scholarly journals Toll-like receptor-4, but not toll-like receptor-2 mediates secretion of tumour necrosis factor α and interleukin-8 in lipopolysaccharide-stimulated mouse mammary epithelial cells

2013 ◽  
Vol 57 (3) ◽  
pp. 393-397 ◽  
Author(s):  
Chang-Liang He ◽  
Qiong Yi ◽  
Yuan-Fang Li ◽  
Hang Yang ◽  
Lu Wang
Keyword(s):  
Epithelial Cells ◽  
Tumour Necrosis ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Tumour Necrosis Factor Α ◽  
Toll Like Receptor ◽  
Tnf Α ◽  
Toll Like Receptor 2 ◽  
Factor Α ◽  
Necrosis Factor

Abstract Mammary epithelial cells (MECs) from Kunming mice were isolated and stimulated in vitro with 10 μg/mL of Escherichia coli lipopolysaccharide (LPS). The release of tumour necrosis factor α (TNF-α) and interleukin-8 (IL-8) into culture supernatants was measured by ELISA. Furthermore, blocking experiments with Toll-like receptor 2 (TLR2) and TLR4 antibodies were performed to verify whether cytokine secretion depended on LPS-induced activation of TLR2 or TLR4. The results revealed that LPS-stimulated mouse MECs significantly secreted TNF-α and IL-8. Blocking of the TLR4 pathway inhibited the secretion of TNF-α and IL-8, while inhibition of LPS-induced TNF-α and IL-8 production was not observed when TLR2 was blocked. Thus, TLR4 can mediate the LPS-induced expression of cytokines such as TNF-α and IL-8 in mouse MECs.

scholarly journals Chinese herbal Jin-Ying-Tang attenuates the inflammatory response by inhibiting the activation of TLR4/MyD88/TRAF-6/NIK pathway at the mRNA level in LPS-stimulated mouse mammary epithelial cells

2016 ◽  
Vol 60 (1) ◽  
pp. 71-80
Author(s):  
Qiong Yi ◽  
Xin Li ◽  
Yuan-Fang Li ◽  
Hang Yang ◽  
Xiao-Yi Zhang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Response ◽  
Mrna Expression ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Mammary Epithelial Cells ◽  
Mrna Level ◽  
Mammary Epithelial ◽  
Tnf Α ◽  
Necrosis Factor

Abstract Introduction: The effects of Jin-Ying-Tang (JYT) on Toll-like Receptor 4 (TLR4) signalling transduction of lipopolysaccharide (LPS)-stimulated mouse mammary epithelial cells (MECs) in vitro were examined. Material and Methods: The cytotoxicity of JYT (0.06-62.50 mg/mL) on mouse MECs was determined by MTT assay. The MECs were co-cultured with LPS in the presence or absence of JYT (39.10 μg/mL, 391 μg/mL, 3910 μg/mL). The concentrations of interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) in the culture supernatants were detected by ELISA. The mRNA expression of TLR4 and downstream TLR4 signalling molecules such as myeloid differentiation factor 88 (MyD88), tumour necrosis factor receptor associated factor 6 (TRAF-6), inhibitor κB (IκB), and nuclear factor κB inducing kinase (NIK) were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Results: The results showed that the IC50 of JYT on MECs was 12.25 mg/mL and JYT could significantly decrease the concentrations of IL-6 and TNF-α in LPS-stimulated MECs (P < 0.05). The mRNA expression of TLR4, MyD88, TRAF-6, IκB, and NIK was also significantly decreased when the LPS-stimulated MECs were cocultured at appropriate concentrations of JYT (P < 0.05, P < 0.01). Conclusion: These observations indicate a potential mechanism through which JYT attenuates the systemic inflammatory response to LPS-stimulated mouse mammary epithelial cells by inhibiting the activation of TLR4/MyD88/ TRAF-6/NIK pathway at the mRNA level.

