Cryptococcus neoformans in Association with Dermatophagoides pteronyssinus has Pro- (IL-6/STAT3 Overproduction) and Anti-inflammatory (CCL2/ERK1/2 Downregulation) Effects on Human Bronchial Epithelial Cells

Inflammation ◽  
2022 ◽  
Author(s):  
Henrique Ismarsi Souza ◽  
Aline Beatriz Mahler Pereira ◽  
Jhony Robison Oliveira ◽  
Paulo Roberto Silva ◽  
David Nascimento Silva Teixeira ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cryptococcus Neoformans ◽  
Dermatophagoides Pteronyssinus ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Anti Inflammatory

scholarly journals Anti-inflammatory effects of antibacterials on human bronchial epithelial cells

2009 ◽  
Vol 10 (1) ◽  
Author(s):  
Gregor S Zimmermann ◽  
Claus Neurohr ◽  
Heidrun Villena-Hermoza ◽  
Rudolf Hatz ◽  
Juergen Behr
Keyword(s):  
Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Anti Inflammatory

scholarly journals Oral feeding with probiotic Lactobacillus rhamnosus attenuates cigarette smoke-induced COPD in C57Bl/6 mice: Relevance to inflammatory markers in human bronchial epithelial cells

2019 ◽  
Author(s):  
J.L. Carvalho ◽  
M. Miranda ◽  
A.K. Fialho ◽  
H. Castro-Faria-Neto ◽  
E. Anatriello ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Inflammatory Cytokines ◽  
Lactobacillus Rhamnosus ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Cytokines And Chemokines ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

AbstractCOPD is a prevalent lung disease with significant impacts on public health. Affected airways exhibit pulmonary neutrophilia and consequent secretion of pro-inflammatory cytokines and proteases, which result in lung emphysema. Probiotics act as nonspecific modulators of the innate immune system that improve several inflammatory responses. To investigate the effect of Lactobacillus rhamnosus (Lr) on cigarette smoke (CS)-induced COPD C57Bl/6 mice were treated with Lr during the week before COPD induction and three times/week until euthanasia. For in vitro assays, murine bronchial epithelial cells as well as human bronchial epithelial cells exposed to cigarette smoke extract during 24 hours were treated with Lr 1 hour before CSE addition. Lr treatment attenuated the inflammatory response both in the airways and lung parenchyma, reducing neutrophilic infiltration and the production of pro-inflammatory cytokines and chemokines. Also, Lr-treated mice presented with lower metalloproteases in lung tissue and lung remodeling. In parallel to the reduction in the expression of TLR2, TLR4, TLR9, STAT3, and NF-κB in lung tissue, Lr increased the levels of IL-10 as well as SOCS3 and TIMP1/2, indicating the induction of an anti-inflammatory environment. Similarly, murine bronchial epithelial cells as well as human bronchial epithelial cells (BEAS) exposed to CSE produced pro-inflammatory cytokines and chemokines, which were inhibited by Lr treatment in association with the production of anti-inflammatory molecules. Moreover, the presence of Lr also modulated the expression of COPD-associated transcription found into BALF of COPD mice group, i.e., Lr downregulated expression of NF-κB and STAT3, and inversely upregulated increased expression of SOCS3. Thus, our findings indicate that Lr modulates the balance between pro- and anti-inflammatory cytokines in human bronchial epithelial cells upon CS exposure and it can be a useful tool to improve the lung inflammatory response associated with COPD.

scholarly journals Molecular Mechanisms of Anti-Inflammatory Action of Erythromycin in Human Bronchial Epithelial Cells: Possible Role in the Signaling Pathway That Regulates Nuclear Factor-κB Activation

2004 ◽  
Vol 48 (5) ◽  
pp. 1581-1585 ◽  
Author(s):  
Masashi Desaki ◽  
Hitoshi Okazaki ◽  
Toshiaki Sunazuka ◽  
Satoshi Omura ◽  
Kazuhiko Yamamoto ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Nuclear Factor Κb ◽  
Bronchial Epithelial Cells ◽  
Nuclear Factor ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Anti Inflammatory ◽  
Inflammatory Action

ABSTRACT Long-term macrolide therapy has been proven to improve survival in patients with diffuse panbronchiolitis. Although its mechanisms remain unknown, previous studies have suggested the effects of macrolide might be anti-inflammatory rather than antibacterial. To elucidate the molecular mechanisms of its action, we studied here the effects of erythromycin (EM) and its new derivative, EM703, which shows no antibacterial action, on the activation of the transcription factor nuclear factor-κB (NF-κB) in human bronchial epithelial cells. Western blotting analysis showed that EM did not inhibit the degradation of IκBα, suggesting the molecular target for EM was not the dissociation of NF-κB from IκB. An electrophoretic mobility shift assay showed that EM did not interrupt the NF-κB DNA-binding activity in the nucleus under the conditions tested. Moreover, not only EM but also EM703 suppressed the activation of NF-κB and the production of interleukin-8, demonstrating that the anti-inflammatory action of the macrolide is independent of its antibacterial activity. Taken together, these data suggest EM has an anti-inflammatory action, presumably via an interaction with the NF-κB signaling pathway in the downstream of the dissociation from IκB, resulting in the inhibition of NF-κB.

scholarly journals HSP60 activity on human bronchial epithelial cells

2017 ◽  
Vol 30 (4) ◽  
pp. 333-340 ◽  
Author(s):  
Claudia Sangiorgi ◽  
Davide Vallese ◽  
Isabella Gnemmi ◽  
Fabio Bucchieri ◽  
Bruno Balbi ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Ex Vivo ◽  
Bronchial Epithelial Cells ◽  
Mitogen Activated Protein Kinase ◽  
Chronic Obstructive ◽  
Human Bronchial Epithelial Cells ◽  
In Vivo Models ◽  
Bronchial Epithelial ◽  
Anti Inflammatory

HSP60 has been implicated in chronic inflammatory disease pathogenesis, including chronic obstructive pulmonary disease (COPD), but the mechanisms by which this chaperonin would act are poorly understood. A number of studies suggest a role for extracellular HSP60, since it can be secreted from cells and bind Toll-like receptors; however, the effects of this stimulation have never been extensively studied. We investigated the effects (pro- or anti-inflammatory) of HSP60 in human bronchial epithelial cells (16-HBE) alone and in comparison with oxidative, inflammatory, or bacterial challenges. 16-HBE cells were cultured for 1–4 h in the absence or presence of HSP60, H2O2, lipopolysaccharide (LPS), or cytomix. The cell response was evaluated by measuring the expression of IL-8 and IL-10, respectively, pro- and anti-inflammatory cytokines involved in COPD pathogenesis, as well as of pertinent TLR-4 pathway mediators. Stimulation with HSP60 up-regulated IL-8 at mRNA and protein levels and down-regulated IL-10 mRNA and protein. Likewise, CREB1 mRNA was up-regulated. H2O2 and LPS up-regulated IL-8. Experiments with an inhibitor for p38 showed that this mitogen-activated protein kinase could be involved in the HSP60-mediated pro-inflammatory effects. HSP60 showed pro-inflammatory properties in bronchial epithelial cells mediated by activation of TLR-4-related molecules. The results should prompt further studies on more complex ex-vivo or in-vivo models with the aim to elucidate further the role of those molecules in the pathogenesis of COPD.

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