Reduced tonsillar expression of human β-defensin 1, 2 and 3 in allergic rhinitis

Abstract

Airway infections are known to cause exacerbations of allergy and asthma. Tonsils constitute a primary site for microbial recognition and triggering of the immune system in the airways. Human β-defensins (HBDs) are antimicrobial peptides with an important role in this defense. Our aim was to investigate HBD1-3 in tonsillar tissue and their potential role in allergic rhinitis (AR). Tonsils, obtained from patients with AR and non-allergic controls, and isolated tonsillar CD4(+), CD8(+) and CD19(+) lymphocytes were analyzed for HBD1-3 expression using real-time RT-PCR and/or immunohistochemistry. Tonsillar tissue, mixed tonsillar lymphocytes and airway epithelial cells (AECs) were cultured with or without IL-4, IL-5, IL-13 or histamine followed by measurements of HBD1-3 release using ELISA. HBD1-3 were present in tonsillar tissue, including epithelial, CD4(+), CD8(+) and CD19(+) cells. The expression was reduced in allergic compared to healthy tonsils. Stimulation of AECs with IL-4, IL-5 and histamine down-regulated the HBD release, whereas no effects were seen in cultured tonsils or lymphocytes. This study demonstrates presence of HBD1-3 in tonsils and that the levels are reduced in patients with AR. Together with the down-regulation of HBDs in epithelial cells in the presence of allergic mediators suggest that AR patients have an impaired antimicrobial defense that might make them more susceptible to respiratory tract infections.

Increased beta 2 defensin in recurrent aphthous ulcer

“…Indeed, it was in the present work found that RAU lesions, both in their ulcer margins and in the inflamed marginal halo surrounding the ulcer, contained highly increased amounts of microbicidal hBD‐2. This was found in resident epithelial cells and macrophages but also in immigrant inflammatory mononuclear cells, which could be newly recruited monocytes and lymphocytes (Häyrinen‐Immonen et al , ; Romano Carratelli et al , ; Bogefors et al , ). These findings confirm our working hypothesis.…”

Evaluation of nasal fluid β-defensin 2 levels in children with allergic rhinitis

“…Thus, the investigators could not clearly determine if the cause of the reduction in BD-2 levels was the caused by the disease itself or the nasal steroids used by the patients. When our findings and the other studies in the literature are evaluated together, we concluded that the reduction in BD-2 levels in the nasal fluid in patients with AR was mainly caused by the disease itself, not steroid treatment (8,18). On the other hand, only 16 patients with AR and 16 controls were included in the present study.…”

“…In previous studies, lysozyme and cathelicidin levels were shown as low in patients with AR (16,17). In the study conducted by Bogefors et al (8), it was found that BD-1 and BD-3 expression in tonsillary tissues was lower in patients with AR compared with healthy controls. In another study, it was shown that BD-1 and BD-3 expressions significantly increased compared with the pre-treatment period in nasal biopsy samples of patients with AR after allergen-specific immunotherapy was completed (9).…”

“…In addition, they have been shown to have a regulatory function in many physiologic processes including antitumoral immunity, cytokine release, chemotaxis, histamine production, inflammation, and wound healing (7). Although there are a few studies conducted with adults in the literature, no studies have investigated the roles of defensins in the pathogenesis of AR in childhood (8,9). In this study, we aimed to investigate the levels of β-defensin 2 (BD-2), which is AMP synthesized in the respiratory tract of pediatric patients with AR.…”

Cigarette Smoke Modulates NOD1 Signal Pathway and Human ß Defensins Expression in Human Oral Mucosa

“…The qPCR primers used for measuring mRNA levels of hBDs crossed exons. Primer sequences were as follow: hBD-1 forward TCA TTA CAA TTG CGT CAG CAG, reverse TTG CAG CAC TTG GCC TTC [13]; hBD-2 forward TCC TCT TCT CGT TCC TCT TCA, reverse AGG GCA AAA GAC TGG ATG AC [13]; hBD-3 forward CCA TTA TCT TCT GTT TGC TTT GCT C, reverse CCG CCT CTG ACT CTG CAA TAA TA [24]; GAPDH forward GCA CCG TCA AGG CTG AGA AC, reverse TGG TGA AGA CGC CAG TGG A [25].…”