Antimicrobial peptides are present in immune and host defense cells of the human respiratory and gastrointestinal tracts

Department of Anatomy, Chair II, Ludwig Maximilian University, 80336 München, Germany.
Cell and Tissue Research (Impact Factor: 3.57). 07/2006; 324(3):449-56. DOI: 10.1007/s00441-005-0127-7
Source: PubMed


Previous studies have implicated antimicrobial peptides in the host defense of the mammalian intestinal and respiratory tract. The aim of the present study has been to characterize further the expression of these molecules in non-epithelial cells of the human pulmonary and digestive systems by detailed immunohistochemical analysis of the small and large bowel and of the large airways and lung parenchyma. Additionally, cells obtained from bronchoalveolar lavage were analyzed by fluorescent activated cell sorting and immunostaining of cytospin preparations. hBD-1, hBD-2, and LL-37 were detected in lymphocytes and macrophages in the large airways, lung parenchyma, duodenum, and colon. Lymphocytes positive for the peptides revealed a staining pattern and distribution that largely matched that of CD3-positive and CD8-positive T-cells. Macrophages with positive staining for the antimicrobial peptides also stained positively for CD68 and CD74. In view of the morphology of the LL-37-positive and hBD-2-positive mucosal lymphocytes, they are probably also B-cells. Thus, antimicrobial peptides of the defensin and cathelicidin families are present in a variety of non-epithelial cells of mucosal organs. These findings confirm that antimicrobial peptides have multiple functions in the biology of the mucosa of these organs.

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Available from: Pia Unterberger, Sep 06, 2015
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    • "In addition to the direct antimicrobial function, they may act as ion channels and stimulators of angiogenesis . Other reports suggest a role in wound repair and in cell proliferation, (Heilborn et al., 2003) or that they function as mediators of inflammation and chemotaxis (Wah et al., 2006). "
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    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.
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    • "HBD-2 has been found in hyperplastic-stratified squamous epithelia in odontogenic keratocysts and radicular cysts (Yoshimoto et al, 2004). HBD-2 was also found in the cytoplasm of epithelial cells located through the upper spinous layer to the parakeratinized layer of the buccal epithelia from subjects with oral candidiasis (Sawaki et al, 2002), in T-lymphocytes cd3, cd8, and macrophages (Wah et al, 2006). The expression of HBD-2 was upregulated by TNF-a in patients with lichen planus (Abiko et al, 2002) and by IL-1b in keratinocytes (Liu et al, 2002). "
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    ABSTRACT: The expressions of human beta defensin-1 (HBD-1), -2 (HBD-2) and -3 (HBD-3) in non-inflamed pseudocysts such as mucoceles were investigated immunohistochemically in this study. Mucocele specimens were obtained from 21 patients. The expression of HBDs was studied immunohistochemically by using antibodies directed against HBD-1, -2, and -3. Statistical analyses were carried out on serial sections stained with antibodies. Cells expressing HBDs were found in mucoceles. The expression of HBD-2 was observed in floating cells in all the specimens, whereas HBD-1 and HBD-3-expressing cells were detected in 93% and 73% of the mucoceles, respectively. The HBD-2 signal was the most intense and the HBD-3 signal intensity was weaker than that of HBD-1. HBDs were expressed in neutrophils and in other floating cells. Interestingly, the signal intensity and the population of positive cells located close to the centers of cysts were higher than those located in the peripheral areas of cysts. The expression of HBDs was found even in non-inflamed pseudocysts such as mucoceles. These results suggest that an unknown mechanism not involved in biophylaxis for the expression of HBDs may exist.
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    • "Although in vitro stimulation with lipopolysaccharide did not have any effect on the S100A7 expression, a significant downregulation of S100A7 was detected in infected tonsils. This is in contrast to other studies concerning AMPs and tonsillar infection, where, in general, an increase of these proteins is described during infection (Song et al., 2006; Wah et al., 2006). Although S100A7 expression is induced in the skin in response to stimulation with bacterial products (Glaser et al., 2005), this does not seem to be the case in palatine tonsils, indicating that S100A7 may have tissuespecific functions. "
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