ArticleThe American journal of pathology2010
Inhibition of NF-kappaB signaling reduces virus load and gammaherpesvirus-induced pulmonary fibrosis.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Idiopathic Pulmonary Fibrosis: Cellular Heterogeneity, Mechanisms, and Therapeutic Implications.MedComm · 2025Review
- IKKα-Mediated Noncanonical NF-κB Signaling Is Required To Support Murine Gammaherpesvirus 68 LatencyJournal of virology · 2022Article
- Nuclear respiratory factor-1 negatively regulates TGF-β1 and attenuates pulmonary fibrosis.iScience · 2022Article
- Ginsenoside Rb1 Alleviates Bleomycin-Induced Pulmonary Inflammation and Fibrosis by Suppressing Central Nucleotide-Binding Oligomerization-, Leucine-Rich Repeat-, and Pyrin Domains-Containing Protein Three Inflammasome Activation and the NF-κB Pathway.Drug design, development and therapy · 2022Article
- Virus infection induced pulmonary fibrosis.Journal of translational medicine · 2021Review
- Conquering the Host: Determinants of Pathogenesis Learned from Murine Gammaherpesvirus 68.Annual review of virology · 2021Article
- Bufei Decoction Alleviated Bleomycin-Induced Idiopathic Pulmonary Fibrosis in Mice by Anti-Inflammation.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Akt1 regulates pulmonary fibrosis via modulating IL-13 expression in macrophages.Innate immunity · 2019Article
- Proteomics of Bronchoalveolar Lavage Fluid Reveals a Lung Oxidative Stress Response in Murine Herpesvirus-68 Infection.Viruses · 2018Article
- Cholesterol-modified Hydroxychloroquine-loaded Nanocarriers in Bleomycin-induced Pulmonary Fibrosis.Scientific reports · 2017Article
- Interplay of Murine Gammaherpesvirus 68 with NF-kappaB Signaling of the Host.Frontiers in microbiology · 2016Review
- High-mobility group box 1 accelerates lipopolysaccharide-induced lung fibroblast proliferation in vitro: involvement of the NF-κB signaling pathway.Laboratory investigation; a journal of technical methods and pathology · 2015Article
- PINK1 deficiency impairs mitochondrial homeostasis and promotes lung fibrosis.The Journal of clinical investigation · 2015Article
- CD8+ T Cell Response to Gammaherpesvirus Infection Mediates Inflammation and Fibrosis in Interferon Gamma Receptor-Deficient Mice.PloS one · 2015Article
- Protective role of andrographolide in bleomycin-induced pulmonary fibrosis in mice.International journal of molecular sciences · 2013Article
- Stem cells, cell therapies, and bioengineering in lung biology and diseases. Comprehensive review of the recent literature 2010-2012.Annals of the American Thoracic Society · 2013Review
- Myxomavirus-derived serpin prolongs survival and reduces inflammation and hemorrhage in an unrelated lethal mouse viral infection.Antimicrobial agents and chemotherapy · 2013Article
- Role of endoplasmic reticulum stress in age-related susceptibility to lung fibrosis.American journal of respiratory cell and molecular biology · 2012Article
- Tiled microarray identification of novel viral transcript structures and distinct transcriptional profiles during two modes of productive murine gammaherpesvirus 68 infection.Journal of virology · 2012Article
- Nuclear factor-κB: a key regulator in health and disease of lungs.Archivum immunologiae et therapiae experimentalis · 2011Review
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Authors and funding
8 authors at 1 institution in 3 countries.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disorder of unknown etiology. Several studies have demonstrated an association between pulmonary infection with a herpesvirus and IPF. Based on those observations, we have developed a mouse model in which interferon (IFN)gammaR(-/-) mice infected intranasally with murine gammaherpesvirus 68 (MHV68) develop lung fibrosis. We hypothesize that viral load was a critical factor for the development of fibrosis. Because nuclear factor (NF)-kappaB signaling is required to efficiently establish gammaherpesvirus, latency we infected IFNgammaR(-/-) mice with a MHV68 virus that expresses a mutant dominant inhibitor of the NF-kappaB signaling pathway, called IkappaBalphaM. Striking differences were observed at the onset of the chronic infection, which correlated with a decreased virus load in mice infected with MHV68-IkappaBalphaM compared with mice infected with control MHV68 (MHV68-MR). IFNgammaR(-/-) mice infected with MHV68-IkappaBalphaM lacked vasculitis and fibrosis 15 to 120 days post infection. Inhibition of NF-kappaB in MHV68-infected cells of the lungs diminished the expression of the fibrocyte recruiting chemokines monocyte chemoattractant protein 1 (MCP-1) and CXCL12, ameliorated macrophage expression of markers of alternative activation, and failed to increase expression of the integrin alphavbeta6, which is implicated in the activation of the profibrotic factor TGF-beta. Thus, the inhibition of NF-kappaB signaling in the infected lung cells of IFNgammaR(-/-) mice reduces virus persistence and ameliorates profibrotic events. Host determinants of latency might therefore represent new therapeutic targets for gammaherpesvirus-associated pulmonary fibrosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.