Escherichia coli–derived and Staphylococcus aureus–derived extracellular vesicles induce MUC5AC expression via extracellular signal related kinase 1/2 and p38 mitogen‐activated protein kinase in human airway epithelial cells

Bae, Chang Hoon; Choi, Yoon Seok; Song, Si-Youn; Kim, Yoon-Keun; Kim, Yong‐Dae

doi:10.1002/alr.21844

Cited by 10 publications

(11 citation statements)

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“…Consequently, our knowledge regarding Gram-positive EVs still remains limited (Brown et al, 2015 ). Since 2009, a few works reported the production and secretion of EVs by S. aureus , with particular emphasis on their protein content characterization and their impact on host cells (Lee et al, 2009 , 2013b ; Gurung et al, 2011 ; Hong et al, 2011 ; Kim et al, 2012 ; Thay et al, 2013 ; Choi et al, 2015 ; Jeon et al, 2016 ; Bae et al, 2017 ; He et al, 2017 ; Im et al, 2017 ; Jun et al, 2017 ; Askarian et al, 2018 ). In analogy with Gram-negative bacteria S. aureus EVs harbor, inter alia , numerous virulence factors, can have cytotoxic effects on host cells in vitro (Gurung et al, 2011 ; Jeon et al, 2016 ) and trigger a pro-inflammatory response both in vitro and in vivo (Hong et al, 2011 ; Kim et al, 2012 ).…”

Section: Introductionmentioning

confidence: 99%

Staphylococcus aureus Extracellular Vesicles Elicit an Immunostimulatory Response in vivo on the Murine Mammary Gland

Tartaglia

Breyne

Meyer

et al. 2018

Front. Cell. Infect. Microbiol.

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Staphylococcus aureus is a major pathogen responsible for bovine mastitis, the most common and costly disease affecting dairy cattle. S. aureus naturally releases extracellular vesicles (EVs) during its growth. EVs play an important role in the bacteria-bacteria and bacteria-host interactions and are notably considered as nanocarriers that deliver virulence factors to the host tissues. Whether EVs play a role in a mastitis context is still unknown. In this work, we showed that S. aureus Newbould 305 (N305), a bovine mastitis isolate, has the ability to generate EVs in vitro with a designated protein content. Purified S. aureus N305-secreted EVs were not cytotoxic when tested in vitro on MAC-T and PS, two bovine mammary epithelial cell lines. However, they induced the gene expression of inflammatory cytokines at levels similar to those induced by live S. aureus N305. The in vivo immune response to purified S. aureus N305-secreted EVs was tested in a mouse model for bovine mastitis and their immunogenic effect was compared to that of live S. aureus N305, heat-killed S. aureus N305 and to S. aureus lipoteichoic acid (LTA). Clinical and histopathological signs were evaluated and pro-inflammatory and chemotactic cytokine levels were measured in the mammary gland 24 h post-inoculation. Live S. aureus induced a significantly stronger inflammatory response than that of any other condition tested. Nevertheless, S. aureus N305-secreted EVs induced a dose-dependent neutrophil recruitment and the production of a selected set of pro-inflammatory mediators as well as chemokines. This immune response elicited by intramammary S. aureus N305-secreted EVs was comparable to that of heat-killed S. aureus N305 and, partly, by LTA. These results demonstrated that S. aureus N305-secreted EVs induce a mild inflammatory response distinct from the live pathogen after intramammary injection. Overall, our combined in vitro and in vivo data suggest that EVs are worth to be investigated to better understand the S. aureus pathogenesis and are relevant tools to develop strategies against bovine S. aureus mastitis.

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Section: Introductionmentioning

confidence: 99%

Staphylococcus aureus Extracellular Vesicles Elicit an Immunostimulatory Response in vivo on the Murine Mammary Gland

Tartaglia

Breyne

Meyer

et al. 2018

Front. Cell. Infect. Microbiol.

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“…1,13 Several inflammatory mediators induce MUC5AC expression in asthma, chronic obstructive pulmonary disease, and chronic bronchitis: inflammatory cytokines, hormones, chemicals, bacterial proteinases, and enzymes significantly induced MUC5AC expression in human airway epithelial cells. [14][15][16] For example, IL-1␤, a member of the IL-1 subfamily, is well known as a inflammatory mediator, which significantly induces MUC5AC expression in various cells, including NCI-H292 cells, hemoglobin subunit epsilon 1 transformed cells, and primary differentiated human nasal epithelial cells. 17 Several studies indicate that IL-36␥ is involved in the response of inflammation in the airway: lipopolysacchardie induces the production and release of IL-36r from monocytes in mouse lungs.…”

