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Evaluation of bronchoalveolar cells in pulmonary paracoccidioidomycosis

¹ Dept of Clinical Pathology, Faculty of Medical Sciences, and ² Dept of Internal Medicine, State University of Campinas (UNICAMP) Medical School, Campinas, São Paulo, Brazil.

CORRESPONDENCE: M.H.S.L. Blotta, Dept of Clinical Pathology, Faculty of Medical Sciences, State University of Campinas (UNICAMP), PO Box 6111, 13083-970, Campinas, São Paulo, Brazil. Fax: 55 1932893273. E-mail: heblotta@fcm.unicamp.br

Keywords: bronchoalveolar lavage, CD8+ T-cells, interleukin-6, macrophage inflammatory protein-1, paracoccidioidomycosis, tumour necrosis factor-

Received: November 30, 2002
Accepted July 18, 2003

To investigate the local immune response, the cellular infiltrate and cytokine levels were analysed in bronchoalveolar lavage (BAL) from patients with pulmonary paracoccidioidomycosis. The group consisted of 19 patients aged 34–65 yrs. The diagnosis was confirmed by demonstration of the fungus in the sputum or BAL fluid and by serological tests.

Cytospin preparations showed an increased number of lymphocytes and neutrophils in BAL. A higher number of CD8+ lymphocytes were observed in BAL compared with peripheral blood. Alveolar macrophages (AM) expressed approximately three-fold more major histocompatibility class II, intercellular adhesion molecule-1 and B7-2 molecules on their surfaces than their circulating counterparts, indicating that they had differentiated into activated macrophages inside the lungs.

Cultured AM produced higher levels of interleukin (IL)-6, tumour necrosis factor (TNF)- and macrophage inflammatory protein (MIP)-1 than peripheral blood monocytes. BAL fluid contained low but detectable amounts of IL-6, TNF- and MIP-1, and specific antibodies to Paracoccidioides brasiliensis, mainly of the immunoglobulin G₂ isotype.

As macrophage inflammatory protein-1 was shown to selectively attract CD8+ T-cells and this population was elevated in bronchoalveolar lavage, the data suggest that, besides macrophages, CD8+ T-cells may have an important role in the pathogenesis of pulmonary paracoccidioidomycosis.