ArticleDevelopmental cell2012
LTB4 is a signal-relay molecule during neutrophil chemotaxis.
Article in Developmental cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 215 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.
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.
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Who cites it
215 citing papers in PubMed, 357 citations in OpenAlex.
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- Targeting the interactions between neutrophils and microglia: a novel strategy for anti-inflammatory treatment of stroke.Acta pharmacologica Sinica · 2026Review
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- Zebrafish macrophages convert physical wound signals into rapid vascular permeabilization.Nature communications · 2026Article
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- Modelling chemotaxis of branched cells in complex environments provides insights into immune cell navigation.PLoS computational biology · 2026Article
- Decoding mitochondrial signaling: neutrophil-tumor cell crosstalk in orchestrating cancer progression.Journal of translational medicine · 2026Review
- AN OPTIMIZED METHOD TO DIFFERENTIATE HL60 CELLS INTO NEUTROPHIL-LIKE CELLS.bioRxiv : the preprint server for biology · 2026Article
155 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
Neutrophil recruitment to inflammation sites purportedly depends on sequential waves of chemoattractants. Current models propose that leukotriene B(4) (LTB(4)), a secondary chemoattractant secreted by neutrophils in response to primary chemoattractants such as formyl peptides, is important in initiating the inflammation process. In this study we demonstrate that LTB(4) plays a central role in neutrophil activation and migration to formyl peptides. We show that LTB(4) production dramatically amplifies formyl peptide-mediated neutrophil polarization and chemotaxis by regulating specific signaling pathways acting upstream of actin polymerization and MyoII phosphorylation. Importantly, by analyzing the migration of neutrophils isolated from wild-type mice and mice lacking the formyl peptide receptor 1, we demonstrate that LTB(4) acts as a signal to relay information from cell to cell over long distances. Together, our findings imply that LTB(4) is a signal-relay molecule that exquisitely regulates neutrophil chemotaxis to formyl peptides, which are produced at the core of inflammation sites.
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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.