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Citations to this article

Intranasal Poly-IC treatment exacerbates tuberculosis in mice through the pulmonary recruitment of a pathogen-permissive monocyte/macrophage population
Lis R.V. Antonelli, … , Carl G. Feng, Alan Sher
Lis R.V. Antonelli, … , Carl G. Feng, Alan Sher
Published April 12, 2010
Citation Information: J Clin Invest. 2010;120(5):1674-1682. https://doi.org/10.1172/JCI40817.
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Research Article Infectious disease Article has an altmetric score of 11

Intranasal Poly-IC treatment exacerbates tuberculosis in mice through the pulmonary recruitment of a pathogen-permissive monocyte/macrophage population

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Abstract

Type I IFN has been demonstrated to have major regulatory effects on the outcome of bacterial infections. To assess the effects of exogenously induced type I IFN on the outcome of Mycobacterium tuberculosis infection, we treated pathogen-exposed mice intranasally with polyinosinic-polycytidylic acid condensed with poly-l-lysine and carboxymethylcellulose (Poly-ICLC), an agent designed to stimulate prolonged, high-level production of type I IFN. Drug-treated, M. tuberculosis–infected WT mice, but not mice lacking IFN-αβ receptor 1 (IFNαβR; also known as IFNAR1), displayed marked elevations in lung bacillary loads, accompanied by widespread pulmonary necrosis without detectable impairment of Th1 effector function. Importantly, lungs from Poly-ICLC–treated M. tuberculosis–infected mice exhibited a striking increase in CD11b+F4/80+Gr1int cells that displayed decreased MHC II expression and enhanced bacterial levels relative to the same subset of cells purified from infected, untreated controls. Moreover, both the Poly-ICLC–triggered pulmonary recruitment of the CD11b+F4/80+Gr1int population and the accompanying exacerbation of infection correlated with type I IFN–induced upregulation of the chemokine-encoding gene Ccl2 and were dependent on host expression of the chemokine receptor CCR2. The above findings suggest that Poly-ICLC treatment can detrimentally affect the outcome of M. tuberculosis infection, by promoting the accumulation of a permissive myeloid population in the lung. In addition, these data suggest that agents that stimulate type I IFN should be used with caution in patients exposed to this pathogen.

Authors

Lis R.V. Antonelli, Antonio Gigliotti Rothfuchs, Ricardo Gonçalves, Ester Roffê, Allen W. Cheever, Andre Bafica, Andres M. Salazar, Carl G. Feng, Alan Sher

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Total citations by year

Year: 2025 2024 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 2010 2009 Total
Citations: 5 10 9 8 6 13 16 12 21 7 19 18 16 9 9 5 1 184
Citation information
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Citations to this article in year 2023 (9)

Title and authors Publication Year
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Suhas Bobba, Nicole Howard, Shibali Das, Mushtaq Ahmed, Nargis Khan, Ignacio Marchante, Linrui Tang, Shyamala Thirunavukkarasu, Michelle Larsen, Luis Barreiro, Barun Mathema, Joaquín Sanz, Maziar Divangahi, Shabaana Khader.
mBio 2023
The Complexity of Interferon Signaling in Host Defense against Protozoan Parasite Infection
Deng S, Graham ML, Chen XM
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Pathogenicity of Type I Interferons in Mycobacterium tuberculosis
Mundra A, Yegiazaryan A, Karsian H, Alsaigh D, Bonavida V, Frame M, May N, Gargaloyan A, Abnousian A, Venketaraman V
International journal of molecular sciences 2023
Inflammatory monocytes promote granuloma control of Yersinia infection.
Sorobetea D, Matsuda R, Peterson ST, Grayczyk JP, Rao I, Krespan E, Lanza M, Assenmacher CA, Mack M, Beiting DP, Radaelli E, Brodsky IE
Nature Microbiology 2023
Mycobacterium tuberculosis and its clever approaches to escape the deadly macrophage.
Krishnan V, Nath S, Nair P, Das B
World Journal of Microbiology & Biotechnology 2023
Co-infection of mice with SARS-CoV-2 and Mycobacterium tuberculosis limits early viral replication but does not affect mycobacterial loads
Baker PJ, Amaral EP, Castro E, Bohrer AC, Torres-Juárez F, Jordan CM, Nelson CE, Barber DL, Johnson RF, Hilligan KL, Mayer-Barber KD
Frontiers in immunology 2023
Host Genetic Impact on Infectious Diseases among Different Ethnic Groups
Naidoo L, Arumugam T, Ramsuran V
2023
Early cellular mechanisms of type I interferon-driven susceptibility to tuberculosis.
Kotov DI, Lee OV, Fattinger SA, Langner CA, Guillen JV, Peters JM, Moon A, Burd EM, Witt KC, Stetson DB, Jaye DL, Bryson BD, Vance RE
Cell 2023
Nucleic acid sensing promotes inflammatory monocyte migration through biased coagulation factor VIIa signaling
Zelaya H, Grunz K, Nguyen TS, Habibi A, Witzler C, Reyda S, Gonzalez-Menendez I, Quintanilla-Martinez L, Bosmann M, Weiler H, Ruf W
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