ArticleJournal of leukocyte biology2011
Endotoxin-induced uveitis is primarily dependent on radiation-resistant cells and on MyD88 but not TRIF.
Article in Journal of leukocyte biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Targeting Lung Damage: Amniotic Mesenchymal Stem Cells Mitigate Lipopolysaccharide-Induced Acute Lung Injury via Multiple Signaling Pathways.International journal of molecular sciences · 2025Article
- The Cellular Composition of the Uveal Immune Environment.Frontiers in medicine · 2021Review
- Article
- Selective Cannabinoid 2 Receptor Agonists as Potential Therapeutic Drugs for the Treatment of Endotoxin-Induced Uveitis.Molecules (Basel, Switzerland) · 2019Article
- Primed Mycobacterial Uveitis (PMU): Histologic and Cytokine Characterization of a Model of Uveitis in Rats.Investigative ophthalmology & visual science · 2015Article
- Unexpected Roles for Toll-Like Receptor 4 and TRIF in Intraocular Infection with Gram-Positive Bacteria.Infection and immunity · 2015Article
- Macrophages and Uveitis in Experimental Animal Models.Mediators of inflammation · 2015Review
- Caveolin-1 increases proinflammatory chemoattractants and blood-retinal barrier breakdown but decreases leukocyte recruitment in inflammation.Investigative ophthalmology & visual science · 2014Article
- Role of toll-like receptors in human iris pigment epithelial cells and their response to pathogen-associated molecular patterns.Journal of inflammation (London, England) · 2014Article
- TLR9 bone marrow chimeric mice define a role for cerebral TNF in neuroprotection induced by CpG preconditioning.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2012Article
- Impact of IL-1 signalling on experimental uveitis and arthritis.Annals of the rheumatic diseases · 2012Article
- Interplay between innate and adaptive immunity in the development of non-infectious uveitis.Progress in retinal and eye research · 2012Review
- Investigation of the differential potentials of TLR agonists to elicit uveitis in mice.Journal of leukocyte biology · 2011Article
- Why HLA-B27? My thirty-year quest: the Friedenwald lecture.Investigative ophthalmology & visual science · 2011Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
TLR4 activation by LPS (endotoxin) is mediated by the MyD88 and TRIF intracellular signaling pathways. We determined the relative activation of these pathways in murine ocular tissue after LPS exposure. Additionally, we explored whether BM-derived or non-BM-derived cells were the major contributors to EIU. Mice deficient in TRIF or MyD88 and their congenic (WT) controls received 250 ng ultrapure LPS ivt at 0 h. Ocular inflammation was assessed by histological analysis at 4, 6, and 24 h, and additionally, in MyD88(-/-) mice, intravital microscopy was performed at 4 h and 6 h to assess adherent, rolling, and infiltrating cells in the iris vasculature and tissue. Cytokines associated with the MyD88 and TRIF intracellular signaling pathways were analyzed in ocular tissue at 4 h. BM chimeric mice (WT→WT, TLR4(-/-)→WT, WT→TLR4(-/-)) received 250 ng LPS by ivt injection, and ocular tissues were examined by histology at 6 h. Lack of MyD88 resulted in a markedly diminished cellular response and reduced production of MyD88-related cytokines 4 h post-LPS treatment. In contrast, lack of TRIF led to reduced production of TRIF-related cytokines and no change in the cellular response to LPS. Therefore, the MyD88 pathway appears to be the dominant TLR4 pathway in EIU. Only WT → TLR4(-/-) chimeric mice were resistant to EIU, and this suggests, surprisingly, that non-BM-derived (radiation-resistant) cells in the eye play a greater role than BM-derived cells.
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