Cited by 162Immune Response and InflammationIron Metabolism and DisordersInflammasome and immune disorders

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Selective modulation of TLR4-activated inflammatory responses by altered iron homeostasis in mice

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Wang, Lijian, Harrington, Lynne, Trebicka, Estela, Shi, Hai Ning, Kagan, Jonathan C., Hong, Charles C., Lin, Herbert Y., Babitt, Jodie L., Cherayil, Bobby J.·2009·Journal of Clinical Investigation

DOI 10.1172/jci39939PMC PMC2769199

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Abstract

Mice deficient in the hemochromatosis gene, Hfe, have attenuated inflammatory responses to Salmonella infection associated with decreased macrophage TNF-alpha and IL-6 biosynthesis after exposure to LPS. In this study, we show that the abnormal cytokine production is related to impaired TLR4 signaling. Despite their abnormal response to LPS, Hfe KO macrophages produced amounts of TNF-alpha similar to those in WT cells after TLR2 stimulation. Consistent with this finding, LPS-induced activation of Mal/MyD88-dependent events was normal in the mutant macrophages. However, LPS-induced IFN-beta expression, a TRAM/TRIF-dependent response activated by TLR4, was reduced by Hfe deficiency. This reduction could be replicated in WT macrophages with the use of iron chelators. In contrast, TLR3-activated expression of IFN-beta, a TRIF-dependent response, was normal in Hfe KO macrophages and was unaffected by iron chelation. Our data suggest that low intracellular iron selectively impairs signaling via the TLR4/TRAM/TRIF pathway proximal to TRIF and results in reduced LPS-induced cytokine expression. Furthermore, by mimicking the altered iron metabolism associated with Hfe deficiency, we found that 3 different inhibitors of hepcidin attenuated Salmonella-induced and noninfectious enterocolitis. Thus, manipulation of iron homeostasis could represent a new therapeutic approach to controlling inflammation.

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Authors: Wang, L., Harrington, L., Trebicka, E., Shi, H. N., Kagan, J. C., Hong, C. C., Lin, H. Y., Babitt, J. L., & Cherayil, B. J.
Affiliations: Harvard University (US)
Massachusetts General Hospital (US)
Boston Children's Hospital (US)
Vanderbilt University Medical Center (US)
Corresponding author: Cherayil, Bobby J.
ORCID: Wang, Lijian
Shi, Hai Ning
Kagan, Jonathan C.
Hong, Charles C.
Lin, Herbert Y.
Babitt, Jodie L.
Cherayil, Bobby J.
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2009-10-05
Volume: 119
Issue: 11
Pages: 3322-8
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci39939
PMC: PMC2769199
OpenAlex: W2167404536
Cited by: 162
References: 44
Citations by year: 2026: 2 · 2025: 9 · 2024: 6 · 2023: 4 · 2022: 7 · 2021: 11 · 2020: 8 · 2019: 14 · 2018: 9 · 2017: 6 · 2016: 7 · 2015: 11 · 2014: 13 · 2013: 10 · 2012: 9
FWCI: 6.47
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health
U.S. Public Health Service (R01 071837)
National Heart, Lung, and Blood Institute (K08HL081535)
National Institute of Allergy and Infectious Diseases (R00AI072955)
National Institute of Diabetes and Digestive and Kidney Diseases (P30DK040561)
Topics: Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Keywords: TLR4 signaling, iron homeostasis, hemochromatosis, macrophages, lipopolysaccharide, interferon-beta, TLR2, TLR3, TNF-α, interleukin-6, salmonellosis, enterocolitis, inflammation, iron chelation
MeSH terms: Animals, Enterocolitis, Gene Expression Regulation, Hemochromatosis, Homeostasis, Immunity, Innate, Inflammation, Iron, Lipopolysaccharides, Macrophages, Mice, Inbred C57BL, Salmonella Infections, Signal Transduction, Mice, Knockout, Toll-Like Receptor 4, Mice, Myeloid Differentiation Factor 88

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Selective modulation of TLR4-activated inflammatory responses by altered iron homeostasis in mice

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