A pathogenic role for tumor necrosis factor-related apoptosis-inducing ligand in chronic obstructive pulmonary disease

Haw, Tatt Jhong; Starkey, Malcolm R.; Nair, Prema M.; Pavlidis, Stelios; Liu, Gang; Nguyen, Duc Hai; Hsu, Alan; Hanish, Irwan; Kim, Richard; Collison, Adam; Inman, Mark D.; Wark, Peter; Foster, Paul S.; Knight, Darryl A.; Mattes, Joërg; Yagita, Hideo; Adcock, Ian M.; Horvat, Jay C.; Hansbro, Philip M.

doi:10.1038/mi.2015.111

Cited by 64 publications

(121 citation statements)

References 54 publications

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“…In this study, we investigated the mechanisms involved using our established experimental systems (27,(32)(33)(34). We found that COPD pBECs and mice with experimental COPD infected with IAV have higher levels of inflammatory cytokines but reduced antiviral responses (30,35). We uncovered that NF-κB-mediated inflammation in IAV infection and in COPD was also exaggerated and resulted from decreased levels of A20 protein, which in turn was caused by elevated levels of miR125a or -b.…”

Section: Introductionmentioning

confidence: 96%

“…In vivo. Experimental COPD and influenza infection were induced; miR-125a and -b were inhibited using specific antagomirs; and histopathology, IHC, immunoblotting, and cytometric bead array and data analyses were performed as previously described and/or as in Supplemental Methods (33,35,39,(59)(60)(61)(62)(63)(64)(65)(66)(67).…”

Section: Methodsmentioning

confidence: 99%

“…In contrast, the induction of IFN-β and IFN-λ1 proteins were reduced in COPD. We then measured the levels of activity of NF-κB by assessing the levels of phosphorylated p65 (phospho-p65) at Ser536 (35,37,38). Infection significantly increased the activation of phospho-p65 in both healthy and smoker pBECs at 6 hours, which was further increased at 24 hours ( Figure 1C and Supplemental Figure 1A; supplemental material available online with this article; https://doi.org/10.1172/jci.insight.90443DS1).…”

Section: Iav Infection Induces Increased Inflammatory But Reduced Antmentioning

confidence: 99%

“…BALB/c mice were exposed to either normal air (Air) or cigarette smoke (Smk) for 8 weeks. The Smk group develops hallmark features of COPD as previously described (27,28,(32)(33)(34)(35)39). Mice were then infected with IAV A/PR/8/34, and viral titers, airway inflammation (histopathological score), and inflammatory and antiviral cytokines were determined at 7 days postinfection (dpi) (Figure 2A).…”

Section: Iav Infection Induces Increased Inflammatory But Reduced Antmentioning

confidence: 99%

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MicroRNA-125a and -b inhibit A20 and MAVS to promote inflammation and impair antiviral response in COPD

et al. 2017

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Section: Introductionmentioning

confidence: 96%

Section: Methodsmentioning

confidence: 99%

Section: Iav Infection Induces Increased Inflammatory But Reduced Antmentioning

confidence: 99%

Section: Iav Infection Induces Increased Inflammatory But Reduced Antmentioning

confidence: 99%

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MicroRNA-125a and -b inhibit A20 and MAVS to promote inflammation and impair antiviral response in COPD

et al. 2017

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“…Analyzing BALf is one of the prime parameters to understand the underlying disease pathology in prominent mice models of major respiratory diseases, including asthma [27][28][29], COPD [30,31], and pulmonary fibrosis [32]. Moreover, the application of BALF is not only restricted to quantifying the inflammatory cells, it is also employed to determine the viral titre in various viral infections [3,30].…”

Section: Clinical Utility Of Balf Collectionmentioning

confidence: 99%

Aspiration techniques for bronchoalveolar lavage in translational respiratory research: Paving the way to develop novel therapeutic moieties

Dua

Shukla

Hansbro³

2017

J Biol Methods

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Bronchoalveolar lavage (BAL) is a simple, yet informative tool in understanding the immunopathology of various lung diseases via quantifying various inflammatory cells, cytokines and growth factors. At present, this traditional method is often blended with several robust and sophisticated molecular and biological techniques sustaining the significance and longevity of this technique. Crucially, the existence of slightly distinct approaches and variables employed at different laboratories around the globe in performing BAL aspiration indeed demands an utmost need to optimize and develop an effective, cost-effective and a reproducible technique. This mini review will be of importance to the biological translational scientist, particularly respiratory researchers in understanding the fundamentals and approaches to apply and consider with BAL aspiration techniques. This will ensure generating a meaningful and clinically relevant data which in turn accelerate the development of new and effective therapeutic moieties for major respiratory conditions.

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Enhancing tristetraprolin activity reduces the severity of cigarette smoke‐induced experimental chronic obstructive pulmonary disease

et al. 2019

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Objective. Chronic obstructive pulmonary disease (COPD) is a progressive disease that causes significant mortality and morbidity worldwide and is primarily caused by the inhalation of cigarette smoke (CS). Lack of effective treatments for COPD means there is an urgent need to identify new therapeutic strategies for the underlying mechanisms of pathogenesis. Tristetraprolin (TTP) encoded by the Zfp36 gene is an anti-inflammatory protein that induces mRNA decay, especially of transcripts encoding inflammatory cytokines, including those implicated in COPD.Methods. Here, we identify a novel protective role for TTP in CSinduced experimental COPD using Zfp36 aa/aa mice, a genetically modified mouse strain in which endogenous TTP cannot be phosphorylated, rendering it constitutively active as an mRNAdestabilising factor. TTP wild-type (Zfp36 +/+ ) and Zfp36 aa/aa active C57BL/6J mice were exposed to CS for four days or eight weeks, and the impact on acute inflammatory responses or chronic features of COPD, respectively, was assessed. Results. After four days of CS exposure, Zfp36 aa/aa mice had reduced numbers of airway neutrophils and lymphocytes and mRNA expression levels of cytokines compared to wild-type controls. After eight weeks, Zfp36 aa/aa mice had reduced pulmonary inflammation, airway remodelling and emphysema-like alveolar enlargement, and lung function was improved. We then used pharmacological treatments in vivo (protein phosphatase 2A activator, AAL (S) , and the proteasome inhibitor, bortezomib) to promote the activation and stabilisation of TTP and show that hallmark features of CS-induced experimental COPD were ameliorated. Conclusion. Collectively, our ª

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A pathogenic role for tumor necrosis factor-related apoptosis-inducing ligand in chronic obstructive pulmonary disease

Abstract: Chronic obstructive pulmonary disease (COPD) is a life-threatening

Cited by 64 publications

References 54 publications

MicroRNA-125a and -b inhibit A20 and MAVS to promote inflammation and impair antiviral response in COPD

MicroRNA-125a and -b inhibit A20 and MAVS to promote inflammation and impair antiviral response in COPD

Aspiration techniques for bronchoalveolar lavage in translational respiratory research: Paving the way to develop novel therapeutic moieties

Enhancing tristetraprolin activity reduces the severity of cigarette smoke‐induced experimental chronic obstructive pulmonary disease

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