Activation of the TLR2-mediated downstream signaling pathways NF-κB and MAPK is responsible for B7-H3-augmented inflammatory response during S. pneumoniae infection

Chen, Xuqin; Meng, Xiangying; Foley, Niamh; Shi, Xiaoyan; Liu, Min; Chai, Yahui; Li, Yiping; Redmond, H. P.; Wang, Jian; Wang, Jiang Huai

doi:10.1016/j.jneuroim.2017.07.002

Cited by 16 publications

(13 citation statements)

References 34 publications

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“…MAPK, a family of serine/threonine protein kinases that includes p38, ERK and JNK, is involved in the regulation of a wide variety of fundamental cellular responses, physiologic functions and pathological processes [ 21 ]. It is widely accepted that the MAPK signaling cascade is activated by bacterial stimuli through TLR2, resulting in the over-expression and production of various pro-inflammatory mediators [ 22 ]. For example, MAPK plays a central role in Streptococcus pneumoniae- or C. acnes -stimulated inflammatory responses in murine microglia and human neonatal epidermal keratinocytes [ 20 , 22 ].…”

Section: Resultsmentioning

confidence: 99%

“…It is widely accepted that the MAPK signaling cascade is activated by bacterial stimuli through TLR2, resulting in the over-expression and production of various pro-inflammatory mediators [ 22 ]. For example, MAPK plays a central role in Streptococcus pneumoniae- or C. acnes -stimulated inflammatory responses in murine microglia and human neonatal epidermal keratinocytes [ 20 , 22 ]. The results of the present study demonstrate that incubation of C. acnes -stimulated THP-1 cells with the ESF significantly attenuates MAPK activation, resulting in the suppression of IL-8 production ( Figure 4 ).…”

Section: Resultsmentioning

confidence: 99%

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In Vitro and In Vivo Screening of Wild Bitter Melon Leaf for Anti-Inflammatory Activity against Cutibacterium acnes

et al. 2020

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Cutibacterium acnes (formerly Propionibacterium acnes) is a key pathogen involved in the development and progression of acne inflammation. The numerous bioactive properties of wild bitter melon (WBM) leaf extract and their medicinal applications have been recognized for many years. In this study, we examined the suppressive effect of a methanolic extract (ME) of WBM leaf and fractionated components thereof on live C. acnes-induced in vitro and in vivo inflammation. Following methanol extraction of WBM leaves, we confirmed anti-inflammatory properties of ME in C. acnes-treated human THP-1 monocyte and mouse ear edema models. Using a bioassay-monitored isolation approach and a combination of liquid–liquid extraction and column chromatography, the ME was then separated into n-hexane, ethyl acetate, n-butanol and water-soluble fractions. The hexane fraction exerted the most potent anti-inflammatory effect, suppressing C. acnes-induced interleukin-8 (IL-8) production by 36%. The ethanol-soluble fraction (ESF), which was separated from the n-hexane fraction, significantly inhibited C. acnes-induced activation of mitogen-activated protein kinase (MAPK)-mediated cellular IL-8 production. Similarly, the ESF protected against C. acnes-stimulated mouse ear swelling, as measured by ear thickness (20%) and biopsy weight (23%). Twenty-four compounds in the ESF were identified using gas chromatograph–mass spectrum (GC/MS) analysis. Using co-cultures of C. acnes and THP-1 cells, β-ionone, a compound of the ESF, reduced the production of IL-1β and IL-8 up to 40% and 18%, respectively. β-ionone also reduced epidermal microabscess, neutrophilic infiltration and IL-1β expression in mouse ear. We also found evidence of the presence of anti-inflammatory substances in an unfractionated phenolic extract of WBM leaf, and demonstrated that the ESF is a potential anti-inflammatory agent for modulating in vitro and in vivo C. acnes-induced inflammatory responses.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

In Vitro and In Vivo Screening of Wild Bitter Melon Leaf for Anti-Inflammatory Activity against Cutibacterium acnes

et al. 2020

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“…During the early stage (0–3 days) of adipogenic differentiation, the expression of multiple proinflammatory cytokines (e.g., IL‐1β, IL‐6, IL‐8, and CCL2) dramatically decreases, which might contribute to suppression of NF‐κB and ERK1/2 pathways, as both can positively regulate proinflammatory cytokines (Al‐Harbi et al, ; Chen et al, ). Dexamethasone in adipogenic medium is a strong inhibitor of NF‐κB (Laberge et al, ; Al‐Harbi et al, ).…”

Section: Discussionmentioning

confidence: 99%

IL‐1α inhibits proliferation and adipogenic differentiation of human adipose‐derived mesenchymal stem cells through NF‐κB‐ and ERK1/2‐mediated proinflammatory cytokines

