Lipopolysaccharide induced Interleukin-6 production is mediated through activation of ERK 1/2, p38 MAPK, MEK, and NFκB in chicken thrombocytes

Winkler, Christine; Ferdous, Farzana; Dimmick, M.A.; Scott, T. R.

doi:10.1016/j.dci.2017.03.017

Cited by 31 publications

(24 citation statements)

References 30 publications

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“…Various stimuli, including ER stress, cause the phosphorylation of IκB, followed by its subsequent degradation. This degradation leads to the phosphorylation of NF‐κB subunits, such as p65, affecting its transcription activation efficiency . The activation of the MAPK pathways includes JNK/stress‐activated protein kinase and p38‐MAPK .…”

Section: Discussionmentioning

confidence: 99%

“…This degradation leads to the phosphorylation of NF-κB subunits, such as p65, affecting its transcription activation efficiency. 18,29 The activation of the MAPK pathways includes JNK/stress-activated protein kinase and p38-MAPK. 29,30 In the current study, TiO 2 NPs induced the inflammation response and activated MAPK pathways at the early stage in the developing mice, which continued to the late stage.…”

Section: Tio 2 Nps Induced Insulin Resistance (Ir) Earlier In Develmentioning

confidence: 99%

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The toxic effects of titanium dioxide nanoparticles on plasma glucose metabolism are more severe in developing mice than in adult mice

Zhang

et al. 2019

Environmental Toxicology

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Titanium dioxide nanoparticles (TiO2 NPs) are authorized food additives, and children have the highest exposure. Therefore, children are likely more susceptible to the adverse effects of TiO2 NPs than adults. Previous study showed that oral administration of 50 mg/kg body weight (bw) TiO2 NPs increase plasma glucose in mice. However, few studies have directly compared the adverse effects of exposure to TiO2 NPs on plasma glucose metabolism of different age groups. In this study, the developing (age 3 weeks) and adult mice (age 10 weeks) were orally administered with 50 mg/kg bw TiO2 NPs per day. The TiO2 NPs induced hyperglycemia earlier in the developing mice than in the adult mice. Then mechanisms were analyzed after mice were oral administration of TiO2 NPs for 8 weeks and 26 weeks, respectively. Results showed that the treatment with TiO2 NPs activated xenobiotic biodegradation in livers of both developing and adult mice at the early stage. However, only in the developing mice, TiO2 NPs induced endoplasmic reticulum (ER) stress in livers and increased reactive oxygen species in livers and sera in the early stage. The ER stress and ROS activated an inflammation response and mitogen‐activated protein kinase pathways, thereby inducing insulin resistance in the livers of developing mice at the early stage. The response of the adult mice was delayed, and these changes were observed in the late stage of the study. The results of this study all suggest that children are more susceptible than adults to the toxicity of orally administered TiO2 NPs.

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Section: Discussionmentioning

confidence: 99%

Section: Tio 2 Nps Induced Insulin Resistance (Ir) Earlier In Develmentioning

confidence: 99%

The toxic effects of titanium dioxide nanoparticles on plasma glucose metabolism are more severe in developing mice than in adult mice

Zhang

et al. 2019

Environmental Toxicology

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“…Although Pam3CSK4 or LPS may induce TNF-α and NF-κB transcriptions in murine C2C12 myoblasts (Frost et al, 2002;Frost et al, 2006), neither Pam3CSK4, FSL-1, nor LPS upregulated TNF-α and NF-κB in chick myoblasts. TNF-α and NF-κB transcriptions were elevated in the bursa of Fabricius of LPS-challenged chickens (Cheng et al, 2014) while phosphorylated NF-κB was not elevated in LPS-treated thrombocytes (Winkler et al, 2017). It is still unclear whether chick TLR1/2 ligands enhance NF-κB expression in other types of cells.…”

Section: Discussionmentioning

confidence: 99%

“…In chickens, Pam3CSK4, FSL-1, or LPS induces the expression of inflammatory cytokines such as interleukin (IL)-1β, IL-6, IL-8, interferon (IFN)-γ, and tumor necrosis factor (TNF)-α in the bursa of Fabricius (Cheng et al, 2014), spleen (Alkie et al, 2017;Li et al, 2017), primary-cultured splenocytes (St. Paul et al, 2013), heterophils (Kogut et al, 2006), thrombocytes (Ferdous and Scott, 2015;Winkler et al, 2017), cecal tonsil cells (Taha-abdelaziz et al, 2016), and the macrophage cell line MQ-NCSU (Barjesteh et al, 2014;Alkie et al, 2017). LPS also induces nuclear factor (NF)-κB, a transcription factor for regulating immune responses, in the bursa of Fabricius (Cheng et al, 2014) but not in thrombocytes (Winkler et al, 2017). In addition to these inflammatory mediators, IL-10, a feedback negative regulator of inflammation, is known to be induced by LPS in macrophage and is detected in serum from the chickens infected with Eimeria tenella (Wu et al, 2016;Qi et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Toll-like receptor ligand-dependent inflammatory responses in chick skeletal muscle myoblasts

