ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014
γ-Herpes virus-68, but not Pseudomonas aeruginosa or influenza A (H1N1), exacerbates established murine lung fibrosis.
Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- The Role of Herpes Viruses in Pulmonary Fibrosis.Frontiers in medicine · 2021Pooled it
- Comparative study on mouse models of acute exacerbation of pulmonary fibrosis.Experimental and therapeutic medicine · 2026Article
- Pulmonary fibrosis: from mechanisms to therapies.Journal of translational medicine · 2025Review
- Current advancements in the mechanisms and animal models of acute exacerbation of pulmonary fibrosis: a systematic review.Frontiers in pharmacology · 2025Review
- Persistent microbial infections and idiopathic pulmonary fibrosis - an insight intoFrontiers in cellular and infection microbiology · 2024Review
- Genetic deficiency of the transcription factor NFAT1 confers protection against fibrogenic responses independent of immune influx.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Animal models of acute exacerbation of pulmonary fibrosis.Respiratory research · 2023Review
- Article
- Fibrotic lung disease inhibits immune responses to staphylococcal pneumonia via impaired neutrophil and macrophage function.JCI insight · 2022Article
- GLUT1-dependent glycolysis regulates exacerbation of fibrosis via AIM2 inflammasome activation.Thorax · 2020Article
- Integrative Analysis of Transcriptome-Wide Association Study and mRNA Expression Profiles Identifies Candidate Genes Associated With Idiopathic Pulmonary Fibrosis.Frontiers in genetics · 2020Article
- IL-17A contributes to HSV1 infection-induced acute lung injury in a mouse model of pulmonary fibrosis.Journal of cellular and molecular medicine · 2019Article
- A pathologic two-way street: how innate immunity impacts lung fibrosis and fibrosis impacts lung immunity.Clinical & translational immunology · 2019Review
- Lung Dysbiosis, Inflammation, and Injury in Hematopoietic Cell Transplantation.American journal of respiratory and critical care medicine · 2018Article
- Role of Microbial Agents in Pulmonary Fibrosis .The Yale journal of biology and medicine · 2017Review
- Periostin regulates fibrocyte function to promote myofibroblast differentiation and lung fibrosis.Mucosal immunology · 2017Article
- Loss of CCR2 signaling alters leukocyte recruitment and exacerbates γ-herpesvirus-induced pneumonitis and fibrosis following bone marrow transplantation.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Influences of innate immunity, autophagy, and fibroblast activation in the pathogenesis of lung fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2016Review
- Vaccinia vaccine-based immunotherapy arrests and reverses established pulmonary fibrosis.JCI insight · 2016Article
- Targeting Inhibitor of Apoptosis Proteins Protects from Bleomycin-Induced Lung Fibrosis.American journal of respiratory cell and molecular biology · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Patients with idiopathic pulmonary fibrosis (IPF) often do worse following infection, but the cause of the decline is not fully understood. We previously demonstrated that infection with a murine gamma herpes virus (γHV-68) could exacerbate established lung fibrosis following administration of fluorescein isothiocyanate (McMillan et al. Am J Respir Crit Care Med 177: 771-780, 2008). In the present study, we anesthetized mice and injected saline or bleomycin intratracheally on day 0. On day 14, mice were anesthetized again and infected with either a Gram-negative bacteria (Pseudomonas aeruginosa), or with H1N1 or γHV-68 viruses. Measurements were then made on days 15, 21, or 35. We demonstrate that infection with P. aeruginosa does not exacerbate extracellular matrix deposition post-bleomycin. Furthermore, fibrotic mice are effectively able to clear P. aeruginosa infection. In contrast, bleomycin-treated mice develop worse lung fibrosis when infected with γHV-68, but not when infected with H1N1. The differential ability of γHV-68 to cause increased collagen deposition could not be explained by differences in inflammatory cell recruitment or whole lung chemokine and cytokine responses. Alveolar epithelial cells from γHV-68-infected mice displayed increased expression of TGFβ receptor 1, increased SMAD3 phosphorylation, and evidence of apoptosis measured by cleaved poly-ADP ribose polymerase (PARP). The ability of γHV-68 to augment fibrosis required the ability of the virus to reactivate from latency. This property appears unique to γHV-68, as the β-herpes virus, cytomegalovirus, did not have the same effect.
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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.