STAT6 and PARP Family Members in the Development of T Cell-dependent Allergic Inflammation

Krishnamurthy, Purna; Kaplan, Mark H.

doi:10.4110/in.2016.16.4.201

Cited by 28 publications

(29 citation statements)

References 83 publications

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“…These reports indicate that each residue of STAT3 has a different role and activates different targets. In the present study, BV had no effect on the activation of NF-κB, which is crucial in the regulation of allergic inflammatory responses (50). As BV inhibited the PMAcI-stimulated phosphorylation of MAPKs, which contribute to the transmission of extracellular signals that can result in the phosphorylation of various transcription factors and alterations in gene expression (51), the present study focused on examining the effects of BV on STAT3 as it is a critical component in multiple aspects of allergic disease.…”

Section: Discussioncontrasting

confidence: 68%

Inhibitory effects of bee venom on mast cell-mediated allergic inflammatory responses

et al. 2018

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Although bee venom (BV) is a toxin that causes bee stings to be painful, it has been widely used clinically for the treatment of certain immune‑associated diseases. BV has been used traditionally for the treatment of chronic inflammatory diseases. In this regard, the present study analyzed the effect of BV on the regulation of inflammatory mediator production by mast cells and their allergic inflammatory responses in an animal model. HMC‑1 cells were treated with BV prior to stimulation with phorbol‑12‑myristate 13‑acetate plus calcium ionophore A23187 (PMACI). The production of allergy‑associated pro‑inflammatory mediators was examined, and the underlying mechanisms were investigated. Furthermore, to investigate whether BV exhibits anti‑inflammatory effects associated with anti‑allergic effects in vivo, a compound 48/80‑induced anaphylaxis model was used. BV inhibited histamine release, mRNA expression and production of cytokines in the PMACI‑stimulated HMC‑1 cells. Furthermore, the inhibitory effects of BV on mitogen‑activated protein kinase (MAPK), MAPK kinase, signal transducer and activator of transcription 3 (STAT3) and Akt were demonstrated. The present study also investigated the ability of BV to inhibit compound 48/80‑induced systemic anaphylaxis in vivo. BV protected the mice against compound 48/80‑induced anaphylactic‑associated mortality. Furthermore, BV suppressed the mRNA expression levels of pro‑inflammatory cytokines, and suppressed the activation of MAPK and STAT3 in this model. These results provide novel insights into the possible role of BV as a modulator for mast cell‑mediated allergic inflammatory disorders.

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Section: Discussioncontrasting

confidence: 68%

Inhibitory effects of bee venom on mast cell-mediated allergic inflammatory responses

et al. 2018

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“…PARP14 (CoaST-6) PARP14 was originally identified as Collaborator of STAT6 (CoaST6) (Goenka and Boothby 2006). It has a range of effects on cell physiology and immunity that were largely anti-inflammatory (Cho et al 2011(Cho et al , 2013Barbarulo et al 2013;Vyas et al 2013;Iansante et al 2015;Iwata et al 2016;Krishnamurthy and Kaplan 2016). In the antiviral response, PARP14 instead is required to enhance IFN-I production in RAW cells (transformed peritoneal macrophages) following LPS treatment (Caprara et al 2018), in primary macrophage cells during CoV infection, and following treatment of human A549 cells with poly(I:C) (Grunewald et al 2019a).…”

Section: Macrodomain-containing Parpsmentioning

confidence: 99%

The impact of PARPs and ADP-ribosylation on inflammation and host–pathogen interactions

et al. 2020

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Poly-adenosine diphosphate-ribose polymerases (PARPs) promote ADP-ribosylation, a highly conserved, fundamental posttranslational modification (PTM). PARP catalytic domains transfer the ADP-ribose moiety from NAD+ to amino acid residues of target proteins, leading to mono- or poly-ADP-ribosylation (MARylation or PARylation). This PTM regulates various key biological and pathological processes. In this review, we focus on the roles of the PARP family members in inflammation and host–pathogen interactions. Here we give an overview the current understanding of the mechanisms by which PARPs promote or suppress proinflammatory activation of macrophages, and various roles PARPs play in virus infections. We also demonstrate how innovative technologies, such as proteomics and systems biology, help to advance this research field and describe unanswered questions.

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“…LXR agonists induce anti‐inflammatory activity but also restore skin barrier function in vivo through direct effects on keratinocytes, hence they present therapeutic potential for AD treatment . Given the relevance of the JAK/STAT pathway in the pathogenesis of AD, we also used an inhibitor of the STAT6 transcription factor and verified that it counteracted the detrimental signalling induced by the Th2 cytokines.…”

Section: Questions Addressedmentioning

confidence: 99%

On the relevance of an in vitro reconstructed human epidermis model for drug screening in atopic dermatitis

Hubaux

Bastin

Salmon

2018

Experimental Dermatology

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Recent advances in the development of human‐based in vitro models offer new tools for drug screening and mechanistic investigations of new therapeutic agents. However, there is a lack of evidence that disease models respond favourably to potential drug candidates. Atopic dermatitis (AD) is a very common disease associated with an altered skin barrier and chronic inflammation. Here, we demonstrate that the AD‐like features of a reconstructed human epidermis (RHE) model treated with Th2 cytokines are reversed in the presence of molecules known to have a beneficial effect on damaged skin as a result of modulating various signalling cascades including the Liver X Receptors and JAK/STAT pathways. This work shows that standardized and reproducible RHE are relevant models for therapeutic research assessing new drug candidates aiming to restore epidermal integrity in an inflammatory environment.

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STAT6 and PARP Family Members in the Development of T Cell-dependent Allergic Inflammation

Cited by 28 publications

References 83 publications

Inhibitory effects of bee venom on mast cell-mediated allergic inflammatory responses

Inhibitory effects of bee venom on mast cell-mediated allergic inflammatory responses

The impact of PARPs and ADP-ribosylation on inflammation and host–pathogen interactions

On the relevance of an in vitro reconstructed human epidermis model for drug screening in atopic dermatitis

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