Antibacterial activity of human defensins on anaerobic intestinal bacterial species: a major role of HBD-3

Nuding, Sabine; Zabel, Lutz; Enders, Corinne; Porter, Edith; Fellermann, Klaus; Wehkamp, Jan; Mueller, Holger A.G.; Stange, Eduard F.

doi:10.1016/j.micinf.2009.01.001

Cited by 52 publications

(46 citation statements)

References 35 publications

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“…This is probably due to the more difficult and time-consuming techniques that are required for culturing of such strains. Hence, few M a n u s c r i p t 9 AMPs have been investigated to date regarding their activity against anaerobic bacteria [14,15].…”

Section: Resultsmentioning

confidence: 99%

The antimicrobial peptide Ci-MAM-A24 is highly active against multidrug-resistant and anaerobic bacteria pathogenic for humans

Fedders

Podschun

Leippe

2010

International Journal of Antimicrobial Agents

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Section: Resultsmentioning

confidence: 99%

The antimicrobial peptide Ci-MAM-A24 is highly active against multidrug-resistant and anaerobic bacteria pathogenic for humans

Fedders

Podschun

Leippe

2010

International Journal of Antimicrobial Agents

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“…To reduce or prevent intestinal infection, the luminal flora and invading pathogens can induce production of epithelial-derived antimicrobial factors such as defensins, cathelicidin LL-37, and antimicrobial proteins. [6][7][8][9] Recently, we demonstrated that stimulation of intestinal epithelial cells with BFT enhanced the expression of the antibacterial peptide human b-defensin (hBD)-2. 10 However, it is possible that other antibacterial factors may be upregulated in the ETBF-infected area of the intestine and contribute to regulation of enteric inflammation.…”

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confidence: 99%

Bacteroides fragilis enterotoxin upregulates lipocalin-2 expression in intestinal epithelial cells

Yoo

Jung

et al. 2013

Laboratory Investigation

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Enterotoxigenic Bacteroides fragilis (ETBF) produces an B20 kDa B. fragilis enterotoxin (BFT), which plays an essential role in mucosal inflammation. Lipocalin (Lcn)-2, a siderophore-binding antimicrobial protein, is critical for control of bacterial infection; however, expression of Lcn-2 in BFT-exposed intestinal epithelial cells has not been elucidated. In the present study, stimulation of human intestinal epithelial cells with BFT resulted in the upregulation of Lcn-2 expression that was a relatively late response of intestinal epithelial cells compared with human b-defensin (hBD)-2 expression. The upregulation of Lcn-2 was dependent on AP-1 but not on NF-kB signaling. Lcn-2 induction via AP-1 was regulated by mitogenactivated protein kinases (MAPKs) including ERK and p38. Lcn-2 was secreted from the apical and basolateral surfaces in BFT-treated cells. These results suggest that a signaling pathway involving MAPKs and AP-1 is required for Lcn-2 induction in intestinal epithelial cells exposed to BFT, after which the secreted Lcn-2 may facilitate antimicrobial activity within ETBF-infected mucosa.

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“…To prevent intestinal infection, the luminal flora and pathogens are controlled by epithelially derived antimicrobial peptides that are constitutively expressed or inducible (29). For example, defensins, cathelicidin LL-37, lysozyme, phospholipase A, and proteins with bactericidal properties such as ubiquicidin, ribosomal proteins, and eosinophilic proteins have been reported (4,11,29,38).…”

mentioning

confidence: 99%

“…For example, defensins, cathelicidin LL-37, lysozyme, phospholipase A, and proteins with bactericidal properties such as ubiquicidin, ribosomal proteins, and eosinophilic proteins have been reported (4,11,29,38).…”

mentioning

confidence: 99%

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Bacteroides fragilisEnterotoxin Induces Human β-Defensin-2 Expression in Intestinal Epithelial Cells via a Mitogen-Activated Protein Kinase/IκB Kinase/NF-κB-Dependent Pathway

et al. 2010

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Enterotoxigenic Bacteroides fragilis (ETBF) produces an approximately 20-kDa heat-labile enterotoxin (BFT) that plays an essential role in mucosal inflammation. Although spontaneous disappearance of ETBF infection is common, little information is available on regulated expression of antibacterial factors in response to BFT stimulation. This study investigates the role of BFT in human β-defensin 2 (hBD-2) induction from intestinal epithelial cells. Stimulation of HT-29 and Caco-2 intestinal epithelial cell lines with BFT resulted in the induction of hBD-2. Activation of a reporter gene for hBD-2 was dependent on the presence of NF-κB binding sites. In contrast, suppression of AP-1 did not affect hBD-2 expression in BFT-stimulated cells. Inhibition of p38 mitogen-activated protein kinase (MAPK) using SB203580 and small interfering RNA (siRNA) transfection resulted in a significant reduction in BFT-induced IκB kinase (IKK)/NF-κB activation and hBD-2 expression. Our results suggest that a pathway including p38 MAPK, IKK, and NF-κB activation is required for hBD-2 induction in intestinal epithelial cells exposed to BFT, and may be involved in the host defense following infection with ETBF.

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Antibacterial activity of human defensins on anaerobic intestinal bacterial species: a major role of HBD-3

Cited by 52 publications

References 35 publications

The antimicrobial peptide Ci-MAM-A24 is highly active against multidrug-resistant and anaerobic bacteria pathogenic for humans

The antimicrobial peptide Ci-MAM-A24 is highly active against multidrug-resistant and anaerobic bacteria pathogenic for humans

Bacteroides fragilis enterotoxin upregulates lipocalin-2 expression in intestinal epithelial cells

Bacteroides fragilisEnterotoxin Induces Human β-Defensin-2 Expression in Intestinal Epithelial Cells via a Mitogen-Activated Protein Kinase/IκB Kinase/NF-κB-Dependent Pathway

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