Evidence map›Paper›PMID 22033934›Full record

ArticleThe Journal of biological chemistry2011

TLR2 and RIP2 pathways mediate autophagy of Listeria monocytogenes via extracellular signal-regulated kinase (ERK) activation.

Paras K Anand, Stephen W G Tait, Mohamed Lamkanfi, Amal O Amer, Gabriel Nunez, Gilles Pagès, Jacques Pouysségur, Maureen A McGargill, Douglas R Green, Thirumala-Devi Kanneganti

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
8.8field-weighted citation impact, top 2% 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

79 citing papers in PubMed, 137 citations in OpenAlex.

  1. Article
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  4. Article
  5. Autophagy and Bacterial infections.Autophagy reports · 2025
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  13. Review
  14. Autophagy in peritoneal fibrosis.Frontiers in physiology · 2023
    Review
  15. Article
  16. International journal of molecular sciences · 2022
    Article
  17. Article
  18. A dynamically evolving war between autophagy and pathogenic microorganisms.Journal of Zhejiang University. Science. B · 2022
    Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 6 institutions in 3 countries.

Paras K AnandDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
Stephen W G Tait
Mohamed Lamkanfi
Amal O Amer
Gabriel Nunez
Gilles Pagès
Jacques Pouysségur
Maureen A McGargill
Douglas R Green
Thirumala-Devi Kanneganti
St. Jude Children's Research Hospital · USCentre Antoine Lacassagne · FRCentre National de la Recherche Scientifique · FRGhent University · BEInterface (United States) · USUniversity of Michigan–Ann Arbor · US

Funding

Role of NLR Inflammasomes in Autoinflammatory Diseases and Host DefenseR01AR056296 · NIAMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2008 to 2022
$5.9M
Role of caspases in Legionella pneumophila pulmonary infectionR01HL094586 · NHLBI · OHIO STATE UNIVERSITY · PI AMER, AMAL O · 2009 to 2013
$1.9M
NLR signaling in intestinal inflammationR21AI088177 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2010 to 2011
$460k
NHLBI NIH HHS R01 HL094586NIAID NIH HHS AI088177NIAID NIH HHS R21 AI088177NIAMS NIH HHS AR056296NIAMS NIH HHS R01 AR056296
6 · The paper itself

Abstract

Listeria monocytogenes is a facultative intracellular pathogen that invades both phagocytic and non-phagocytic cells. Recent studies have shown that L. monocytogenes infection activates the autophagy pathway. However, the innate immune receptors involved and the downstream signaling pathways remain unknown. Here, we show that macrophages deficient in the TLR2 and NOD/RIP2 pathway display defective autophagy induction in response to L. monocytogenes. Inefficient autophagy in Tlr2(-/-) and Nod2(-/-) macrophages led to a defect in bacteria colocalization with the autophagosomal marker GFP-LC3. Consequently, macrophages lacking TLR2 and NOD2 were found to be more susceptible to L. monocytogenes infection, as were the Rip2(-/-) mice. Tlr2(-/-) and Nod2(-/-) cells showed perturbed NF-κB and ERK signaling. However, autophagy against L. monocytogenes was dependent selectively on the ERK pathway. In agreement, wild-type cells treated with a pharmacological inhibitor of ERK or ERK-deficient cells displayed inefficient autophagy activation in response to L. monocytogenes. Accordingly, fewer bacteria were targeted to the autophagosomes and, consequently, higher bacterial growth was observed in cells deficient in the ERK signaling pathway. These findings thus demonstrate that TLR2 and NOD proteins, acting via the downstream ERK pathway, are crucial to autophagy activation and provide a mechanistic link between innate immune receptors and induction of autophagy against cytoplasm-invading microbes, such as L. monocytogenes.

Indexed as

AnimalsAutophagyBlotting, WesternCell LineCells, CulturedExtracellular Signal-Regulated MAP KinasesListeria monocytogenesListeriosisMacrophagesMiceMice, Mutant StrainsMicroscopy, Electron, TransmissionNod2 Signaling Adaptor ProteinReceptor-Interacting Protein Serine-Threonine Kinase 2Receptor-Interacting Protein Serine-Threonine KinasesSignal TransductionExtracellular Signal-Regulated MAP KinasesNod2 protein, mouseNod2 Signaling Adaptor ProteinReceptor-Interacting Protein Serine-Threonine Kinase 2Receptor-Interacting Protein Serine-Threonine KinasesRipk2 protein, mouseToll-Like Receptor 2

Identifiers

PMID22033934
PMCPMC3234870
OpenAlexW2065609114

What OpenQuestion holds

Textmetadata
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.