title: Cytokine Profiles from Antigen-Stimulated Whole-Blood Samples among Patients with Pulmonary or Nonmeningeal Disseminated Coccidioidomycosis.
abstract: 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.
authors.affiliation: Medical and Research Services, Southern Arizona Veterans Affairs Health Care System, Tucson, Arizona, USA nampel@email.arizona.edu.
authors.forename: Neil M
authors.initials: NM
authors.lastname: Ampel
authors.affiliation: Medical and Research Services, Southern Arizona Veterans Affairs Health Care System, Tucson, Arizona, USA Pulmonary Division, Department of Medicine, University of Arizona, Tucson, Arizona, USA.
authors.forename: Lance A
authors.initials: LA
authors.lastname: Nesbit
authors.affiliation: Medical and Research Services, Southern Arizona Veterans Affairs Health Care System, Tucson, Arizona, USA.
authors.forename: Chinh T
authors.initials: CT
authors.lastname: Nguyen
authors.affiliation: Medical and Research Services, Southern Arizona Veterans Affairs Health Care System, Tucson, Arizona, USA.
authors.forename: Suzette
authors.initials: S
authors.lastname: Chavez
authors.affiliation: Pulmonary Division, Department of Medicine, University of Arizona, Tucson, Arizona, USA.
authors.forename: Kenneth S
authors.initials: KS
authors.lastname: Knox
authors.affiliation: Department of Microbiology/Immunology, University of California at Davis, Davis, California, USA.
authors.forename: Suzanne M
authors.initials: SM
authors.lastname: Johnson
authors.affiliation: Department of Microbiology/Immunology, University of California at Davis, Davis, California, USA.
authors.forename: Demosthenes
authors.initials: D
authors.lastname: Pappagianis
mesh_terms: D000328:Adult; D000368:Aged; D000946:Antigens, Fungal / Q000276:immunology*; D001769:Blood / Q000276:immunology*; D003045:Coccidioides / Q000276:immunology*; D003047:Coccidioidomycosis / Q000276:immunology*; D016207:Cytokines / Q000378:metabolism*; D005260:Female; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000276:immunology*; D008297:Male; D008875:Middle Aged
chemical_list: D000946:Antigens, Fungal; D016207:Cytokines