Section: Discussionmentioning

confidence: 99%

“…With regard to the signaling pathway of IL-36␥ and MUC5AC expression, two studies reported on activation of the IL-36 receptor and the phosphorylation of ERK1/2, p38, and NF-B: IL-36 activates the IL-36 receptor and induces mitogen-activated protein kinases and NF-kB in bronchial epithelial cells, 7,10 and several inflammatory mediators induce MUC5AC expression via ERK1/2, p38, and NF-B in human airway epithelial cells [14][15][16] ; therefore, this study focused on the IL-36 receptor, ERK1/2, p38, and NF-B in signaling pathway of IL-36␥-induced MUC5AC expression. The results of this study showed that IL-36␥ activated the phosphorylation of ERK1/2, p38, and NF-B.…”

Section: Figure 3 the Activation Of The Il-36 Receptor-mediated Erk1mentioning

confidence: 99%

Interleukin (IL) 36 gamma induces mucin 5AC, oligomeric mucus/gel-forming expressionviaIL-36 receptor–extracellular signal regulated kinase 1 and 2, and p38–nuclear factor kappa-light-chain-enhancer of activated B cells in human airway epithelial cells

Bae

Choi

et al. 2018

Am J Rhinol�Allergy

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“…The results were as described. 22 PCR products were quantified and normalized to glyceraldehyde-3phosphate dehydrogenase (GAPDH). Products were then detected using 2% agarose gel and visualized by staining with SYBR Safe DNA gel stain (Invitrogen, Carlsbad, CA) and transilluminated with an ultraviolet (UV) light source.…”

Section: Reverse-transcription Polymerase Chain Reaction Analysismentioning

confidence: 99%

“…The primer sequences and conditions used were according to published protocols. 22 Enzyme-linked immunosorbent assay…”

Section: Real-time Pcr Analysismentioning

confidence: 99%

Pepsin exposure in a non‐acidic environment upregulates mucin 5AC (MUC5AC) expression via matrix metalloproteinase 9 (MMP9)/nuclear factor κB (NF‐κB) in human airway epithelial cells

Choi

Bae

et al. 2020

Int Forum Allergy Rhinol

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Background Gastric reflux GR is a backflow of gastric content to the aerodigestive tract GR was previously found to be associated with inflammatory airway diseases and a potential cause of airway remodeling Chronic exposure to gastric content may induce damage from nose to lung because digestive enzymes and acidity are toxic to airway epithelial cells Recently the toxicity of pepsin in a non-acidic environment was found to increase proinflammatory cytokines and receptors in the epithelium of the aerodigestive tract However the effect of pepsin in non-acidic conditions on mucin expression has not been investigated in human airway epithelial cells The purpose of this study was to evaluate the effect of pepsin on mucin AC MUC AC expression in upper and lower airway epithelial cells as an important potential factor of non-acidic GR-related airway inflammation Methods In NCI-H cells and human nasal epithelial cells HNEpCs the effects and signaling pathways of pepsin on MUC AC expression were examined using reverse-transcription polymerase chain reaction RT-PCR real-time PCR enzyme immunoassay zymography Western blot and immunofluorescence staining ResultsPepsin increased MUC AC expression in non-acidic condition of NCI-H cells and HNEpCs Further pepsin activated matrix metalloproteinase MMP and phosphorylated nuclear factor κB NF-κB Moreover inhibitors of MMP and NF-κB significantly attenuated pepsin-induced MUC AC expression and the knockdown of NF-κB by small interfering RNA siRNA significantly blocked pepsin-induced MUC AC expression in human airway epithelial cells Conclusion These findings suggest that pepsin increased MUC AC expression in non-acidic conditions via the activation of MMP and NF-κB in human airway epithelial cells

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Escherichia coli–derived and Staphylococcus aureus–derived extracellular vesicles induce MUC5AC expression via extracellular signal related kinase 1/2 and p38 mitogen‐activated protein kinase in human airway epithelial cells

Abstract: The results of this study suggest that E. coli-derived and S. aureus-derived EVs induced MUC5AC expression via ERK1/2 and p38 MAPK signaling pathways in human airway epithelial cells.

Cited by 10 publications

References 20 publications

Staphylococcus aureus Extracellular Vesicles Elicit an Immunostimulatory Response in vivo on the Murine Mammary Gland

Staphylococcus aureus Extracellular Vesicles Elicit an Immunostimulatory Response in vivo on the Murine Mammary Gland

Interleukin (IL) 36 gamma induces mucin 5AC, oligomeric mucus/gel-forming expressionviaIL-36 receptor–extracellular signal regulated kinase 1 and 2, and p38–nuclear factor kappa-light-chain-enhancer of activated B cells in human airway epithelial cells

Pepsin exposure in a non‐acidic environment upregulates mucin 5AC (MUC5AC) expression via matrix metalloproteinase 9 (MMP9)/nuclear factor κB (NF‐κB) in human airway epithelial cells

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