Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Publication alerts by email
  • Advertising
  • Job board
  • Contact
  • Clinical Research and Public Health
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Video Abstracts
  • Reviews
    • View all reviews ...
    • Pancreatic Cancer (Jul 2025)
    • Complement Biology and Therapeutics (May 2025)
    • Evolving insights into MASLD and MASH pathogenesis and treatment (Apr 2025)
    • Microbiome in Health and Disease (Feb 2025)
    • Substance Use Disorders (Oct 2024)
    • Clonal Hematopoiesis (Oct 2024)
    • Sex Differences in Medicine (Sep 2024)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Clinical Research and Public Health
    • Research Letters
    • Letters to the Editor
    • Editorials
    • Commentaries
    • Editor's notes
    • Reviews
    • Viewpoints
    • 100th anniversary
    • Top read articles

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Video Abstracts
  • In-Press Preview
  • Clinical Research and Public Health
  • Research Letters
  • Letters to the Editor
  • Editorials
  • Commentaries
  • Editor's notes
  • Reviews
  • Viewpoints
  • 100th anniversary
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Publication alerts by email
  • Advertising
  • Job board
  • Contact

The requested figure was not found.

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.
View: Text | PDF
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

  • Text
  • PDF
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

×

Total citations by year

Year: 2025 2024 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 2010 2009 Total
Citations: 6 10 9 8 6 13 16 12 21 7 19 18 16 9 9 5 1 185
Citation information
This citation data is accumulated from CrossRef, which receives citation information from participating publishers, including this journal. Not all publishers participate in CrossRef, so this information is not comprehensive. Additionally, data may not reflect the most current citations to this article, and the data may differ from citation information available from other sources (for example, Google Scholar, Web of Science, and Scopus).

Citations to this article in year 2024 (10)

Title and authors Publication Year
Exposure to Mycobacterium remodels alveolar macrophages and the early innate response to Mycobacterium tuberculosis infection
Mai D, Jahn A, Murray T, Morikubo M, Lim PN, Cervantes MM, Pham LK, Nemeth J, Urdahl K, Diercks AH, Aderem A, Rothchild AC
PLoS pathogens 2024
Aromatic amino acid metabolites alter interferon signaling and influenza pathogenesis
Anand G, Clark-Dinovo C, Perry AM, Goodwin VM, St. Raymond E, Sakleshpur S, Steed AL
Frontiers in Molecular Biosciences 2024
Zebrafish tsc1 and cxcl12a increase susceptibility to mycobacterial infection
Wright K, Han DJ, Song R, de Silva K, Plain KM, Purdie AC, Shepherd A, Chin M, Hortle E, Wong JJ, Britton WJ, Oehlers SH
Life science alliance 2024
A protective role for type I interferon signaling following infection with Mycobacterium tuberculosis carrying the rifampicin drug resistance-conferring RpoB mutation H445Y
Bobba S, Chauhan KS, Akter S, Das S, Mittal E, Mathema B, Philips JA, Khader SA
PLoS pathogens 2024
Mycobacterial CpsA activates type I IFN signaling in macrophages via cGAS-mediated pathway
Ding Y, Tong J, Luo G, Sun R, Bei C, Feng Z, Meng L, Wang F, Zhou J, Chen Z, Li D, Fan Y, Song S, Wang D, Feng CG, Liu H, Chen Q, Yan B, Gao Q
iScience 2024
Antimycobacterial and healing effects of Pranlukast against MTB infection and pathogenesis in a preclinical mouse model of tuberculosis
Rajmani RS, Surolia A
Frontiers in immunology 2024
Increased serum interferon activity in sarcoidosis compared to that in tuberculosis: Implication for diagnosis?
Schrijver B, Göpfert J, La Distia Nora R, Putera I, Nagtzaam NMAN, Smits Te Nijenhuis MAW, van Rijswijk ALCT, Ten Berge JCEM, van Laar JAM, van Hagen PM, Dik WA
Heliyon 2024
Intranasal vaccination with engineered BCG expressing CCL2 induces a stronger immune barrier against Mycobacterium tuberculosis than BCG.
Guo S, Ouyang J, Hu Z, Cao T, Huang C, Mou J, Gu X, Liu J
Molecular therapy : the journal of the American Society of Gene Therapy 2024
APOE Protects Against Severe Infection with Mycobacterium tuberculosis by Restraining Production of Neutrophil Extracellular Traps
Liu D, Mai D, Jahn AN, Murray TA, Aitchison JD, Gern BH, Urdahl KB, Aderem A, Diercks AH, Gold ES
bioRxiv 2024
Unmasking the hidden impact of viruses on tuberculosis risk
Darboe F, Reijneveld JF, Maison DP, Martinez L, Suliman S
Trends in immunology 2024

Advertisement

Copyright © 2025 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts

Blogged by 2
Highlighted by 1 platforms
178 readers on Mendeley
See more details