Nihashi

Ono

Kono

et al. 2019

Developmental & Comparative Immunology

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Toll-like receptors (TLRs) are a group of sensory receptors which are capable of recognizing a microbial invasion and activating innate immune system responses, including inflammatory responses, in both immune and non-immune cells. However, TLR functions in chick myoblasts, which are myogenic precursor cells contributing to skeletal muscle development and growth, have not been studied. Here, we report the expression patterns of TLR genes as well as TLR ligand-dependent transcriptions of interleukin (IL) genes in primary-cultured chick myoblasts. Almost TLR genes were expressed both in layer and broiler myoblasts but TLR1A was detected only in embryonic layer chick myoblasts. Chick TLR1/2 ligands, Pam3CSK4 and FSL-1, induced inflammatory ILs in both broiler and layer myoblasts but a TLR4 ligand, lipopolysaccharide, scarcely promoted. This is the first report on TLR ligand-dependent inflammatory responses in chick myoblasts, which may provide useful information to chicken breeding and meat production industries.

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“…Thrombocytes respond to LPS, lipoteichoic acid (LTA), thymidine homopolymer phosphorothioate oligonucleotide [Poly(dT)], and polyinosinic-polycytidylic acid [Poly(I:C)] (8,11), and this stimulation takes place through TLR signal pathways, specifically TLR4, TLR2, TLR7, and TLR3, respectively. Use of inhibitors has provided evidence to map LPS stimulation of thrombocytes to activation through mitogenactivated protein kinase (ERK, MEK1, and p38 MAPK) and NF-k L-chain-enhancer of activated B cells (NF-kB) pathways (8,12).…”

mentioning

confidence: 99%

Bacterial and Viral Products Affect Differential Pattern Recognition Receptor Activation of Chicken Thrombocytes Evidenced through RNA Sequencing

Ferdous

Saski

Bridges

et al. 2017

The Journal of Immunology

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It is now well understood that thrombocytes (nucleated platelets) express TLRs and respond to both bacterial and viral products. Release of proinflammatory molecules can be expected following relatively short exposure times to LPS, lipoteichoic acid (LTA), thymidine homopolymer phosphorothioate oligonucleotide [Poly(dT)], and polyinosinic-polycytidylic acid [Poly(I:C)]. This study reports the varied expressions of genes encoded for components of the TLR, nucleotide binding oligomerization domain-like receptor, and retinoic acid-inducible gene RIG-like receptor signaling pathways in response to the TLR ligands listed above. Highly sensitive RNA-sequencing technologies were used to analyze the complete transcriptome of thrombocytes treated with all four microbial products for a period of 1 h. A total of 14,326 gene transcripts were found in chicken thrombocytes across all ligand exposures. After 1 h of stimulation with ligands, 87, 138, 1013, and 22 genes were upregulated for LTA, LPS, Poly(dT), and Poly(I:C), and 12, 142, 249, and 16 genes were downregulated for LTA, LPS, Poly(dT), and Poly(I:C), respectively, with at least a 1-fold change relative to unexposed thrombocytes. Summarizations of biological processes, protein classes, and biochemical pathways reveal the role of chicken thrombocytes in proinflammatory responses linked to key signaling pathways. TLR, nucleotide binding oligomerization domain-like receptor, and retinoic acid-inducible gene RIG-like receptor pathways were mapped based on the transcriptome results with gene expression for common signal and proinflammatory mediators highlighted. The information reported in this study is useful for defining a limited set of proinflammatory molecules to evaluate in cases of either bacterial or viral disease monitoring.

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Lipopolysaccharide induced Interleukin-6 production is mediated through activation of ERK 1/2, p38 MAPK, MEK, and NFκB in chicken thrombocytes

Cited by 31 publications

References 30 publications

The toxic effects of titanium dioxide nanoparticles on plasma glucose metabolism are more severe in developing mice than in adult mice

The toxic effects of titanium dioxide nanoparticles on plasma glucose metabolism are more severe in developing mice than in adult mice

Toll-like receptor ligand-dependent inflammatory responses in chick skeletal muscle myoblasts

Bacterial and Viral Products Affect Differential Pattern Recognition Receptor Activation of Chicken Thrombocytes Evidenced through RNA Sequencing

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