Sun

Zou

Zuo

et al. 2018

Cell Biology International

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Dysfunctional adipogenesis such as subcutaneous lipoatrophy is closely related to insulin resistance and metabolic disorders. Although the expression or release of the cytokine interleukin-1α (IL-1α) is known to increase in adipose tissue in response to cell death, cell senescence, aging, or solar radiation, the regulatory role of IL-1α in adipogenesis has not been sufficiently investigated. To investigate the problem, we explored the effect of IL-1α on the proliferation and adipogenic differentiation of human adipose-derived mesenchymal stem cells (ADSCs) using cell counting, alamarBlue assay, oil red O staining, Western blot, among others. The results showed that IL-1α evidently inhibited the proliferation and adipogenic differentiation of ADSCs, which might be related with the activated nuclear factor-κB (NF-κB) and extracellular signal-regulated kinase (ERK) 1/2 pathways. Early-stage adipogenic differentiation was more sensitive to IL-1α than late-stage differentiation. After differentiation of ADSCs into mature adipocytes, adding of IL-1α had no obvious influence on the cellular morphology, including lipid droplet accumulation. IL-1α enhanced the expression of proinflammatory cytokines, such as IL-8, IL-6, CCL2 (C-C motif chemokine ligand 2), and IL-1β, when added into the adipogenic medium of ADSCs. Blocking IL-8 and IL-6 with neutralizing antibodies partially alleviated the inhibitory effect of IL-1α on the proliferation and adipogenic differentiation. The results suggest that IL-1α inhibits adipogenesis through activation of NF-κB and ERK1/2 pathways and subsequent upregulation of proinflammatory cytokines in ADSCs. IL-1α might play an important role in mediating lipoatrophy by regulation of ADSCs.

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“…A previous result also showed that regulation of TLR2 expression provided a pivotal target for the treatment of inflammatory acne (Jung et al, ). In addition, activation of TLR2 could stimulate the downstream gene NF‐κB in inflammatory response (Chen et al, ; Wu et al, ). NF‐κB was a key transcription factor and its activation was a necessary step in the transcriptional induction of adhesion molecules (Sun et al, ), which mediated cellular inflammatory response (Kim et al, ).…”

Section: Discussionmentioning

confidence: 99%

The therapeutic effect of tanshinone IIA onPropionibacterium acnes-induced inflammation in vitro

Zhou

2018

Dermatologic Therapy

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Acne vulgaris, a chronic inflammatory skin disease, affects many adolescents. New therapeutic agents for acne allow for a higher therapeutic activity, but fewer side effects. Tanshinone IIA, a natural product, has been proved to exhibit antibacterial and anti‐inflammatory abilities in many diseases. However, its antibacterial and anti‐inflammatory activities against Propionibacterium acnes have not been described. In the present study, the broth microdilution method was used to evaluate the antibacterial activity of tanshinone IIA and it had an inhibitory effect on the growth of P. acnes. Enzyme‐linked immunosorbent assay and quantitative real‐time PCR were used to investigate the effect of tanshinone IIA on IL‐1β, IL‐8, and TNF‐α expression, and western blot was used to examine TLR2, NF‐κB, and intercellular cell adhesion molecule‐1 (ICAM‐1) protein level induced by P. acnes in THP‐1 cells. Results showed that the expression of inflammatory cytokines and TLR2, NF‐κB, ICAM‐1 protein levels were inhibited by Tanshinone IIA, suggesting that tanshinone IIA appeared to suppress P. acnes‐induced inflammation by blockade of TLR2/NF‐κB signaling pathway. In conclusion, the present study revealed the inhibitory effect of tanshinone IIA on P. acnes‐induced inflammation, providing an evidence to support the mechanism of anti‐acne properties of tanshinone IIA.

show abstract

Activation of the TLR2-mediated downstream signaling pathways NF-κB and MAPK is responsible for B7-H3-augmented inflammatory response during S. pneumoniae infection

Cited by 16 publications

References 34 publications

In Vitro and In Vivo Screening of Wild Bitter Melon Leaf for Anti-Inflammatory Activity against Cutibacterium acnes

In Vitro and In Vivo Screening of Wild Bitter Melon Leaf for Anti-Inflammatory Activity against Cutibacterium acnes

IL‐1α inhibits proliferation and adipogenic differentiation of human adipose‐derived mesenchymal stem cells through NF‐κB‐ and ERK1/2‐mediated proinflammatory cytokines

The therapeutic effect of tanshinone IIA onPropionibacterium acnes-induced inflammation in vitro

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