title: Mucosal leishmaniasis: in situ characterization of the host inflammatory response, before and after treatment.
abstract: Mucosal leishmaniasis (ML) generally shows progressive tissue destruction, not yet fully elucidated, associated with an intense inflammatory response. To contribute to the understanding of this process and of how treatment interferes with it, we studied several anatomopathological parameters, including those analyzed by immunohistochemistry, such as Leishmania antigens, cells participating in the immune response and cytokine expression. Biopsies were taken from 20 patients with ML before and after treatment. A mixed Th1 and Th2 pattern response occurred inside ML before treatment, persist after treatment. Nevertheless, this mixed response was smaller than in active lesions, with reduced but present numbers of cells expressing TNF-alpha, IFN-gamma and IL-4 and sustained numbers of cells expressing IL-10. We may conclude that specific treatment causes a reduction of inflammatory lesions and disappearance of amastigote forms of Leishmania although the factors related to the pathogenesis of the lesion, such as T CD4+ and T CD8+ lymphocytes and Leishmania antigens, persist in treated lesions. The maintenance of these inflammatory patterns may be due to a specific host-parasite relationship response, strongly indicating the need for continuous surveillance of LM patients at risk of reactivation, despite effective cicatrization after therapy.
authors.affiliation: Department of Infectious and Parasitic Diseases, School of Medicine, University of São Paulo, Av Dr Enéas de Carvalho Aguiar, 255, 05403-010 SP, Sao Paulo, Brazil. valdirsa@netpoint.com.br
authors.forename: Valdir Sabbaga
authors.initials: VS
authors.lastname: Amato
authors.forename: Heitor Franco
authors.initials: HF
authors.lastname: de Andrade
authors.forename: Maria Irma Seixas
authors.initials: MI
authors.lastname: Duarte
mesh_terms: D000328:Adult; D000368:Aged; D000818:Animals; D000911:Antibodies, Monoclonal; D000954:Antigens, Surface / Q000032:analysis / Q000145:classification; D000981:Antiprotozoal Agents / Q000627:therapeutic use; D016207:Cytokines / Q000032:analysis; D005260:Female; D006790:Host-Parasite Interactions; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000276:immunology; D007371:Interferon-gamma / Q000032:analysis; D016753:Interleukin-10 / Q000032:analysis; D015847:Interleukin-4 / Q000032:analysis; D007897:Leishmaniasis, Mucocutaneous / Q000188:drug therapy* / Q000276:immunology* / Q000473:pathology; D008297:Male; D010641:Phenotype; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D000911:Antibodies, Monoclonal; D000954:Antigens, Surface; D000981:Antiprotozoal Agents; D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D015847:Interleukin-4; D007371:Interferon-gamma