Syndecan-4 assists Mycobacterium tuberculosis entry into lung epithelial cells by regulating the Cdc42, N-WASP, and Arp2/3 signaling pathways

2022 ◽  
pp. 104931
Author(s):  
Da Wen ◽  
Jia Cui ◽  
Ping Li ◽  
Qiuhong Xiong ◽  
Guangxin Chen ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Epithelial Cells ◽  
Signaling Pathways ◽  
Lung Epithelial Cells ◽  
Lung Epithelial

Metformin promotes Mycobacterium tuberculosis killing and increases the production of human β-defensins in lung epithelial cells and macrophages

2020 ◽  
Vol 22 (3) ◽  
pp. 111-118 ◽  
Author(s):  
Adrian Rodriguez-Carlos ◽  
Claudia Valdez-Miramontes ◽  
Paulina Marin-Luevano ◽  
Irma González-Curiel ◽  
Jose A. Enciso-Moreno ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Lung Epithelial

scholarly journals MAPK signaling pathways regulate IL-8 mRNA stability and IL-8 protein expression in cystic fibrosis lung epithelial cell lines

2011 ◽  
Vol 300 (1) ◽  
pp. L81-L87 ◽  
Author(s):  
Sharmistha Bhattacharyya ◽  
Usha Gutti ◽  
Jose Mercado ◽  
Chad Moore ◽  
Harvey B. Pollard ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Cells ◽  
Protein Expression ◽  
Signaling Pathways ◽  
Mrna Stability ◽  
Mapk Signaling ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
The Stability ◽  
Mapk Signaling Pathways

Cystic fibrosis (CF) is characterized by a massive proinflammatory phenotype in the lung, caused by mutations in the CFTR gene. IL-8 and other proinflammatory mediators are elevated in the CF airway, and the immediate mechanism may depend on disease-specific stabilization of IL-8 mRNA in CF lung epithelial cells. MAPK signaling pathways impact directly on IL-8 protein expression in CF cells, and we have hypothesized that the mechanism may also involve stabilization of the IL-8 mRNA. To test this hypothesis, we have examined the effects of pharmacological and molecular inhibitors of p38, and downstream MK2, ERK1/2, and JNK, on stability of IL-8 mRNA in CF lung epithelial cells. We previously showed that tristetraprolin (TTP) was constitutively low in CF and that raising TTP destabilized the IL-8 mRNA. We therefore also tested these effects on CF lung epithelial cells stably expressing TTP. TTP binds to AU-rich elements in the 3′-UTR of the IL-8 mRNA. We find that inhibition of p38 and ERK1/2 reduces the stability of IL-8 mRNA in parental CF cells. However, neither intervention further lowers TTP-dependent destabilization of IL-8 mRNA. By contrast, inhibition of the JNK-2 pathway has no effect on IL-8 mRNA stability in parental CF cell, but rather increases the stability of the message in cells expressing high levels of TTP. However, we find that inhibition of ERK1/2 or p38 leads to suppression of the effect of JNK-2 inhibition on IL-8 mRNA stability. These data thus lend support to our hypothesis that constitutive MAPK signaling and proteasomal activity might also contribute, along with aberrantly lower TTP, to the proinflammatory phenotype in CF lung epithelial cells by increasing IL-8 mRNA stability and IL-8 protein expression.

scholarly journals Human Lung Epithelial Cells Contain Mycobacterium tuberculosis in a Late Endosomal Vacuole and Are Efficiently Recognized by CD8+ T Cells

PLoS ONE ◽  
2014 ◽  
Vol 9 (5) ◽  
pp. e97515 ◽  
Author(s):  
Melanie J. Harriff ◽  
Meghan E. Cansler ◽  
Katelynne Gardner Toren ◽  
Elizabeth T. Canfield ◽  
Stephen Kwak ◽  
...  
Keyword(s):  
T Cells ◽  
Mycobacterium Tuberculosis ◽  
Epithelial Cells ◽  
Cd8 T Cells ◽  
Human Lung ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Human Lung Epithelial Cells

scholarly journals Kurarinone Attenuates BLM-Induced Pulmonary Fibrosis via Inhibiting TGF-β Signaling Pathways

2021 ◽  
Vol 22 (16) ◽  
pp. 8388
Author(s):  
Soo-Jin Park ◽  
Tae-hyoun Kim ◽  
Kiram Lee ◽  
Min-Ah Kang ◽  
Hyun-Jae Jang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Pulmonary Fibrosis ◽  
Signaling Pathways ◽  
Epithelial Mesenchymal Transition ◽  
Lung Epithelial Cells ◽  
Drug Candidate ◽  
Therapeutic Effects ◽  
Mesenchymal Transition ◽  
Lung Epithelial ◽  
Novel Drug

Idiopathic pulmonary fibrosis (IPF) is a refractory interstitial lung disease for which there is no effective treatment. Although the pathogenesis of IPF is not fully understood, TGF-β and epithelial–mesenchymal transition (EMT) have been shown to be involved in the fibrotic changes of lung tissues. Kurarinone is a prenylated flavonoid isolated from Sophora Flavescens with antioxidant and anti-inflammatory properties. In this study, we investigated the effect of kurarinone on pulmonary fibrosis. Kurarinone suppressed the TGF-β-induced EMT of lung epithelial cells. To assess the therapeutic effects of kurarinone in bleomycin (BLM)-induced pulmonary fibrosis, mice were treated with kurarinone daily for 2 weeks starting 7 days after BLM instillation. Oral administration of kurarinone attenuated the fibrotic changes of lung tissues, including accumulation of collagen and improved mechanical pulmonary functions. Mechanistically, kurarinone suppressed phosphorylation of Smad2/3 and AKT induced by TGF-β1 in lung epithelial cells, as well as in lung tissues treated with BLM. Taken together, these results suggest that kurarinone has a therapeutic effect on pulmonary fibrosis via suppressing TGF-β signaling pathways and may be a novel drug candidate for pulmonary fibrosis.

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