ArticleAmerican journal of respiratory and critical care medicine2009
Toll-like receptor 9 activation is a key mechanism for the maintenance of chronic lung inflammation.
Article in American journal of respiratory and critical care medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Toll-like Receptor 9 Inhibition Mitigates Fibroproliferative Responses in Translational Models of Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2025Article
- Mitochondrial DNA Sensing Pathogen Recognition Receptors in Systemic Sclerosis Associated Interstitial Lung Disease: A Review.Current treatment options in rheumatology · 2023Article
- Differential Analysis of Key Proteins Related to Fibrosis and Inflammation in Soluble Egg Antigen ofPathogens (Basel, Switzerland) · 2023Article
- Toll-like receptor 9 deficiency induces osteoclastic bone loss via gut microbiota-associated systemic chronic inflammation.Bone research · 2022Article
- The role of the adaptor molecule STING during Schistosoma mansoni infection.Scientific reports · 2020Article
- Toll-like Receptor 9 Signaling Is Augmented in Systemic Sclerosis and Elicits Transforming Growth Factor β-Dependent Fibroblast Activation.Arthritis & rheumatology (Hoboken, N.J.) · 2016Article
- Article
- Upregulation of cannabinoid receptor-1 and fibrotic activation of mouse hepatic stellate cells during Schistosoma J. infection: role of NADPH oxidase.Free radical biology & medicine · 2014Article
- The in vivo fibrotic role of FIZZ1 in pulmonary fibrosis.PloS one · 2014Article
- MHV68 latency modulates the host immune response to influenza A virus.Inflammation · 2013Article
- The linkage of innate and adaptive immune response during granulomatous development.Frontiers in immunology · 2013Article
- Alternaria induces STAT6-dependent acute airway eosinophilia and epithelial FIZZ1 expression that promotes airway fibrosis and epithelial thickness.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Toll like receptors in diseases of the lung.International immunopharmacology · 2011Review
- TLR9-induced interferon β is associated with protection from gammaherpesvirus-induced exacerbation of lung fibrosis.Fibrogenesis & tissue repair · 2011Article
- Therapeutic DNA vaccine reduces schistosoma mansoni-induced tissue damage through cytokine balance and decreased migration of myofibroblasts.The American journal of pathology · 2011Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
rationaleAccumulating evidence supports the hypothesis that the continuous host response to a persistent challenge can polarize the cytokine environment toward a Th2 cytokine phenotype, but the mechanisms responsible for this skewing are not clear.
objectivesWe investigated the role of Toll-like receptor 9 (TLR9) in a Th2-driven pulmonary granulomatous response initiated via the embolization of Schistosoma mansoni eggs to the lungs of mice.
methodsMice were intravenously injected with S. mansoni eggs. Histological and flow cytometric analysis, cytokine measurement, adoptive transfer of bone marrow (BM)-derived dendritic cells (DCs), and in vitro T-cell treatments with antigen-presenting cells were examined. MEASUREMENTS AND MAIN
resultsIn comparison to wild-type mice, TLR9(-/-) mice showed increased pulmonary granuloma size, augmented collagen deposition, increased Th2 cytokine phenotype, and impaired accumulation of DCs. BM-derived DCs, but not macrophages, recovered from animals with developed Th2-type lung granulomas promoted the production of type 2 cytokines from CD4(+) T cells. BM-derived DCs from TLR9(-/-) mice induced impaired Th1 cytokine and enhanced Th2 cytokine production by T cells, compared with DCs from WT mice. Macrophages from TLR9(-/-) mice expressed a significantly higher alternatively activated (M2) phenotype characterized by increased "found in inflammatory zone-1" (FIZZ1) and arginase-1 expression. The adoptive transfer of BM-derived DCs from syngeneic WT mice into TLR9(-/-) mice restored the granuloma phenotype seen in WT mice.
conclusionsThese studies suggest that TLR9 plays an important mechanistic role in the maintenance of the pulmonary granulomatous response.
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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.