LPS enhances TLR4 expression and IFN-γ production via the TLR4/IRAK/NF-κB signaling pathway in rat pulmonary arterial smooth muscle cells

Wang, Pengyan; Han, Xuhui; Mo, Biwen; Huang, Guojin; Wang, Changming

doi:10.3892/mmr.2017.6983

Cited by 47 publications

(44 citation statements)

References 16 publications

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“…Monocytes circulate in blood and mature upon entering tissues where they receive local tissue signals that shape their phenotype . Mϕs are tissue‐resident leukocytes that exhibit an array of pattern recognition receptors (PRRs), which recognize a diverse collection of foreign invaders through sensing of non‐self‐molecular motifs called pathogen‐associated molecular patterns (PAMPs) . Upon activation of PRRs, communicational proteins (e.g., cytokines) are manufactured by the cell, cueing and mobilizing a repertoire of effector cells to the compromised locale (Fig.…”

Section: Introductionmentioning

confidence: 99%

“… Illustration of broad communication and crosstalk among innate immune cells and signaling cascades . The success of innate immunity to recognize a diverse collection of foreign invaders relies on PRRs that sense non‐self‐molecular motifs (i.e., PAMPs) . Upon activation of PRRs, commonly characterized as Toll‐like receptors (TLRs), C‐type lectins (CLRs), retinoic acid‐inducible gene (RIG)‐I like receptors (RLRs), and nucleotide oligomerization domain (NOD)‐like receptors (NLRs), antimicrobial communicational proteins (e.g., cytokines) are manufactured by the cell .…”

Section: Introductionmentioning

confidence: 99%

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Decoding communication patterns of the innate immune system by quantitative proteomics

Sukumaran

Coish

Yeung

et al. 2019

Journal of Leukocyte Biology

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The innate immune system is a collective network of cell types involved in cell recruitment and activation using a robust and refined communication system. Engagement of receptor-mediated intracellular signaling initiates communication cascades by conveying information about the host cell status to surrounding cells for surveillance and protection. Comprehensive profiling of innate immune cells is challenging due to low cell numbers, high dynamic range of the cellular proteome, low abundance of secreted proteins, and the release of degradative enzymes (e.g., proteases).However, recent advances in mass spectrometry-based proteomics provides the capability to overcome these limitations through profiling the dynamics of cellular processes, signaling cascades, post-translational modifications, and interaction networks. Moreover, integration of technologies and molecular datasets provide a holistic view of a complex and intricate network of communications underscoring host defense and tissue homeostasis mechanisms. In this Review, we explore the diverse applications of mass spectrometry-based proteomics in innate immunity to define communication patterns of the innate immune cells during health and disease. We also provide a technical overview of mass spectrometry-based proteomic workflows, with a focus on bottom-up approaches, and we present the emerging role of proteomics in immune-based drug discovery while providing a perspective on new applications in the future.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Decoding communication patterns of the innate immune system by quantitative proteomics

Sukumaran

Coish

Yeung

et al. 2019

Journal of Leukocyte Biology

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“…TLR3 and TLR9 are considered as one of the important receptors of antiviral immunity. TLR signaling pathway involves many factors such as interferon regulatory factors (IRFs), IKK epsilon/TBK1, interferon regulatory factors (IRFs), and interferon (IFN) . Studies have shown that the activation of TLRs receptor can activate the immune signaling pathway of TLRs‐IKK epsilon‐IRFs‐IFN in host cells and induce immune inflammation.…”

Section: Introductionmentioning

confidence: 99%

“…TLR signaling pathway involves many factors such as interferon regulatory factors (IRFs), IKK epsilon/TBK1, interferon regulatory factors (IRFs), and interferon (IFN). 5 Studies have shown that the activation of TLRs receptor can activate the immune signaling pathway of TLRs-IKK epsilon-IRFs-IFN in host cells and induce immune inflammation. The immune inflammatory factors produced can activate immune cells Th1, Th2, Th17, and Treg cells and produce immune cascade effect.…”

Section: Introductionmentioning

confidence: 99%

Molecular immune mechanisms of HPV‐infected HaCaT cells in vitro based on toll‐like receptors signaling pathway

