Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (690 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The major metabolite in neutrophil polymorphonuclear leukocytes. It stimulates polymorphonuclear cell function (degranulation, formation of oxygen-centered free radicals, arachidonic acid release, and metabolism). (From Dictionary of Prostaglandins and Related Compounds, 1990)
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Leukotriene B-4; B-4, Leukotriene; Leukotriene B 4; LTB4; 5,12-diHETE; 5,12 diHETE; 5,12-HETE; 5,12 HETE.
Where it fits in the MeSH classification
- Broader topics
- Leukotrienes
Research landscape
PubMed indexes 6,012 records tagged with the MeSH heading “Leukotriene B4” (counts retrieved 2026-10-31). 245 of them (4.1%) were published from 2020 onward, and the busiest period so far is through 1999 with 4,021 records.
Reviews account for 365 records (6.1%) and meta-analyses for 2. Randomized controlled trials number 158 (2.6%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 4,021 |
| 2000-2009 | 1,026 |
| 2010-2019 | 720 |
| 2020 onward | 245 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 365 | 6.1% |
| Meta-analyses | 2 | 0.0% |
| Randomized controlled trials | 158 | 2.6% |
Method: PubMed query "Leukotriene B4"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
Opposing roles of LTB4 and PGE2 in regulating the inflammasome-dependent scorpion venom-induced mortality [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Tityus serrulatus sting causes thousands of deaths annually worldwide.
- Closing excerpt
- We suggest COX1/2 inhibition as an effective therapeutic intervention for scorpion envenomation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (148 words)
Tityus serrulatus sting causes thousands of deaths annually worldwide. T. serrulatus-envenomed victims exhibit local or systemic reaction that culminates in pulmonary oedema, potentially leading to death. However, the molecular mechanisms underlying T. serrulatus venom (TsV) activity remain unknown. Here we show that TsV triggers NLRP3 inflammasome activation via K(+) efflux. Mechanistically, TsV triggers lung-resident cells to release PGE2, which induces IL-1β production via E prostanoid receptor 2/4-cAMP-PKA-NFκB-dependent mechanisms. IL-1β/IL-1R actions account for oedema and neutrophil recruitment to the lungs, leading to TsV-induced mortality. Inflammasome activation triggers LTB4 production and further PGE2 via IL-1β/IL-1R signalling. Activation of LTB4-BLT1/2 pathway decreases cAMP generation, controlling TsV-induced inflammation. Exogenous administration confirms LTB4 anti-inflammatory activity and abrogates TsV-induced mortality. These results suggest that the balance between LTB4 and PGE2 determines the amount of IL-1β inflammasome-dependent release and the outcome of envenomation. We suggest COX1/2 inhibition as an effective therapeutic intervention for scorpion envenomation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26907476 · DOI · PMC4766425
Liquid chromatography/mass spectrometry analysis of exhaled leukotriene B4 in asthmatic children [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundThe role of leukotriene (LT) B4, a potent inflammatory mediator, in atopic asthmatic and atopic nonasthmatic children is largely unknown.
- Closing excerpt
- LC/MS/MS analysis of exhaled LTB4 might provide a non-invasive, sensitive, and quantitative method for airway inflammation assessment in asthmatic children.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (235 words)
BackgroundThe role of leukotriene (LT) B4, a potent inflammatory mediator, in atopic asthmatic and atopic nonasthmatic children is largely unknown. The lack of a gold standard technique for measuring LTB4 in exhaled breath condensate (EBC) has hampered its quantitative assessment in this biological fluid. We sought to measure LTB4 in EBC in atopic asthmatic children and atopic nonasthmatic children. Exhaled nitric oxide (NO) was measured as an independent marker of airway inflammation.MethodsFifteen healthy children, 20 atopic nonasthmatic children, 25 steroid-naïve atopic asthmatic children, and 22 atopic asthmatic children receiving inhaled corticosteroids were studied. The study design was of cross-sectional type. Exhaled LTB4 concentrations were measured using liquid chromatography/mass spectrometry-mass spectrometry (LC/MS/MS) with a triple quadrupole mass spectrometer. Exhaled NO was measured by chemiluminescence with a single breath on-line method. LTB4 values were expressed as the total amount (in pg) of eicosanoid expired in the 15-minute breath test. Kruskal-Wallis test was used to compare groups.ResultsCompared with healthy children [87.5 (82.5-102.5) pg, median and interquartile range], exhaled LTB4 was increased in steroid-naïve atopic asthmatic [255.1 (175.0-314.7) pg, p ConclusionIn contrast to exhaled NO concentrations, exhaled LTB4 values are selectively elevated in steroid-naïve atopic asthmatic children, but not in atopic nonasthmatic children. Although placebo control studies are warranted, inhaled corticosteroids seem to reduce exhaled LTB4 in asthmatic children. LC/MS/MS analysis of exhaled LTB4 might provide a non-invasive, sensitive, and quantitative method for airway inflammation assessment in asthmatic children.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 16236169 · DOI · PMC1283153
Effects of perioperative supplementation with omega-3 fatty acids on leukotriene B₄ and leukotriene B₅ production by stimulated neutrophils in patients with colorectal cancer: a randomized, placebo-controlled intervention trial [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Omega-3 fatty acids (n-3 FA) may have beneficial clinical and immune-modulating effects in surgical patients.
