scholarly journals Honokiol Reduces Fungal Load, Toll-Like Receptor-2, and Inflammatory Cytokines in Aspergillus fumigatus Keratitis

2020 ◽  
Vol 61 (4) ◽  
pp. 48 ◽  
Author(s):  
Lu Zhan ◽  
Xudong Peng ◽  
Jing Lin ◽  
Yingxue Zhang ◽  
Han Gao ◽  
...  
Keyword(s):  
Aspergillus Fumigatus ◽  
Inflammatory Cytokines ◽  
Toll Like Receptor ◽  
Fungal Load ◽  
Toll Like Receptor 2

scholarly journals β-arrestin-2 up-regulates toll-like receptor 2 signaling and inhibits apoptosis in human endometrial cancer heterotransplants in nude mice

BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Fanling Hong ◽  
Yujun Zhang ◽  
Wenjin Cheng ◽  
Xiuli Sun ◽  
Jianliu Wang
Keyword(s):  
Inflammatory Cytokines ◽  
Nude Mice ◽  
Caspase 3 ◽  
Glycogen Synthase ◽  
Inflammatory Factors ◽  
Toll Like Receptor ◽  
Caspase 9 ◽  
Serine Threonine Kinase ◽  
Tnf Α ◽  
Toll Like Receptor 2

Abstract Background β-arrestin-2(Arr2) functions as an anti-apoptotic factor and affects cell proliferation, but its downstream molecular pathway in endometrial carcinoma (EC) is still unclear. This study aimed to investigate the effects of the stable overexpression of Arr2 on the proliferation and apoptosis of human EC heterotransplants and the expression of associated molecules, including Toll-like receptor 2(TLR2), serine-threonine kinase Akt (Akt), glycogen synthase kinase-3β(GSK3β) and some typical inflammatory cytokines such as NF-κB p56, TNF-α and IL-6 & IL-8. Methods Human EC cell line Ishikawa, stably transfected with Arr2 full-length plasmid, was injected subcutaneously into nude mice. They were treated with 0, 10, 20 mg/kg paclitaxel and the volume and weight of the tumor tissue were measured and calculated. The necrotic index were assessed by H&E staining and microscopic observation. The levels of caspase-3, caspase-9, TLR2, NF-κB p56, Akt, GSK3β were measured by western blot, and the levels of TNF-α, IL-6, IL-8 were measured by real-time PCR. Results We found that Arr2 overexpression promoted the growth of human EC heterotransplants. Arr2 attenuated the promotion of caspase-3 and caspase-9 by paclitaxel and mediated the increase of TLR2 and several inflammatory cytokines. The levels of Akt and GSK3β were not affected. Conclusion Arr2 overexpression was associated with the increase of TLR2 and several inflammatory factors, meanwhile inhibited paclitaxel-induced anti-tumor effect on human EC heterotransplants.

Phagocytosis of Aspergillus fumigatus conidia by murine macrophages involves recognition by the dectin-1 beta-glucan receptor and Toll-like receptor 2

2007 ◽  
Vol 9 (2) ◽  
pp. 368-381 ◽  
Author(s):  
Kathrin Luther ◽  
Antonella Torosantucci ◽  
Axel A. Brakhage ◽  
Jürgen Heesemann ◽  
Frank Ebel
Keyword(s):  
Aspergillus Fumigatus ◽  
Toll Like Receptor ◽  
Beta Glucan ◽  
Murine Macrophages ◽  
Toll Like Receptor 2

scholarly journals Enteropathogenic infections modulate intestinal serotonin transporter (SERT) function by activating Toll-like receptor 2 (TLR-2) in Crohn’s disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ahmad Qasem ◽  
Abed Elrahman Naser ◽  
Saleh A. Naser
Keyword(s):  
Oxidative Stress ◽  
Crohn’S Disease ◽  
P38 Mapk ◽  
Serotonin Transporter ◽  
Inflammatory Cytokines ◽  
Tissue Damage ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
Sert Activity ◽  
Pro Inflammatory Cytokines

AbstractSerotonin (5-hydroxytryptamine [5-HT]) is an intestinal neuromodulator that regulates several essential enteric physiological functions such as absorption or secretion of fluids, and peristaltic reflexes. Availability of the intestinal 5-HT is dependent on serotonin transporter (SERT), which uptakes 5-HT and facilitates its degradation. Interestingly, Toll-like receptor 2 (TLR-2) is co-localized with 5-HT, which suggests a possible impact of neuroendocrine cells in the inflammatory response through TLR-2 activation. Serum 5-HT levels were measured in 80 Crohn’s disease (CD) patients and 40 healthy control subjects. Additionally, fully differentiated Caco-2 monolayers were infected with Mycobacteria paratuberculosis (MAP), L. monocytogenes, or M. smegmatis in the presence of exogenous 5-HT at different concentrations. Cells were subsequently harvested and used for measuring SERT activity, RNA isolation followed by RT-PCR, protein quantification, and tissue damage markers (DHE, LDH, GSH and MDA). TLR-2 intracellular signaling pathways were assessed by pre-incubating Caco-2 monolayers with selective blockers of ERK, cAMP/PKA, p38 MAPK, and 5-HT3 receptors. MAP-infected CD patients (N = 40) had higher serum 5-HT levels (462.95 ± 8.55 ng/mL, N = 40) than those without MAP infection (385.33 ± 10.3 ng/mL, N = 40). TLR-2 activation by enteropathogenic bacteria inhibited SERT activity in the presence of exogenous 5-HT by up to 50%. These effects were increasing gradually over 72 h, and MAP infection had the greatest effect on SERT inhibition when cells were exposed to 5-HT in a concentration dependent manner. Additionally, inhibition of SERT activity was accompanied with higher levels of pro-inflammatory cytokines (TNF-α, IL-6, IL-8) and oxidative stress markers (DHE, LDH and MDA), whereas SERT expression and protein level were downregulated. Consequently, inhibition of TLR-2 and p38 MAPK signaling or blocking 5-HT3 receptors restored SERT activity and reduced the production of pro-inflammatory cytokines, as reflected by the downregulation of oxidative stress and tissue damage markers. The involvement of TLR-2 in the intestinal pathology might be concluded not only from its innate immune role, but also from its effect on modulating the intestinal serotonergic response. Ultimately, regulating the intestinal serotonergic system can be therapeutically exploited to mitigate other enteropathogenic infections, which will help in understanding the gut-microbiome-brain connection.

scholarly journals Stimulation of Toll-like Receptor 2 byCoxiella burnetiiIs Required for Macrophage Production of Pro-inflammatory Cytokines and Resistance to Infection

2004 ◽  
Vol 279 (52) ◽  
pp. 54405-54415 ◽  
Author(s):  
Dario S. Zamboni ◽  
Marco A. Campos ◽  
Ana C. T. Torrecilhas ◽  
Kati Kiss ◽  
James E. Samuel ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
Resistance To Infection ◽  
Stimulation Of ◽  
Pro Inflammatory Cytokines
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