a link.) The current findings add to an evolving understanding of allergic diseases that suggests symptoms may stem from a combination of Th1 and Th2 cytokines.