Human beta-defensin-2

Schröder, Jens‐M.; Harder, Jürgen

doi:10.1016/s1357-2725(99)00013-8

Cited by 421 publications

(291 citation statements)

References 14 publications

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“…Interestingly, hBD2 is known for its low bactericidal activity against Gram-positive bacteria (e.g. S. aureus) [33,34], therefore other AMPs and antimicrobial genes such as LL-37 are likely to be up-regulated in HCECs challenged with S. aureus or TLR2 ligands. Indeed, using RT-PCR and slot blot, we showed rapid induction of LL-37 expression and its abundant production in HUCL cells challenged with saLP.…”

Section: Discussionmentioning

confidence: 99%

Staphylococcus aureus lipoproteins trigger human corneal epithelial innate response through toll-like receptor-2

Kumar

Gui

et al. 2008

Microbial Pathogenesis

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Bacterial lipoproteins (LP) are a family of cell wall components found in a wide variety of bacteria. In this study, we characterized the response of HUCL, a telomerase-immortalized human corneal epithelial cell (HCEC) line, to LP isolated from Staphylococcus (S) aureus. S. aureus LP (saLP) prepared by Triton X-114 extraction stimulated the activation of NF-kB, JNK, and P38 signaling pathways in HUCL cells. The extracts failed to stimulate NF-kB activation in HUCL cells after lipoprotein lipase treatment and in cell lines expressing TLR4 or TLR9, but not TLR2, indicating lipoprotein nature of the extracts. saLP induced the up-regulation of a variety of inflammatory cytokines and chemokines (IL-6, IL-8, ICAM-1), antimicrobial molecules (hBD-2, LL-37, and iNOS), and homeostasis genes (Mn-SOD) at both the mRNA level and protein level. Similar inflammatory response to saLP was also observed in primarily cultured HCECs using the production of IL-6 as readout. Moreover, TLR2 neutralizing antibody blocked the saLP-induced secretion of IL-6, IL-8 and hBD2 in HUCL cells. Our findings suggest that saLP activates TLR2 and triggers innate immune response in the cornea to S. aureus infection via production of proinflammatory cytokines and defense molecules. r

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Section: Discussionmentioning

confidence: 99%

Staphylococcus aureus lipoproteins trigger human corneal epithelial innate response through toll-like receptor-2

Kumar

Gui

et al. 2008

Microbial Pathogenesis

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“…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 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]. 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].…”

Section: Defensinsmentioning

confidence: 99%

“…The bacteria or bacterial component, ie lipopolysaccharide and peptidoglycan, causes this induction. α-defensins are constitutively expressed, accumulating in granules [43,63,64,72]. Therefore, the α-defensins are not regulated at the transcriptional level but at the post-translational level when induction occurs to mobilize them within cells.…”

Section: Regulation Of Anti-microbial Peptide Expressionmentioning

confidence: 99%

See 2 more Smart Citations

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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Human Toll-like receptor 2 mediates induction of the antimicrobial peptide human beta-defensin 2 in response to bacterial lipoprotein

et al. 2001

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Human beta-defensin-2

Cited by 421 publications

References 14 publications

Staphylococcus aureus lipoproteins trigger human corneal epithelial innate response through toll-like receptor-2

Staphylococcus aureus lipoproteins trigger human corneal epithelial innate response through toll-like receptor-2

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

Human Toll-like receptor 2 mediates induction of the antimicrobial peptide human beta-defensin 2 in response to bacterial lipoprotein

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