Nerve Growth Factor Modulates Toll-like Receptor Expression In A Human Conjunctival Epithelial Cell Line

Micera, Alessandra; Lambìase, Alessandro; Stampachiacchiere, Barbara; Bonini, Sergio

doi:10.1016/j.jaci.2007.12.1092

Cited by 11 publications

(14 citation statements)

References 31 publications

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“…Thus, the increased expression levels of NGF appear to result in increased neuropeptide expression in patients with conjunctivitis (25). The phenomenon of increased NGF expression levels is not exclusive to conjunctivitis but also exists in other systemic allergic diseases (26). In the present study, it was revealed that carvedilol significantly increases the suppression of NGF protein expression levels in rat models B A of conjunctivitis.…”

Section: Discussionsupporting

confidence: 56%

Effects of carvedilol reduce conjunctivitis through changes in inflammation, NGF and VEGF levels in a rat model

Chen¹,

Hong²

2016

Experimental and Therapeutic Medicine

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Abstract. Carvedilol is a novel third generation β-blocker that acts as an antagonist of β and α adrenergic receptors, and is able to regulate various cell factors. In addition, it possesses antioxidant activity, is capable of reversing cardiac remodeling effects and has anti-arrhythmic effects. The present study aimed to investigate whether the effects of carvedilol were able to reduce conjunctivitis clinical scores. Initially, 24 Sprague Dawley (SD) rats were randomly divided into three equal groups as follows: Control group, model group and carvedilol group. The model and carvedilol group adult SD rats were injected with lipopolysaccharide (LPS) to induce conjunctivitis. In the carvedilol group, the eight SD rats with LPS-induced conjunctivitis also received 50 mg/kg/day of carvedilol for 4 weeks. Next, the effects carvedilol were assessed utilizing a system of clinical sign scores, and an enzyme-linked immunosorbent assay was used to determine the expression levels of interleukin-1β (IL-1β), IL-6, IL-8 and tumor necrosis factor-α (TNF-α). Finally, nuclear factor-κB (NF-κB), nerve growth factor (NGF) and vascular endothelial growth factor (VEGF) were analyzed by western blotting. Carvedilol was observed to significantly reduce clinical sign scores in a dose-dependent manner (P<0.01), and reduce IL-1β, IL-6, IL-8 and TNF-α expression levels (P<0.01) in the LPS-induced rat model of conjunctivitis. Carvedilol was also able to significantly reduce the protein expression levels of NF-κB, and induce the protein expression levels of NGF and VEGF in the LPS-induced rat model of conjunctivitis (P<0.01). In conclusion, the effects of carvedilol may reduce conjunctivitis clinical scores through inflammation, NGF and VEGF in LPS-induced rat models.

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Section: Discussionsupporting

confidence: 56%

Effects of carvedilol reduce conjunctivitis through changes in inflammation, NGF and VEGF levels in a rat model

Chen¹,

Hong²

2016

Experimental and Therapeutic Medicine

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“…It was indicated that some cytokines, including proinflammatory cytokines, can modulate the expression of TLR2 and/or TLR4 on macrophages [39], monocytes [40], endothelial cells [41], neutrophils [42], and epithelial cells [43]. Several reports described the effect of bacterial components on TLR expression, as well.…”

Section: Discussionmentioning

confidence: 99%

Surface TLR2 and TLR4 Expression on Mature Rat Mast Cells Can Be Affected by Some Bacterial Components and Proinflammatory Cytokines

Pietrzak

Wierzbicki

Wiktorska

et al. 2011

Mediators of Inflammation

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The aim of our study was to determine whether some bacterial components as well as some proinflammatory cytokines can affect surface mast cell levels. By the use of flow cytometry technique, we documented that freshly isolated mature rat peritoneal mast cells do express surface TLR2 and TLR4 protein, but not CD14 molecules, and respond to stimulation with TLR2 and TLR4 ligands by cysteinyl leukotriene generation. The level of TLR2 protein is modulated by PGN and CCL5 treatment, but not by LPS, LAM, TNF, or IL-6. Surface mast cell TLR4 expression is affected by LPS, LAM, IL-6, and CCL5. Considering that TLR-mediated activation conditions not only engaged these cells in antibacterial defense and development of inflammation but also might influence allergic processes, our observations that surface TLR2 and TLR4 expression can be regulated both bacterial components and proinflammatory cytokines seem to be very intriguing and importance.

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“…This is the first report, to our knowledge, demonstrating induced TLR4 upregulation in response to human liver fluke parasite in biliary cells. Upregulation of TLR4 has been reported in several conditions, such as in chronic hepatitis B virus infection [23], mechanical cyclic stretch in cultured cardiocytes [24] and certain growth factor stimulation [25]. Pinlaor et al [26] recently reported that O. viverrini somatic extracts can induce upregulation of TLR2 but not TLR4 in Raw 264.7 macrophage cells and triggered NF-κB signaling, stimulate inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression.…”

Section: Discussionmentioning

confidence: 99%

Opisthorchis viverrini excretory/secretory products induce toll-like receptor 4 upregulation and production of interleukin 6 and 8 in cholangiocyte

Ninlawan

O'Hara

Splinter

et al. 2010

Parasitology International

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Biliary tract infection with the Group I carcinogenic liver fluke Opisthorchis viverrini is associated with severe inflammation leading to cholangiocarcinoma – a major biliary cancer in Southeast Asia. However, mechanism(s) by which the liver fluke induces host mucosal immune/inflammatory responses are unclear. In the present study we address whether a normal immortalized human cholangiocyte cell line (H69 cells) recognizes and responds to O. viverrini excretory/secretory products (OVES). Expression of multiple TLRs, activation of NF-κB, and expression of proinflammatory cytokines were monitored in the presence and absence of OVES. Our results showed that OVES induced increased cholangiocyte TLR4 mRNA expression, induced IκB-α degradation in a MyD88-dependent manner, and activated NF-κB nuclear translocation. Moreover, OVES induced expression and secretion of the strong chemoattractant chemokine interleukin 8 (IL-8) and pro-inflammatory cytokine IL-6. These results demonstrate that secreted/excreted products of O. viverrini are recognized by human cholangiocytes and initiate innate mucosal immunity/inflammatory cascades, a primary event in the pathogenesis of opisthorchiasis and cholangiocarcinoma.

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Nerve Growth Factor Modulates Toll-like Receptor Expression In A Human Conjunctival Epithelial Cell Line

Cited by 11 publications

References 31 publications

Effects of carvedilol reduce conjunctivitis through changes in inflammation, NGF and VEGF levels in a rat model

Effects of carvedilol reduce conjunctivitis through changes in inflammation, NGF and VEGF levels in a rat model

Surface TLR2 and TLR4 Expression on Mature Rat Mast Cells Can Be Affected by Some Bacterial Components and Proinflammatory Cytokines

Opisthorchis viverrini excretory/secretory products induce toll-like receptor 4 upregulation and production of interleukin 6 and 8 in cholangiocyte

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