Zhao

Hong

et al. 2019

Clinical Laboratory Analysis

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Objective To explore the molecular immune mechanism of HPV‐infected HaCaT cells in vitro based on TLRs signaling pathway by analyzing the effects of interfering TLRs on inflammatory and immune factors in the signaling pathway. Methods FCM was used to analyze the proportion of Th1, Th2, Th17, and Treg cells in blood samples. HPV‐infected HaCaT cells were divided into five groups: A, B, C, D, and E. Group A added TLR3 antagonist, group B added TLR9 antagonist, group C added equivalent saline, group D added IRF3 agonist, and group E added IRF3 inhibitor. Immunohistochemistry was used to analyze the expression of TLR3 and TLR9 in HaCaT cell model; ELISA was used to analyze the expression of inflammatory factors IL‐2, TNF‐a, and IFN‐beta; WB was used to analyze the expression of TRAF3, IKK epsilon, and TBK1; RT‐PCR was used to analyze the expression of IRF3 and IRF7 in each cell model. Results The proportion of blood immune cells in patients with HPV infection was Th1, Th17, Th2, and Treg, with statistical significance (P < .05); the expression of TLR3 and TLR9 in HPV‐infected cells was higher than that in negative control group, with statistical significance (P < .05); TLR3 was higher than TLR9, with no significant difference (P > .05); the expression of IL‐2, TNF‐alpha, IFN‐beta in each group, TLR3, and TLR9 was higher than that in negative control group (P < .05). The expression of TRAF3, IKK epsilon, and TBK1 in the control group was higher than that in the TLR3 and TLR9 inhibitor groups, and the expression of IRF3 and IRF7 in the TLR9 inhibitor group was higher than that in the TLR3 inhibitor group (P < .05); the expression of IRF3 and IRF7 in the TLR3i and TLR9i inhibitor groups was lower than that in the TLR3 inhibitor group (P < .05). Compared with the control group, IRF3a group was higher than the control group, IRF3i group was lower than the control group, the difference was statistically significant (P < .05). Conclusion TLR3 and TLR9, the key factors of TLRs, are highly expressed in HaCaT cells infected with HPV. Through TLRs‐IKK‐e‐IRFs‐IFN signaling pathway, they can induce high expression of inflammatory factors, IKK‐e, IRFs, and IFN, and improve immunity.

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“…NF-κB, an important nuclear transcription factor, were activated by various inflammatory cytokines such as TGF-β1, TNF-α, and IL-1β. NF-κB activation can in turn promote the expression of inflammatory cytokines such as INF-γ, TGF-β1, TNF-α, and IL-1β [27,28]. A previous study showed that NF-κB activation occurred in the lungs of patients with ARDS and may contribute to the increased expression of immunoregulatory cytokines and other proinflammatory cytokines [29].…”

mentioning

confidence: 99%

Acute Respiratory Distress Syndrome Induced by White Smoke Inhalation: a Potential Animal Model For Evaluating Pathological Changes and Underlying Mechanisms

Cui

Feng

Zhu

et al. 2018

Cell Physiol Biochem

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Background/Aims: White smoke inhalation (WSI) is an uncommon but potentially deadly cause of acute respiratory distress syndrome (ARDS). However, no clinical treatment protocol has been established for the treatment of WSI-induced ARDS. Therefore, it is necessary to investigate the effects of WSI in ARDS and the mechanisms underlying the effects of WSI to determine a novel therapeutic target. Methods: On the basis of the duration of continued inhalation of white smoke (3 min, 5 min, and 7 min), rats were divided into three groups (WSI-3 min, WSI-5 min, and WSI-7 min). The survival rate, pathological change, and computed tomography (CT) score were evaluated to determine the modeling conditions. In the established WSI-5 min models, evaluations were performed to evaluate the following: arterial blood gas levels, lung wet/dry weight ratio, the expression of inflammatory cytokines, and the effect of NF-κB signaling pathway. Results: The survival rate of rats at 72 h post-WSI in the WSI-3 min, WSI-5 min, and WSI-7 min groups was 83.33%, 75%, and 25%, respectively. Results from evaluation of H&E staining, CT scan, arterial blood gas levels, and lung wet/dry weight ratio suggest that the pathological changes in the rat in the WSI-5 min and WSI-7 min groups are very similar to those in patients with ARDS induced by WSI. Additionally, the expression of INF-γ, TGF-β1, TNF-α, and IL-1β were increased, and the NF-κB signaling pathway was activated in the WSI-5 min group. Conclusion: The rat model of WSI-5 min can be used as a WSI-induced ALI model for further experiments. The NF-κB signaling pathway may be a potential therapeutic target for the treatment of WSI- induced ARDS.

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LPS enhances TLR4 expression and IFN-γ production via the TLR4/IRAK/NF-κB signaling pathway in rat pulmonary arterial smooth muscle cells

Cited by 47 publications

References 16 publications

Decoding communication patterns of the innate immune system by quantitative proteomics

Decoding communication patterns of the innate immune system by quantitative proteomics

Molecular immune mechanisms of HPV‐infected HaCaT cells in vitro based on toll‐like receptors signaling pathway

Acute Respiratory Distress Syndrome Induced by White Smoke Inhalation: a Potential Animal Model For Evaluating Pathological Changes and Underlying Mechanisms

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