Interleukin-10 up-regulates tumour-necrosis-factor-α-related apoptosis-inducing ligand (TRAIL) gene expression in mammary epithelial cells at the involution stage

2001 ◽  
Vol 360 (1) ◽  
pp. 31-38 ◽  
Author(s):  
B. Hwa SOHN ◽  
Hyung-Bae MOON ◽  
Tae-Yoon KIM ◽  
Han-Sung KANG ◽  
Yoon Soo BAE ◽  
...  
Keyword(s):  
Tumour Necrosis ◽  
Mammary Epithelial Cells ◽  
Mammary Glands ◽  
Interleukin 10 ◽  
Mammary Epithelial ◽  
Tumour Necrosis Factor Α ◽  
Lactation Stage ◽  
Elevated Expression ◽  
Factor Α ◽  
Necrosis Factor

Although interleukin-10 (IL-10) is known to contribute to inflammation and pathogenesis in mammalian organs, little is known about its precise role in the mammary gland. We found that IL-10 levels fluctuated during the mouse mammary cycle, showing little expression at the lactation stage and the highest expression at the involution stage. To reveal the effects of IL-10 on involution, expression profiles of apoptosis-related genes were examined in mice transgenic for IL-10 as well as in IL-10−/− mice. Mild inflammatory lesions by lymphocytes were observed in the mammary glands from four of seven transgenic lines at the lactation stage. It was striking that the expression of tumour-necrosis-factor-α-related apoptosis-inducing ligand (TRAIL) among the apoptosis-related genes was elevated approx. 7-fold in the transgenic mice, whereas others were almost unchanged. Furthermore, TRAIL was down-regulated 4-fold in the IL-10−/− mice at the involution stage. Elevated expression of TRAIL and of death receptor 4 (DR4) protein was identified at the involution stage of normal mammary glands as well as at the lactation stage of the IL-10 transgenic mice. These results indicate that the elevated expression of IL-10 at the involution stage recruits lymphocytes and induces the expression of TRAIL and DR4. These phenomena might partly contribute to apoptosis in the mammary epithelial cells for entering involution.

Differential effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α, interleukin-6 and corticosterone induced by bacterial lipopolysaccharide in mice

1995 ◽  
Vol 144 (3) ◽  
pp. 457-462 ◽  
Author(s):  
G Haskó ◽  
I J Elenkov ◽  
V Kvetan ◽  
E S Vizi
Keyword(s):  
Tumour Necrosis Factor ◽  
Interleukin 6 ◽  
Plasma Levels ◽  
Tumour Necrosis ◽  
Endotoxin Shock ◽  
Bacterial Lipopolysaccharide ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Abstract The effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and corticosterone induced by bacterial lipopolysaccharide (LPS) was investigated in mice using ELISA and RIA. It was found that the LPS-induced TNF-α response was significantly blunted in mice pretreated with CH-38083, a novel and highly selective α2-adrenoreceptor antagonist (the α2/α1 ratio is >2000). In contrast, LPS-induced increases in both corticosterone and IL-6 plasma levels were further increased by CH-38083. Since it has recently been shown that the selective block of α2-adrenoreceptors located on noradrenergic axon terminals resulted in an increase in the release of noradrenaline (NA), both in the central and peripheral nervous systems, and, in our experiments, that propranolol prevented the effect of α2-adrenoreceptor blockade on TNF-α plasma levels induced by LPS, it seems likely that the excessive stimulation by NA of β-adrenoreceptors located on cytokine-secreting immune cells is responsible for this action. Since it is generally accepted that increased production of TNF-α is involved in the pathogenesis of inflammation and endotoxin shock on the one hand, and corticosterone and even IL-6 are known to possess anti-inflammatory properties on the other hand, it is suggested that the selective block of α2-adrenoreceptors might be beneficial in the treatment of inflammation and/or endotoxin shock. Journal of Endocrinology (1995) 144, 457–462

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