ArticleImmunity2010
Cell-cell propagation of NF-κB transcription factor and MAP kinase activation amplifies innate immunity against bacterial infection.
Article in Immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
What it found
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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.
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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.
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Who cites it
69 citing papers in PubMed, 111 citations in OpenAlex.
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- Protective and pathogenic antibody responses from a primate Shigella outbreak inform vaccine design.bioRxiv : the preprint server for biology · 2025Article
- Propagation of monocyte exhaustion memory and underlying mechanisms.Cell communication and signaling : CCS · 2025Article
- Microgravity activates monocyte ERK1/2 signaling and modulates the response to lipopolysaccharide.Molecular medicine (Cambridge, Mass.) · 2025Article
- Mechanism of lactic acidemia-promoted pulmonary endothelial cells death in sepsis: role for CIRP-ZBP1-PANoptosis pathway.Military Medical Research · 2024Article
- DAMP sensing and sterile inflammation: intracellular, intercellular and inter-organ pathways.Nature reviews. Immunology · 2024Review
- Platelet transcription factors license the pro-inflammatory cytokine response of human monocytes.EMBO molecular medicine · 2024Article
- A two-step activation mechanism enables mast cells to differentiate their response between extracellular and invasive enterobacterial infection.Nature communications · 2024Article
- IFN-λ derived from nonsusceptible enterocytes acts on tuft cells to limit persistent norovirus.Science advances · 2023Article
- Mitogen-Activated Protein Kinases (MAPKs) and Enteric Bacterial Pathogens: A Complex Interplay.International journal of molecular sciences · 2023Review
- Know your neighbors: microbial recognition at the intestinal barrier and its implications for gut homeostasis and inflammatory bowel disease.Frontiers in cell and developmental biology · 2023Review
- Invading Bacterial Pathogens Activate Transcription Factor EB in Epithelial Cells through the Amino Acid Starvation Pathway of mTORC1 Inhibition.Molecular and cellular biology · 2022Article
- Mechanical Forces Govern Interactions of Host Cells with Intracellular Bacterial Pathogens.Microbiology and molecular biology reviews : MMBR · 2022Review
- NF-κB, a culprit of both inflamm-ageing and declining immunity?Immunity & ageing : I & A · 2022Review
- Ex Vivo Infection of Human Placental Explants byPathogens (Basel, Switzerland) · 2022Article
- Reprogramming of microRNA expression via E2F1 downregulation promotes Salmonella infection both in infected and bystander cells.Nature communications · 2021Article
- Bacterial detection by NAIP/NLRC4 elicits prompt contractions of intestinal epithelial cell layers.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Mechanical competition triggered by innate immune signaling drives the collective extrusion of bacterially infected epithelial cells.Developmental cell · 2021Article
- Immunity in Space: Prokaryote Adaptations and Immune Response in Microgravity.Life (Basel, Switzerland) · 2021Review
- Intercellular Transmission of Hepatic ER Stress in Obesity Disrupts Systemic Metabolism.Cell metabolism · 2021Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The enteroinvasive bacterium Shigella flexneri uses multiple secreted effector proteins to downregulate interleukin-8 (IL-8) expression in infected epithelial cells. Yet, massive IL-8 secretion is observed in Shigellosis. Here we report a host mechanism of cell-cell communication that circumvents the effector proteins and strongly amplifies IL-8 expression during bacterial infection. By monitoring proinflammatory signals at the single-cell level, we found that the activation of the transcription factor NF-κB and the MAP kinases JNK, ERK, and p38 rapidly propagated from infected to uninfected adjacent cells, leading to IL-8 production by uninfected bystander cells. Bystander IL-8 production was also observed during Listeria monocytogenes and Salmonella typhimurium infection. This response could be triggered by recognition of peptidoglycan and is mediated by gap junctions. Thus, we have identified a mechanism of cell-cell communication that amplifies innate immunity against bacterial infection by rapidly spreading proinflammatory signals via gap junctions to yet uninfected cells.
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Registered trials
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.