The outcome of
coccidioidomycosis depends on a robust specific cellular immune response. A T-helper type 1 (Th1) cellular immune response has been previously associated with resolution of clinical illness. However, the precise elements of this response and whether
cytokines not involved with the Th1 response play a role in
coccidioidomycosis are not known. Whole-blood samples were obtained from subjects with active
coccidioidomycosis and controls and incubated for 18 h with T27K, a coccidioidal
antigen preparation. The supernatant was then assayed for
gamma interferon (IFN-γ),
interleukin-2 (IL-2),
tumor necrosis factor alpha (TNF-α),
IL-4,
IL-6,
IL-10, and
IL-17A. A total of 43 subjects, 16 with acute
pneumonia, 9 with pulmonary sequelae of nodules and cavities, and 18 with nonmeningeal disseminated
coccidioidomycosis, were studied. Compared to concentrations in healthy immune and nonimmune donors, the median concentration of
IL-17A was significantly higher in those with active
coccidioidomycosis (for both, P < 0.01). In addition,
IL-6 concentrations were higher while
IL-2 and IFN-γ concentrations were significantly lower in those with nonmeningeal disseminated disease diagnosed within 12 months than in those with acute
pneumonia (for all, P < 0.05). The
cytokine profile among patients with active
coccidioidomycosis is distinct in that
IL-17A is persistently present. In addition, those with nonmeningeal disseminated disease have an increased inflammatory
cytokine response and diminished Th1 responses that modulate over time.