Expression of Toll-like receptors in cultured nasal epithelial cells

Lin, Chih‐Feng; Tsai, Ching-Hwa; Cheng, Chiung-Hsiang; Chen, Yuh‐Shyan; Tournier, Frédéric; Yeh, Te‐Huei

doi:10.1080/00016480601089416

Cited by 27 publications

(30 citation statements)

References 27 publications

(32 reference statements)

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“…Nasal epithelial cells (hNECs) located at mucosal surface serve as the first barrier to microbial challenge and are permissive to drug or vaccine delivery [1], [2]. Epithelial cells are capable of producing various cytokines, chemokines, and growth factors by recognizing microbial-associated molecular patterns (MAMPs) from colonizing microbes or invading pathogens through pathogen recognition receptors, such as Toll-like receptors (TLRs).…”

Section: Introductionmentioning

confidence: 99%

“…We have established a system for culturing human primary nasal epithelial cells in vitro to subsequently harvest well-differentiated hNECs, as determined by cililary differentiation [11], which express both TLR2 and TLR4 [2]. We previously demonstrated that immunodominant glycoprotein 60 (IDG60) from oral commensal Streptococcus mutans is an immunodominat antigen that elucidates a relatively high secretory IgA, serum IgG, and memory CD4+ T cell proliferative responses in the general population [12], [13].…”

Section: Introductionmentioning

confidence: 99%

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Activated Human Nasal Epithelial Cells Modulate Specific Antibody Response against Bacterial or Viral Antigens

Yeh

Jung

et al. 2013

PLoS ONE

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Nasal mucosa is an immune responsive organ evidenced by eliciting both specific local secretory IgA and systemic IgG antibody responses with intra-nasal administration of antigens. Nevertheless, the role of nasal epithelial cells in modulating such responses is unclear. Human nasal epithelial cells (hNECs) obtained from sinus mucosa of patients with chronic rhinosinusitis were cultured in vitro and firstly were stimulated by Lactococcus lactis bacterium-like particles (BLPs) in order to examine their role on antibody production. Secondly, both antigens of immunodominant protein IDG60 from oral Streptococcus mutans and hemagglutinin (HA) from influenza virus were tested to evaluate the specific antibody response. Stimulated hNECs by BLPs exhibited a significant increase in the production of interleukin-6 (IL-6), and thymic stromal lymphopoietin (TSLP). Conditioned medium of stimulated hNECs has effects on enhancing the proliferation of CD4+ T cells together with interferon-γ and IL-5 production, increasing the costimulatory molecules on dendritic cells and augmenting the production of IDG60 specific IgA, HA specific IgG, IgA by human peripheral blood lymphocytes. Such production of antigen specific IgG and IgA is significantly counteracted in the presence of IL-6 and TSLP neutralizing antibodies. In conclusion, properly stimulated hNECs may impart immuno-modulatory effects on the antigen-specific antibody response at least through the production of IL-6 and TSLP.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Activated Human Nasal Epithelial Cells Modulate Specific Antibody Response against Bacterial or Viral Antigens

Yeh

Jung

et al. 2013

PLoS ONE

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“…In addition to innate immune cells [8,9] , a number of other cell types express TLR3, including nasal [10] , intestinal [11] and endometrial [12,13] epithelium. Signaling through TLR3 results in downstream activation of proinflammatory genes such as TNF-␣ and IL-12 [14] , which inhibit viral replication [15] and stimulate T cells [16] , respectively.…”

Section: Introductionmentioning

confidence: 99%

Choroidal Neovascular Membranes Express Toll-Like Receptor 3

Maloney

Antecka²,

Orellana³

et al. 2010

Ophthalmic Res

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Background: Recent evidence has suggested a role for toll-like receptor 3 (TLR3) in experimental models of age-related macular degeneration (AMD). To date, however, few data exist about TLR3 in human AMD. The purpose of this study was to investigate the expression of TLR3 in human choroidal neovascular (CNV) membranes. Methods: Immunostaining for TLR3 was performed on sections of CNV membranes from 8 AMD patients and eyes from 4 donors without CNV. Results: All CNV membranes expressed TLR3 in retinal pigment epithelial (RPE) cells. One was classified as having strong intensity, 5 as having moderate intensity and 2 as having weak intensity. All cases had ≧30% of the RPE cells staining for TLR3, ranging from 30 to 90%. No expression of TLR3 was observed in vascular endothelial cells or fibroblasts in any CNV membrane. In the donor eyes, the RPE cells near the ora serrata stained stronger than those at the posterior pole, where no staining was observed in 3 out of 4 cases. Conclusion: TLR3 was found in all CNV membranes and was expressed exclusively in RPE cells. The observed difference in RPE staining for TLR3 in donor eyes and CNV membranes suggests a possible role for this receptor in human neovascular AMD.

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“…Messenger RNA (mRNA) for all 10 TLRs have been identified in SNECs, and their function has been demonstrated by induced production of innate immune effectors such as human β-defensin 2, serum amyloid A, and surfactant proteins A and D [64]. The activity of SNEC TLRs is abnormally diminished in recalcitrant CRSwNP [65–67]. In addition, expression of the antimicrobial protein, lactoferrin, is decreased at the mRNA and protein level in the nasal mucosa of CRS patients [28•, 68].…”

Section: Inflammation Caused By Intrinsic Host Factorsmentioning

confidence: 99%

Chronic Rhinosinusitis as a Multifactorial Inflammatory Disorder

Lee

Lane

2011

Curr Infect Dis Rep

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Chronic rhinosinusitis (CRS) is a prevalent health condition characterized by sinonasal mucosal inflammation lasting at least 12 weeks. Heterogeneous in clinical presentation, histopathology, and therapeutic response, CRS represents a spectrum of disease entities with variable pathophysiology. Increased knowledge of cellular and molecular derangements in CRS suggests potential etiologies and targets for therapy. Microbial elements including fungi, staphylococcal enterotoxin, and biofilms have been implicated as inflammatory stimuli, along with airborne irritants and allergens. Defects in innate immunity have gained increased attention as contributors to the chronic inflammatory state. A combination of host susceptibility and environmental exposure is widely believed to underlie CRS, although direct evidence is lacking. Presently, without precise disease definitions and identifiable universal triggers, CRS pathogenesis is broadly described as multifactorial. Current research is beginning to unravel complex and diverse effects of chronic inflammation on sinonasal mucosal homeostasis, but dysfunctional pathways of inflammatory regulation and resolution require further elucidation.

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Expression of Toll-like receptors in cultured nasal epithelial cells

Cited by 27 publications

References 27 publications

Activated Human Nasal Epithelial Cells Modulate Specific Antibody Response against Bacterial or Viral Antigens

Activated Human Nasal Epithelial Cells Modulate Specific Antibody Response against Bacterial or Viral Antigens

Choroidal Neovascular Membranes Express Toll-Like Receptor 3

Chronic Rhinosinusitis as a Multifactorial Inflammatory Disorder

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