Cited by 732Inflammasome and immune disordersImmune Response and InflammationBacillus and Francisella bacterial research

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The AIM2 inflammasome is critical for innate immunity to Francisella tularensis

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Fernandes-Alnemri, Teresa, Yu, Je-Wook, Juliana, Christine, Solorzano, Leobaldo, Kang, Seokwon, Wu, Jianghong, Datta, Pinaki, McCormick, Margaret, Huang, Lan, McDermott, Erin, Eisenlohr, Laurence, Landel, Carlisle P, Alnemri, Emad S·2010·Nature Immunology

DOI 10.1038/ni.1859PMC PMC3111085

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Abstract

Francisella tularensis, the causative agent of tularemia, infects host macrophages, which triggers production of the proinflammatory cytokines interleukin 1beta (IL-1beta) and IL-18. We elucidate here how host macrophages recognize F. tularensis and elicit this proinflammatory response. Using mice deficient in the DNA-sensing inflammasome component AIM2, we demonstrate here that AIM2 is required for sensing F. tularensis. AIM2-deficient mice were extremely susceptible to F. tularensis infection, with greater mortality and bacterial burden than that of wild-type mice. Caspase-1 activation, IL-1beta secretion and cell death were absent in Aim2(-/-) macrophages in response to F. tularensis infection or the presence of cytoplasmic DNA. Our study identifies AIM2 as a crucial sensor of F. tularensis infection and provides genetic proof of its critical role in host innate immunity to intracellular pathogens.

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Authors: Fernandes-Alnemri, T., Yu, J.-W., Juliana, C., Solorzano, L., Kang, S., Wu, J., Datta, P., McCormick, M., Huang, L., McDermott, E., Eisenlohr, L., Landel, C. P., & Alnemri, E. S.
Affiliations: Thomas Jefferson University (US)
Corresponding author: Alnemri, Emad S
ORCID: Yu, Je-Wook
Juliana, Christine
Kang, Seokwon
Huang, Lan
Eisenlohr, Laurence
Alnemri, Emad S
Venue: Nature Immunology
Publisher: Springer Science and Business Media LLC
Published: 2010-03-28
Volume: 11
Issue: 5
Pages: 385-393
ISSN: 1529-2908 (ISSN-L)
1529-2916
DOI: 10.1038/ni.1859
PMC: PMC3111085
OpenAlex: W2157305255
Cited by: 732
References: 45
Citations by year: 2026: 26 · 2025: 19 · 2024: 34 · 2023: 22 · 2022: 25 · 2021: 35 · 2020: 30 · 2019: 39 · 2018: 42 · 2017: 60 · 2016: 53 · 2015: 57 · 2014: 58 · 2013: 73 · 2012: 51
FWCI: 29.95
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springernature.com/gp/researchers/text-and-data-mining (tdm)
www.springernature.com/gp/researchers/text-and-data-mining (vor)
Locations: Nature Immunology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
YUHSpace (Yonsei University Medical Library) (submittedVersion, cc-by-nc-nd)
eScholarship (California Digital Library) (submittedVersion)
Funders: Harvard University
National Institutes of Health
National Institute on Aging (AG14357, R01AG014357)
National Cancer Institute (T32 CA09678, T32CA009678)
National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR-055398, R01AR055398)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bacillus and Francisella bacterial research
Keywords: AIM2 inflammasome, Francisella tularensis, tularemia, innate immunity, macrophages, cytosolic DNA sensing, caspase-1 activation, IL-1β, IL-18, intracellular bacterial infection, host defense
MeSH terms: Animals, Cells, Cultured, DNA-Binding Proteins, Francisella tularensis, Humans, Immunity, Innate, Interferon Type I, L-Lactate Dehydrogenase, Macrophages, Nuclear Proteins, Tularemia, Mice, Knockout, Calcium Signaling, Caspase 1, Multiprotein Complexes, Interferon Regulatory Factor-3, Mice, Interleukin-1beta, Protein Multimerization

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The AIM2 inflammasome is critical for innate immunity to Francisella tularensis

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