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“Mucosal Leishmaniasis (ML) may occur in both nasal and oral mucosa. However, despite the impressive tissue destruction, little is known about the oral involvement. To compare some changes underlying inflammation in oral and nasal ML, we performed immunohistochemistry on mucosal tissue of 20 patients with ML (nasal [n = 12]; oral [n = 8] lesions) and 20 healthy donors using antibodies that recognize inflammatory markers (CD3, CD4, CD8, CD22, CD68, neutrophil elastase, CD1a, CLA, Ki67, Bcl-2, NOS2, CD62E, Fas and FasL). A significantly larger number of cells, mainly T cells and macrophages, were observed in lesions than in healthy tissue. In addition, high nitric oxide synthase 2 (NOS2) expression
was associated with a reduced detection of parasites, highlighting the https://www.selleckchem.com/products/Gefitinib.html importance of NOS2 for parasite elimination. Oral lesions had higher numbers of neutrophils, parasites, proliferating cells and NOS2 than nasal lesions. These findings, together with the shorter duration of oral lesions and more intense symptoms, suggest a more recent inflammatory process. It could be explained by lesion-induced oral cavity changes that lead to eating difficulties and social stigma. In addition, the frequent poor Buparlisib tooth conservation and gingival inflammation tend to amplify tissue destruction and symptoms and may impair and confuse the correct diagnosis,
thus delaying the onset of specific treatment. American tegumentary leishmaniasis (ATL) is a parasitic disease caused by Leishmania protozoa, which are transmitted by insects of the genus Lutzomyia (1). The most common clinical presentation is the presence of cutaneous lesions (2). However, about 3–5% of patients infected with Leishmania (Viannia) braziliensis progress to mucosal leishmaniasis, which mainly affects nasal, oral and laryngeal mucosae (2–4). They are characterized by difficulties in parasite identification and large tissue 5-FU datasheet destruction (5–7). However, the exact mechanisms underlying the formation of mucosal lesions remain unknown (1). The affected mucosa is pale and hyperemic and appears rough, crusty and ulcerative. Nasal septal perforation might be observed in severe cases. Oral lesions frequently involve the lip and palate, although lesions in the uvula, gingiva, tonsils and tongue are reported. The oral mucosa generally appears swollen, ulcerated with a granular bottom and/or presents ulcerovegetative lesions (2–4). To our knowledge, few studies have investigated the in situ immune response in mucosal leishmaniasis (4,6,8–13), and there are no studies comparing the inflammatory activity between nasal and oral infected or healthy mucosae. Here, we characterize the inflammatory infiltrate of oral and nasal lesions or healthy tissues by immunohistochemistry. Forty oral (O) and nasal (N) mucosa samples obtained by biopsy were examined.