Evidence map›Paper›PMID 21825018›Full record

ArticleThe Journal of experimental medicine2011

Preexisting helminth infection induces inhibition of innate pulmonary anti-tuberculosis defense by engaging the IL-4 receptor pathway.

Julius A Potian, Wasiulla Rafi, Kamlesh Bhatt, Amanda McBride, William C Gause, Padmini Salgame

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed, 1 pooled it
13.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

121 citing papers in PubMed, 1 synthesis or guideline pooled it, 215 citations in OpenAlex.

  1. Pooled it
  2. Pre-vaccinationFrontiers in immunology · 2024
    Trial
  3. Trial
  4. Trial
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Cytokine Responses duringMicroorganisms · 2023
    Article
  17. Article
  18. Article
  19. Mouse Models forPathogens (Basel, Switzerland) · 2022
    Review
  20. Article

61 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Julius A PotianDepartment of Medicine, University of Medicine and Dentistry of New Jersey, Newark, NJ 07101, USA.
Wasiulla Rafi
Kamlesh Bhatt
Amanda McBride
William C Gause
Padmini Salgame
National Center for Emerging and Zoonotic Infectious Diseases · USRutgers, The State University of New Jersey · US

Funding

Heminth Modulation of MtbR01AI069395 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SALGAME, PADMINI · 2007 to 2011
$2.8M
Helminth Modulation of the Protective Immune Response to TuberculosisF31AI075859 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI POTIAN, JULIUS ANDREW · 2007 to 2008
$50k
NIAID NIH HHS AI 069395NIAID NIH HHS AI075859NIAID NIH HHS F31 AI075859NIAID NIH HHS R01 AI069395
6 · The paper itself

Abstract

Tuberculosis and helminthic infections coexist in many parts of the world, yet the impact of helminth-elicited Th2 responses on the ability of the host to control Mycobacterium tuberculosis (Mtb) infection has not been fully explored. We show that mice infected with the intestinal helminth Nippostrongylus brasiliensis (Nb) exhibit a transitory impairment of resistance to airborne Mtb infection. Furthermore, a second dose of Nb infection substantially increases the bacterial burden in the lungs of co-infected mice. Interestingly, the Th2 response in the co-infected animals did not impair the onset and development of the protective Mtb-specific Th1 cellular immune responses. However, the helminth-induced Th2 environment resulted in the accumulation of alternatively activated macrophages (AAMs) in the lung. Co-infected mice lacking interleukin (IL) 4Rα exhibited improved ability to control Mtb infection, which was accompanied by significantly reduced accumulation of AAMs. Moreover, IL-4Rα(-/-) mice adoptively transferred with wild-type macrophages had a significantly higher Mtb load in their lungs compared with those that received IL-4Rα(-/-) macrophages, suggesting a direct contribution for the IL-4R pathway to the heightened susceptibility of co-infected animals. The Th2 response can thus enhance the intracellular persistence of Mtb, in part by mediating the alternative activation of macrophages via the IL-4Rα signaling pathway.

Indexed as

Immunity, InnateAnimalsImmunity, CellularInterleukin-4 Receptor alpha SubunitLungMacrophagesMiceMice, Inbred BALB CMice, KnockoutMycobacterium tuberculosisNippostrongylusReceptors, Cell SurfaceSignal TransductionStrongylida InfectionsTh1 CellsTh2 CellsIl4ra protein, mouseInterleukin-4 Receptor alpha SubunitReceptors, Cell Surface

Identifiers

PMID21825018
PMCPMC3171086
OpenAlexW2153234950

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.