Even though it appeared as the HBD1 and HBD3 mRNA expression was down-regulated by Th2 cytokines and histamine, no statistical differences were found (Fig. 4a–c). Moreover, high levels of HBD1-3 were excreted from tonsils, but the levels remained unchanged upon stimulation (Fig. 4d–f). However, our impression was that the outcome of these Raf inhibitor analyses

was dependent on where the excised tonsillar piece was taken. It was technically very difficult to know in advance the relation between epithelial and lymphoid cells as well as the infectious and allergic status of the tonsil and donor, respectively. Therefore, the experiments were repeated with mixed tonsillar lymphocytes and AECs cultured for 4, 16 and 24 h with and without IL-4, IL-5 and histamine. For both cell types, 4 and 16 h were insufficient to induce AMP generation (data not shown). However, after 24 h of culture the effects on the lymphocyte-induced HBD release were negligible (Fig. 5a–c), whereas a marked reduction in the epithelium-derived HBDs in the culture medium was seen in response to these agents (Fig. 6a–c). The present study describes HBD1-3 in tonsillar tissue and their regulation

in allergic rhinitis. mRNA and protein expression of HBD1-3 are shown in epithelial and lymphoid cells along with tonsillar secretion of HBD1-3. Allergic individuals are found to have reduced levels of HBD1-3. In addition, culture of mixed tonsillar lymphocytes and AECs with Th2-associated

cytokines and histamine causes a down-regulation of HBDs in the latter, indicating that the epithelial tissue is the regulatory site for the production of HBDs. Respiratory infections are Opaganib datasheet known to cause exacerbations of allergic disease. AMPs, including HBDs, are key players in the first line defense against such infections. The present study demonstrates the presence of HBD1-3 in tonsils and that they originate from the epithelium as well as CD4+, CD8+ and CD19+ lymphocytes. Presence of AMPs in tonsillar tissue as well as their association with airway infections has previously been thoroughly described (Ball et al., 2007; Schwaab et al., 2009). Tieu et al. (2010) have investigated Florfenicol members of the S100 family in chronic rhinosinusitis, and reported diminished levels of epithelial psoriasin (S100A7) and calprotectin (S100A8/A9). In analogy, reduced mRNA levels of psoriasin have been observed in infected tonsils (Bryborn et al., 2008). Claeys et al. (2003) have demonstrated high levels of mRNA encoding HBD2 and HBD3 in tonsils with no significant difference between idiopathic hypertrophic tonsillar disease and recurrent tonsillitis. Another group found presence of HBD1-3 in tonsils and that the concentrations were similar during different states of tonsillar disease (Schwaab et al., 2010). The reduced HBD1-3 levels found in tonsils from AR patients are in line with previous studies reporting a reduction in AMP synthesis in allergic individuals.