Production of β‐defensin‐2 by human colonic epithelial cells induced by <i>Salmonella enteritidis</i> flagella filament structural protein

Takahashi, Akira; Wada, Akihiro; Ogushi, Ken-ichi; Maeda, Kyoko; Kawahara, Tsukasa; Mawatari, Kazuaki; Kurazono, Hisao; Moss, Joel; Hirayama, Toshiya; Nakaya, Yutaka

doi:10.1016/s0014-5793(01)03088-5

Cited by 61 publications

(47 citation statements)

References 32 publications

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“…The increase in ␤-defensin-2 expression correlates with an increase in the related ␤-defensin-3 but does not correlate with expression of TNF-␣, suggesting that other factors are involved in its regulation (28). Our coauthors have demonstrated that Salmonella enteritidis flagellin increases ␤-defensin-2 promoter activation in IEC (26,29). Human ␤-defensin gene expression is increased in tracheobronchial epithelial cells in response to LPS (30) and in lung and skin epithelial cells in response to TLR2 stimulation (31)(32)(33)(34).…”

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confidence: 85%

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β-Defensin-2 Expression Is Regulated by TLR Signaling in Intestinal Epithelial Cells

Vora¹,

Youdim²,

Thomas³

et al. 2004

The Journal of Immunology

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The intestinal epithelium serves as a barrier to the intestinal flora. In response to pathogens, intestinal epithelial cells (IEC) secrete proinflammatory cytokines. To aid in defense against bacteria, IEC also secrete antimicrobial peptides, termed defensins. The aim of our studies was to understand the role of TLR signaling in regulation of β-defensin expression by IEC. The effect of LPS and peptidoglycan on β-defensin-2 expression was examined in IEC lines constitutively or transgenically expressing TLRs. Regulation of β-defensin-2 was assessed using promoter-reporter constructs of the human β-defensin-2 gene. LPS and peptidoglycan stimulated β-defensin-2 promoter activation in a TLR4- and TLR2-dependent manner, respectively. A mutation in the NF-κB or AP-1 site within the β-defensin-2 promoter abrogated this response. In addition, inhibition of Jun kinase prevents up-regulation of β-defensin-2 protein expression in response to LPS. IEC respond to pathogen-associated molecular patterns with expression of the antimicrobial peptide β-defensin-2. This mechanism may protect the intestinal epithelium from pathogen invasion and from potential invaders among the commensal flora.

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confidence: 85%

“…␤-Defensins are synthesized by various epithelial cells such as in the skin, respiratory tract, and gastrointestinal tract (24,25). Whereas expression of human ␤-defensin-1 may be constitutive, ␤-defensin-2 is induced by bacterial infection (26,27).…”

mentioning

confidence: 99%

β-Defensin-2 Expression Is Regulated by TLR Signaling in Intestinal Epithelial Cells

Vora¹,

Youdim²,

Thomas³

et al. 2004

The Journal of Immunology

Self Cite

320

225

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“…Because FliC is reported to activate the NF-kB pathway in epithelial cells Reed et al, 2002;Takahashi et al, 2001) and because the NF-kB pathway participates in the induction of SOCS-3 expression (Hayashi et al, 2002), we investigated the participation of the NF-kB signalling pathway in SPI-2-dependent expression of SOCS-3. As shown in Fig.…”

Section: Detection Of Flic In Salmonella-infected Macrophagesmentioning

confidence: 99%

Salmonella virulence factor SpiC is involved in expression of flagellin protein and mediates activation of the signal transduction pathways in macrophages

Uchiya

Nikai

2008

Microbiology

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“…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%

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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Production of β‐defensin‐2 by human colonic epithelial cells induced by Salmonella enteritidis flagella filament structural protein

Cited by 61 publications

References 32 publications

β-Defensin-2 Expression Is Regulated by TLR Signaling in Intestinal Epithelial Cells

β-Defensin-2 Expression Is Regulated by TLR Signaling in Intestinal Epithelial Cells

Salmonella virulence factor SpiC is involved in expression of flagellin protein and mediates activation of the signal transduction pathways in macrophages

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

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