CD14-dependent Lipopolysaccharide-induced β-Defensin-2 Expression in Human Tracheobronchial Epithelium

Becker, Marie N.; Diamond, Gill; Verghese, Margrith W.; Randell, Scott H.

doi:10.1074/jbc.m000184200

Cited by 294 publications

(247 citation statements)

References 48 publications

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“…Perhaps most confusing are the data on gastrointestinal epithelial cells, where the ability of LPS to up-regulate proinflammatory cytokines appears to vary with the cell line tested (67)(68)(69)(70). In addition, airway epithelial cells have demonstrated sensitivity to LPS by NF-B activation, cytokine production, and up-regulation of various defense molecules (71)(72)(73)(74), and LPS has been shown to simulated cytokine expression by human gingival epithelial cells (75)(76)(77). None of these studies identified host cell surface moieties linked to epithelial-LPS interactions.…”

Section: Discussionmentioning

confidence: 99%

Response toNeisseria gonorrhoeaeby Cervicovaginal Epithelial Cells Occurs in the Absence of Toll-Like Receptor 4-Mediated Signaling

Fichorova

Cronin

Lien

et al. 2002

The Journal of Immunology

212

174

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Toll-like receptors (TLRs) have recently been identified as fundamental components of the innate immune response to bacterial pathogens. We investigated the role of TLR signaling in immune defense of the mucosal epithelial cells of the lower female genital tract. This site provides first line defense against microbial pathogens while remaining tolerant to a complex biosystem of resident microbiota. Epithelial cells derived from normal human vagina, ectocervix, and endocervix expressed mRNA for TLR1, -2, -3, -5, and -6. However, they failed to express TLR4 as well as MD2, two essential components of the receptor complex for LPS in phagocytes and endothelial cells. Consistent with this, endocervical epithelial cells were unresponsive to protein-free preparations of lipooligosaccharide from Neisseria gonorrhoeae and LPS from Escherichia coli. However, they were capable of responding to whole Gram-negative bacteria and bacterial lysates, as demonstrated by NF-κB activation and proinflammatory cytokine production. The presence of soluble CD14, a high-affinity receptor for LPS and other bacterial ligands, enhanced the sensitivity of genital tract epithelial cells to both low and high concentrations of bacteria, suggesting that soluble CD14 can act as a coreceptor for non-TLR4 ligands. These data demonstrate that the response to N. gonorrhoeae and other Gram-negative bacteria at the mucosal surface of the female genital tract occurs in the absence of endotoxin recognition and TLR4-mediated signaling.

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Section: Discussionmentioning

confidence: 99%

Response toNeisseria gonorrhoeaeby Cervicovaginal Epithelial Cells Occurs in the Absence of Toll-Like Receptor 4-Mediated Signaling

Fichorova

Cronin

Lien

et al. 2002

The Journal of Immunology

212

174

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“…64,65 In vitro studies showed upregulation of hBD-2 in primary airway epithelial cells in response to P. aeruginosa LPS and inflammatory cytokines such as IL-1b and TNF-a. [66][67][68] P. aeruginosa and TNF-a both induced expression of hBD-3 in lung cells in vitro 69 or cultured fetal lung explants. 70 Analysis of the putative promoter regions of hBD-2 and hBD-3 genes reveals consensus sequence sites for the regulators of transcription nuclear factor kB (NF-kB), CCAAT/ enhancer binding protein (c/EBP) and activating protein 1 (AP-1) 67,71 which are activated in airway epithelial cells by bacterial ligands.…”

Section: Airway Epithelial Cell Responses To Bacteriamentioning

confidence: 99%

Airway epithelial cell signaling in response to bacterial pathogens

Gómez

Prince

2007

Pediatric Pulmonology

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Summary. The airway epithelium represents a primary site for the introduction and deposition of potentially pathogenic microorganisms into the body, through inspired air. The epithelial mucosa is an important component of the innate immune system that recognizes conserved structures in microorganisms and initiates appropriate signaling to recruit and activate phagocytic cells to the airways. This review focuses on how airway epithelial cells sense and respond to the presence of bacterial pathogens. The major signaling cascades initiated by epithelial receptors that lead to phagocyte recruitment to the airways as well as the ability of the epithelium to regulate inflammation are discussed.

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“…No NF-B consensus sites were found within the 5-kb promoter of the hBD-5 gene. The hBD-6 gene contains the NF-B consensus sequence (GGGRNTYC) 5 and 1.3 kbp upstream of the start codon like the hBD-2 gene, which contains multiple NF-B binding sites (29,34).…”

Section: Identification Of Two Novel Hbd Genesmentioning

confidence: 99%

Identification of Multiple Novel Epididymis-Specific β-Defensin Isoforms in Humans and Mice

Yamaguchi

Nagase

Makita

et al. 2002

The Journal of Immunology

217

168

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Defensins comprise a family of cationic antimicrobial peptides that are characterized by the presence of six conserved cysteine residues. We identified two novel human β-defensin (hBD) isoforms by mining the public human genomic sequences. The predicted peptides conserve the six-cysteine motif identical with hBD-4, termed hBD-5 and hBD-6. We also evaluated the characteristics of the mouse homologs of hBD-5, hBD-6, and HE2β1, termed mouse β-defensin (mBD)-12, mBD-11, and mouse EP2e (mEP2e). The mBD-12 synthetic peptide showed salt-dependent antimicrobial activity. We demonstrate the epididymis-specific expression pattern of hBD-5, hBD-6, mBD-11, mBD-12, and mEP2e. In situ hybridization revealed mBD-11, mBD-12, and mEP2e expression in the columnar epithelium of the caput epididymis, contrasting with the predominant expression of mBD-3 in the capsule or septum of the whole epididymis. In addition, the regional specificity of mBD-11, mBD-12, and mEP2e was somewhat overlapping, but not identical, in the caput epididymis, suggesting that specific regulation may work for each member of the β-defensin family. Our findings indicated that multiple β-defensin isoforms specifically and cooperatively contribute to the innate immunity of the urogenital system.

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CD14-dependent Lipopolysaccharide-induced β-Defensin-2 Expression in Human Tracheobronchial Epithelium

Cited by 294 publications

References 48 publications

Response toNeisseria gonorrhoeaeby Cervicovaginal Epithelial Cells Occurs in the Absence of Toll-Like Receptor 4-Mediated Signaling

Response toNeisseria gonorrhoeaeby Cervicovaginal Epithelial Cells Occurs in the Absence of Toll-Like Receptor 4-Mediated Signaling

Airway epithelial cell signaling in response to bacterial pathogens

Identification of Multiple Novel Epididymis-Specific β-Defensin Isoforms in Humans and Mice

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