- Closing excerpt
- In conclusion, oral n-3 FA exerts anti-inflammatory effects in surgical patients, without reducing the risk of postoperative complications.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (157 words)
Omega-3 fatty acids (n-3 FA) may have beneficial clinical and immune-modulating effects in surgical patients. In a randomized, double-blind, prospective, placebo-controlled trial, 148 patients referred for elective colorectal cancer surgery received an n-3 FA-enriched oral nutritional supplement (ONS) providing 2.0 g of eicosapentaenoic acid (EPA) and 1.0 g of docosahexaenoic acid (DHA) per day or a standard ONS for seven days before surgery. On the day of operation, there was a significant increase in the production of leukotriene B5 (LTB5) (p < 0.01) and 5-hydroxyeicosapentaenoic acid (5-HEPE) (p < 0.01), a significant decrease in the production of leukotriene B4 (LTB4) (p < 0.01) and a trend for a decrease in the production of 5-hydroxyeicosatetraenoic acid (5-HETE) (p < 0.1) from stimulated neutrophils in the active group compared with controls. There was no association between LTB4 values and postoperative complications. In conclusion, oral n-3 FA exerts anti-inflammatory effects in surgical patients, without reducing the risk of postoperative complications.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 25268838 · DOI · PMC4210906
A genetically encoded sensor for visualizing leukotriene B4 gradients in vivo [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Leukotriene B4 (LTB4) is a potent lipid chemoattractant driving inflammatory responses during host defense, allergy, autoimmune and metabolic diseases.
- Closing excerpt
- GEM-LTB4 thus serves as a broadly applicable tool for analyzing LTB4 dynamics in various experimental systems and model organisms.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (150 words)
Leukotriene B4 (LTB4) is a potent lipid chemoattractant driving inflammatory responses during host defense, allergy, autoimmune and metabolic diseases. Gradients of LTB4 orchestrate leukocyte recruitment and swarming to sites of tissue damage and infection. How LTB4 gradients form and spread in live tissues to regulate these processes remains largely elusive due to the lack of suitable tools for monitoring LTB4 levels in vivo. Here, we develop GEM-LTB4, a genetically encoded green fluorescent LTB4 biosensor based on the human G-protein-coupled receptor BLT1. GEM-LTB4 shows high sensitivity, specificity and a robust fluorescence increase in response to LTB4 without affecting downstream signaling pathways. We use GEM-LTB4 to measure ex vivo LTB4 production of murine neutrophils. Transgenic expression of GEM-LTB4 in zebrafish allows the real-time visualization of both exogenously applied and endogenously produced LTB4 gradients. GEM-LTB4 thus serves as a broadly applicable tool for analyzing LTB4 dynamics in various experimental systems and model organisms.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37528073 · DOI · PMC10393954
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Leukotrienes and lipoxins: structures, biosynthesis, and biological effects [5]
- Research article The role of arachidonic acid oxygenation products in pain and inflammation [6]
- Research article Leukotrienes [7]
- Research article Leukotriene B4 in inflammation [8]
- Research article Leukotrienes and airway responses [9]
- Research article Leukotriene B4 [10]
References
- Zoccal KF, Sorgi CA, Hori JI, Paula-Silva FW, Arantes EC, Serezani CH, et al.. Opposing roles of LTB4 and PGE2 in regulating the inflammasome-dependent scorpion venom-induced mortality. . 2016. PMID 26907476 · DOI · PMC4766425
- Montuschi P, Martello S, Felli M, Mondino C, Barnes PJ, Chiarotti M. Liquid chromatography/mass spectrometry analysis of exhaled leukotriene B4 in asthmatic children. . 2005. PMID 16236169 · DOI · PMC1283153
- Sorensen LS, Thorlacius-Ussing O, Rasmussen HH, Lundbye-Christensen S, Calder PC, Lindorff-Larsen K, et al.. Effects of perioperative supplementation with omega-3 fatty acids on leukotriene B₄ and leukotriene B₅ production by stimulated neutrophils in patients with colorectal cancer: a randomized, placebo-controlled intervention trial. . 2014. PMID 25268838 · DOI · PMC4210906
- Tamás SX, Roux BT, Vámosi B, Dehne FG, Török A, Fazekas L, et al.. A genetically encoded sensor for visualizing leukotriene B4 gradients in vivo. . 2023. PMID 37528073 · DOI · PMC10393954
- Samuelsson B, Dahlén SE, Lindgren JA, Rouzer CA, Serhan CN. Leukotrienes and lipoxins: structures, biosynthesis, and biological effects. Science. 1987. PMID 2820055 · DOI
- Davies P, Bailey PJ, Goldenberg MM, Ford-Hutchinson AW. The role of arachidonic acid oxygenation products in pain and inflammation. Annu Rev Immunol. 1984. PMID 6100476 · DOI
- Hammarström S. Leukotrienes. Annu Rev Biochem. 1983. PMID 6311078 · DOI
- Ford-Hutchinson AW. Leukotriene B4 in inflammation. Crit Rev Immunol. 1990. PMID 2155000
- Drazen JM, Austen KF. Leukotrienes and airway responses. Am Rev Respir Dis. 1987. PMID 2821857 · DOI
- Crooks SW, Stockley RA. Leukotriene B4. Int J Biochem Cell Biol. 1998. PMID 9608670 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.