Serum from patients with invasive fungal infections inhibits the adherence of polymorphonuclear leukocytes and alveolar macrophages.

Adherence of various combinations of polymorphonuclear leukocytes (PMN) or alveolar macrophages (AM) and serum from nonimmunosuppressed patients wit culture-proved, invasive fungal infections or control subjects was evaluated in vitro using the standard nylon fiber pipette technique. In autologous serum, adherence of PMN from patients with wide variety of untreated fungal infections, including blastomycosis, histoplasmosis, cryptococcosis, coccidiodomycosis, and spirotrichosis, was significantly (p less than 0.001) decreased when compared with PMN from uninfected control subjects or patients with untreated bacterial infections. Studies using various combinations of PMN and serums from patients with blastomycosis suggested that the adherence defect was due to a serum disorder rather than an intrinsic cellular abnormality. Preincubation in serum from patients with blastomycosis decreased the adherence of control PMN. Preincubation in control serum corrected the decreased adherence of PMN from patients with blastomycosis. Additional studies revealed that the inhibitor was heat-stable and reversible, being present before, but not after, treatment or spontaneous resolution of the patient's infections. Adherence of AM from patients with fungal infection was also normal except when AM were preincubated in serum from patients with untreated fungal infections. We concluded that the intrinsic adherence of PMN and AM from patients with untreated fungal infections is normal, but that these patients do have an extrinsic heat-labile serum factor that can decrease the adherence of PMN and AM.