Haemophilus parasuis induces activation of NF-κB and MAP kinase signaling pathways mediated by toll-like receptors

Chen, Yu‐Shan; Liu, Ting; Langford, Paul R.; Hua, Kexin; Zhou, Shenghan; Zhai, Yajun; Xiao, Haiyan; Luo, Rui; Bi, Dingren; Jin, Hui; Zhou, Rui

doi:10.1016/j.molimm.2015.02.016

Cited by 35 publications

(22 citation statements)

References 37 publications

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“…It is well documented that cells use TLR2 and TLR4 to recognize PAMPs expressed by bacteria. Activation of TLR2 and TLR4 leads to activation of MAPK and NF- κ B pathways and production of inflammatory cytokines, including IL-1, IL-6, and TNF- α [ 20 – 22 ]. In this study, we showed that LPS promoted expression of TLR2 and TLR4 in alveolar macrophages and HUVECs.…”

Section: Discussionmentioning

confidence: 99%

Bone Marrow Mesenchymal Stem Cells Inhibit Lipopolysaccharide-Induced Inflammatory Reactions in Macrophages and Endothelial Cells

Chi

Wang

et al. 2016

Mediators of Inflammation

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Background. Systemic inflammatory response syndrome (SIRS) accompanied by trauma can lead to multiple organ dysfunction syndrome (MODS) and even death. Early inhibition of the inflammation is necessary for damage control. Bone marrow mesenchymal stem cells (BMSCs), as a novel therapy modality, have been shown to reduce inflammatory responses in human and animal models. Methods. In this study, we used Western blot, quantitative PCR, and enzyme-linked immunosorbent assay (ELISA) to assess the activity of BMSCs to suppress the inflammation induced by lipopolysaccharide (LPS) in human umbilical cord endothelial cells (HUVECs) and alveolar macrophages. Results. Our results demonstrated that LPS caused an inflammatory response in alveolar macrophages and HUVECs, increased permeability of HUVEC, upregulated expression of toll-like receptor (TLR) 2, TLR4, phosphorylated p65, downregulated release of IL10, and promoted release of TNF-α in both cells. Coculture with BMSCs attenuated all of these activities induced by LPS in the two tested cell types. Conclusions. Together, our results demonstrate that BMSCs dosage dependently attenuates the inflammation damage of alveolar macrophages and HUVECs induced by LPS.

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Section: Discussionmentioning

confidence: 99%

Bone Marrow Mesenchymal Stem Cells Inhibit Lipopolysaccharide-Induced Inflammatory Reactions in Macrophages and Endothelial Cells

Chi

Wang

et al. 2016

Mediators of Inflammation

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“…Previous studies have shown that H. parasuis infects PUVEC, pig kidney epithelial cells (PK‐15), and porcine brain microvascular endothelial cells (Vanier et al, ; Zhang et al, ). In PK‐15 cells, H. parasuis activates NF‐κB and MAP kinase signalling pathways mediated by toll‐like receptors and the NOD1/2‐RIP2 signalling pathway (Chen et al, ; Ma et al, ). Porcine alveolar macrophages are an important line of defense against H. parasuis .…”

Section: Introductionmentioning

confidence: 99%

Haemophilus parasuis infection in 3D4/21 cells induces autophagy through the AMPK pathway

Shen

Zhou

et al. 2019

Cellular Microbiology

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Haemophilus parasuis (H. parasuis) is a common commensal in the upper respiratory tract of pigs, but causes Glässer's disease in stress conditions. To date, many studies focused on the immune evasion and virulence of H. parasuis; very few have focused on the role autophagy played in H. parasuis infection, particularly in porcine alveolar macrophages (PAMs). In this study, a PAM cell line, 3D4/21 cells were used to study the role of autophagy in H. parasuis infection. 3D4/21 cells tandemly expressing GFP, mCherry, and LC3 were infected with H. parasuis serovar 5 (Hps5). Western blot analysis and confocal and transmission electron microscopy showed that H. parasuis infection effectively induces autophagy. Using Hps strains of varying virulence (Hps4, Hps5, and Hps7) and UV-inactivated Hps5, we demonstrated that autophagy is associated with the internalisation of living virulent strains into cells. In 3D4/21 cells pretreated with rapamycin and 3-MA then infected by Hps4, Hps5, and Hps7, we demonstrated that autophagy affects invasion of H. parasuis in cells. AMPK signal results showed that Hps5 infection can upregulate the phosphorylation level of AMPK, which is consistent with the autophagy development. 3D4/21 cells pretreated with AICAR or Compound C then infected by Hps5 revealed that the autophagy induced by Hps5 infection is associated with the AMPK pathway. Our study contributes to the theoretical basis for the study of H. parasuis pathogenesis and development of novel drugs target for prevention Glässer's disease.

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“…Of note, in Kupffer cells and liver injury in mice, miR‐181b can mediate TLR4 signaling in response to ethanol, and miR‐181b can target TLR4 to regulate the proliferation of epidermal keratinocytes in human pasoriasis . Moreover, TLR4 was responsible for the activation of p38 and JNK, and there was evidence that selective targeting of JNK over p38 has become a potential therapeutic approach to neurological disorders, as well as epilepsy. However, whether miR‐181b could mediate P38/JNK signaling pathway via regulating TLR4 to affect further the occurrence and development of epilepsy is still unknown.…”

Section: Introductionmentioning

confidence: 99%

MiR‐181b inhibits P38/JNK signaling pathway to attenuate autophagy and apoptosis in juvenile rats with kainic acid‐induced epilepsy via targeting TLR4

et al. 2018

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Haemophilus parasuis induces activation of NF-κB and MAP kinase signaling pathways mediated by toll-like receptors

Cited by 35 publications

References 37 publications

Bone Marrow Mesenchymal Stem Cells Inhibit Lipopolysaccharide-Induced Inflammatory Reactions in Macrophages and Endothelial Cells

Bone Marrow Mesenchymal Stem Cells Inhibit Lipopolysaccharide-Induced Inflammatory Reactions in Macrophages and Endothelial Cells

Haemophilus parasuis infection in 3D4/21 cells induces autophagy through the AMPK pathway

MiR‐181b inhibits P38/JNK signaling pathway to attenuate autophagy and apoptosis in juvenile rats with kainic acid‐induced epilepsy via targeting TLR4

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