Human beta-defensin-1: an antimicrobial peptide of urogenital tissues.

Valore, Erika V.; Park, C H; Quayle, Alison J.; Wiles, Kerry; McCray, Paul B.; Ganz, Tomas

doi:10.1172/jci1861

Cited by 668 publications

(609 citation statements)

References 44 publications

(44 reference statements)

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“…7 DEFB1 is constitutively expressed mainly in kidney, keratinocytes, oral cavity, as well as in urogenital tract. 8,9 The in vitro expression of DEFB1 can be upregulated by LPS, IL-1b, interferon-g (IFN-g) and arginine. [10][11][12] In vivo, elevated levels of DEFB1 in body fluid were observed in individuals suffering from sepsis and infectious diseases.…”

Section: Introductionmentioning

confidence: 99%

Genomic variations within DEFB1 are associated with the susceptibility to and the fatal outcome of severe sepsis in Chinese Han population

Huang

et al. 2007

Genes Immun

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Sepsis is a systemic inflammatory response syndrome to infection. Human b-defensin 1 (DEFB1) is a multifunctional mediator in infection and inflammation, which has been largely explored in ex vivo studies. The present case-control study was designed to investigate whether DEFB1 genomic variations are associated with the susceptibility to and the outcome of severe sepsis in 211 patients with severe sepsis and 157 ethnic-matched healthy controls. After correcting for multiple testing, the À44G/C was the only polymorphism found to show significant associations with both the susceptibility to and the fatal outcome of severe sepsis (P ¼ 0.0049, odd ratio (OR) 1.971 and P ¼ 0.002, OR 2.406, respectively). Haplotype À20A/À44C/À52G showed a protective role against severe sepsis (P ¼ 0.0066, OR 0.6751), whereas haplotype À20G/À44G/À52G served as a risk factor for the fatal outcome of severe sepsis (P ¼ 0.0052, OR 2.427). These findings provide further evidence that b-defensin 1 may play a role in the pathogenesis of severe sepsis.

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Section: Introductionmentioning

confidence: 99%

Genomic variations within DEFB1 are associated with the susceptibility to and the fatal outcome of severe sepsis in Chinese Han population

Huang

et al. 2007

Genes Immun

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“…We used the killing rate because the antibacterial effect was observed at low concentrations of the peptides (1-10 µg/ml). Because the concentrations expressed in vivo are from 1 to 100 µg/ml [61,71,77,125], the killing rate in vitro is relatively similar to the amount that is expressed in vivo. The antibacterial assay showed that all synthetic peptides of hBD1-3 and LL37 have dose-dependent antibacterial activity against S. aureus, although the effect was different among peptides.…”

Section: Anti-s Aureus Activity Of Anti-microbial Peptidesmentioning

confidence: 99%

“…β-defensin Four β-defensins (hBD1-4) have been identified and found to be expressed in various epithelial tissues: the trachea, skin, and intestine; and in monocytes and dendritic cells [8,[60][61][62][63][64][65][66][67][68][69]. Like α-defensins, hBDs have three disulphide moieties of cysteine linking residues 1-5, 2-4, and 3-6. hBD1 was first identified in haemodialysate fluid [70] and then from urogenital tissues, skin, intestine, and other tissues [61][62][63][64][65][66][67][68][69]71].…”

Section: Defensinsmentioning

confidence: 99%

“…Like α-defensins, hBDs have three disulphide moieties of cysteine linking residues 1-5, 2-4, and 3-6. hBD1 was first identified in haemodialysate fluid [70] and then from urogenital tissues, skin, intestine, and other tissues [61][62][63][64][65][66][67][68][69]71]. In vitro experiments show that hBD1 is constitutively expressed and that its production is not influenced by bacterial exposure, while other hBDs are inducible when exposed to bacteria [67,[72][73][74][75].…”

Section: Defensinsmentioning

confidence: 99%

“…In particular, hBD2, first identified from skin [8], is highly responsive to bacteria, pro-inflammatory stimuli (IL−1β, TNFα, LPS), and phorbol myristate acetate [63,72,74,[76][77][78][79]. Previous reports show that hBD1 and hBD2 have strong antibacterial activity against Gram-negative bacteria and weak (or no) activity against Gram-positive bacteria, while hBD3 and hBD4 have strong activity against both Gram-positive and Gram-negative bacteria [8,41,50,61,66,[80][81][82][83]. hBD1 is primarily found in differentiated keratinocytes, suggesting that the regulation of hBD1 is linked to cell differentiation [84,85].…”

Section: Defensinsmentioning

confidence: 99%

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Innate defences against methicillin‐resistant Staphylococcus aureus (MRSA) infection

Komatsuzawa

Ouhara

Yamada

et al. 2005

The Journal of Pathology

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The innate immune system is the primary defence against bacterial infection. Among the factors involved in innate defence, anti-microbial peptides produced by humans have recently attracted attention due to their relevance to some diseases and also to the development of new chemotherapeutic agents. Staphylococcus aureus is one of the major human pathogens, causing a variety of infections from suppurative disease to food poisoning. Methicillin-resistant S. aureus (MRSA) is a clinical problem and with the recent emergence of a vancomycin-resistant strain, this will pose serious problems in the near future. In investigating the molecular biology of S. aureus infections to develop new chemotherapeutic agents against MRSA infections, knowledge of the interaction of innate anti-microbial peptides with S. aureus is important. In vitro and in vivo experiments demonstrate that exposure of S. aureus to host cells can induce the anti-microbial peptides β-defensin-2 (hBD2), hBD3, and LL37/CAP18. The induction level of these peptides differs among strains, as does the susceptibility of the strains, with MRSA strains exhibiting lower susceptibility. In summary, the susceptibility of S. aureus strains, including MRSA strains, to components of the innate immune system varies, with the MRSA strains showing more resistance to both innate immune factors and chemotherapeutic agents.

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