The expression of the β-defensins hBD-2 and hBD-3 is differentially regulated by NF-κB and MAPK/AP-1 pathways in an in vitro model of Candida esophagitis

Steubesand, Nadine; Kiehne, Karlheinz; Brunke, Gabriele; Pahl, René; Reiß, Karina; Herzig, Karl‐Heinz; Schubert, Sabine; Schreiber, Stefan; Fölsch, Ulrich R.; Rosenstiel, Philip; Arlt, Alexander

doi:10.1186/1471-2172-10-36

Cited by 65 publications

(69 citation statements)

References 58 publications

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“…Analysis of the promoter region of hBD3 reveals the presence of AP-1 binding motifs but not NF-B binding sites (36). Most studies, including ours, support the involvement of MAPKs in hBD3 expression (7,48,67; also this study) and the lack of a role for NF-B (7,10,48,67; also this study). As with hBD2, different MAPKs mediate hBD3 expression depending on the stimulus and cell type.…”

Section: Discussionsupporting

confidence: 69%

Klebsiella pneumoniae Capsule Polysaccharide Impedes the Expression of β-Defensins by Airway Epithelial Cells

et al. 2010

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Section: Discussionsupporting

confidence: 69%

Klebsiella pneumoniae Capsule Polysaccharide Impedes the Expression of β-Defensins by Airway Epithelial Cells

et al. 2010

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“…3C). These findings are consistent with previous reports that hBD-2 induction is regulated by NF-B and not EGFR (32,33).…”

Section: Hbd-3 Induction By a Baumannii Is Egfr Dependentsupporting

confidence: 94%

Epithelial Innate Immune Response to Acinetobacter baumannii Challenge

et al. 2014

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dCurrently, Acinetobacter baumannii is recognized as one of the major pathogens seriously threatening our health care delivery system. Aspects of the innate immune response to A. baumannii infection are not yet well understood. Human ␤-defensins (hBDs) are epithelial cell-derived cationic antimicrobial peptides (AMPs) that also function to bridge the innate and adaptive immune system. We tested the induction of hBD-2 and -3 by A. baumannii on primary oral and skin epithelial cells and found that A. baumannii induces hBD-3 transcripts to a greater extent than it induces hBD-2 transcripts on both types of cells. In addition, we found that A. baumannii is susceptible to hBD-2 and -3 killing at submicromolar concentrations. Moreover, hBD-3 induction by A. baumannii was found to be dependent on epidermal growth factor receptor (EGFR) signaling. Inhibition of mitogen-activated protein kinase resulted in reduced expression of both hBD-2 and -3. Lastly, a disintegrin and metalloprotease 17 (ADAM17; also known as TACE) was found to be critical for hBD-3 induction, while ADAM10 and dual oxidase 1 (Duox1) were not required for hBD-3 induction. Induction of AMPs is an important component of innate sensing of pathogens and may play an important role in triggering systemic immune responses to A. baumannii infection. Further studies on the interactions between epithelial cells and A. baumannii will help us understand early stages of infection and may shed light on why some individuals are more vulnerable to A. baumannii infection.

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“…Absence of this cytokine strongly impairs neutrophil recruitment and effective phagocytosis of C. albicans (Netea et al, 1999). In an in vitro model of esophageal candidiasis, co-incubation of PMNs with C. albicans leads to a significant up-regulation of hBD-2 and hBD-3 in esophageal cells compared with effects of PMNs or C. albicans alone (Steubesand et al, 2009). Thus, increased PMN-dependent production of antimicrobial peptides by epithelial cells could contribute to the protective effect and further underlines the important role for PMNs in clearance of experimental oral candidiasis.…”

Section: Regulation Of Innate Immune Pathways By C Albicansmentioning

confidence: 89%

Epithelial Cells and Innate Antifungal Defense

2010

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The human pathogenic fungus Candida albicans is the predominant cause of both superficial and invasive forms of candidiasis. Clinical observations indicate that mucocutaneous Candida infections are commonly associated with defective cell-mediated immune responses. The importance of the innate immune system as a first-line defense against pathogenic challenge has long been recognized. Over the last decade, many key molecules mediating innate host defense have been identified. Central to these developments is the discovery of pattern recognition receptors such as Toll-like receptors and C-type lectin-receptors that induce innate immune responses and also modulate cellular and humoral adaptive immunity during Candida infections. Although a large amount of information is now available in systemic infections, little is known about localized infections. We address the most relevant pattern recognition receptors and their signaling mechanisms in oral epithelial cells, to gain a better understanding of their contributions to antifungal innate immunity.

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The expression of the β-defensins hBD-2 and hBD-3 is differentially regulated by NF-κB and MAPK/AP-1 pathways in an in vitro model of Candida esophagitis

Cited by 65 publications

References 58 publications

Klebsiella pneumoniae Capsule Polysaccharide Impedes the Expression of β-Defensins by Airway Epithelial Cells

Klebsiella pneumoniae Capsule Polysaccharide Impedes the Expression of β-Defensins by Airway Epithelial Cells

Epithelial Innate Immune Response to Acinetobacter baumannii Challenge

Epithelial Cells and Innate Antifungal Defense

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