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 (654 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
An amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter.
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: Peremin; Histamine Dihydrochloride; Ceplene; Histamine Hydrochloride.
Where it fits in the MeSH classification
- Broader topics
- Biogenic Monoamines; Ethylamines; Imidazoles; Autacoids
- Narrower topics
- Methylhistamines
- See also
- Histamine Release; Hypersensitivity, Immediate; Receptors, Histamine
Related concepts
- Histidine
Research landscape
PubMed indexes 38,853 records tagged with the MeSH heading “Histamine” (counts retrieved 2026-10-31). 1,653 of them (4.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 29,929 records.
Reviews account for 2,114 records (5.4%) and meta-analyses for 23. Randomized controlled trials number 839 (2.2%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 29,929 |
| 2000-2009 | 4,207 |
| 2010-2019 | 3,064 |
| 2020 onward | 1,653 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,114 | 5.4% |
| Meta-analyses | 23 | 0.1% |
| Randomized controlled trials | 839 | 2.2% |
Method: PubMed query "Histamine"[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.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| The Role of Histamine and Histamine Receptors in Mast Cell-Mediated Allergy and Inflammation: The Hunt for New Therapeutic Targets | 2018 | Review article Design not recorded in structured metadata | 401 | cc by PMID 30150993 · DOI · PMC6099187 |
| Role of Histamine in Modulating the Immune Response and Inflammation | 2018 | Review article Design not recorded in structured metadata | 265 | cc by PMID 30224900 · DOI · PMC6129797 |
| Histamine Intolerance: The Current State of the Art | 2020 | Review article Design not recorded in structured metadata | 144 | cc by PMID 32824107 · DOI · PMC7463562 |
| Histaminylation alters collagen matrix mechanics and attenuates cardiac fibrosis post-myocardial infarction via mechanotransduction signaling axis | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42270610 · DOI · PMC13254370 |
The Role of Histamine and Histamine Receptors in Mast Cell-Mediated Allergy and Inflammation: The Hunt for New Therapeutic Targets [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Histamine and its receptors (H1R-H4R) play a crucial and significant role in the development of various allergic diseases.
- Closing excerpt
- In the present review, we examine the accumulating evidence suggesting novel therapeutic approaches that explore both H1R and H4R as therapeutic targets for histamine-mediated allergic diseases.
- 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 (170 words)
Histamine and its receptors (H1R-H4R) play a crucial and significant role in the development of various allergic diseases. Mast cells are multifunctional bone marrow-derived tissue-dwelling cells that are the major producer of histamine in the body. H1R are expressed in many cells, including mast cells, and are involved in Type 1 hypersensitivity reactions. H2R are involved in Th1 lymphocyte cytokine production. H3R are mainly involved in blood-brain barrier function. H4R are highly expressed on mast cells where their stimulation exacerbates histamine and cytokine generation. Both H1R and H4R have important roles in the progression and modulation of histamine-mediated allergic diseases. Antihistamines that target H1R alone are not entirely effective in the treatment of acute pruritus, atopic dermatitis, allergic asthma, and other allergic diseases. However, antagonists that target H4R have shown promising effects in preclinical and clinical studies in the treatment of several allergic diseases. In the present review, we examine the accumulating evidence suggesting novel therapeutic approaches that explore both H1R and H4R as therapeutic targets for histamine-mediated allergic diseases.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30150993 · DOI · PMC6099187
Role of Histamine in Modulating the Immune Response and Inflammation [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Inflammatory mediators, including cytokines, histamine, bradykinin, prostaglandins, and leukotrienes, impact the immune system, usually as proinflammatory factors.
- Closing excerpt
- We also evaluate the interactions between these effects.
- 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 (116 words)
Inflammatory mediators, including cytokines, histamine, bradykinin, prostaglandins, and leukotrienes, impact the immune system, usually as proinflammatory factors. Other mediators act as regulatory components to establish homeostasis after injury or prevent the inflammatory process. Histamine, a biogenic vasoactive amine, causes symptoms such as allergies and has a pleiotropic effect that is dependent on its interaction with its four histamine receptors. In this review, we discuss the dualistic effects of histamine: how histamine affects inflammation of the immune system through the activation of intracellular pathways that induce the production of inflammatory mediators and cytokines in different immune cells and how histamine exerts regulatory functions in innate and adaptive immune responses. We also evaluate the interactions between these effects.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30224900 · DOI · PMC6129797
Histamine Intolerance: The Current State of the Art [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Histamine intolerance, also referred to as enteral histaminosis or sensitivity to dietary histamine, is a disorder associated with an impaired ability to metabolize ingested histamine that was described at the beginning of the 21st century.
- Closing excerpt
- In this work, a glance on histamine intoxication will also be provided, as well as the analysis of some uncertainties historically associated to histamine intoxication outbreaks that may be better explained by the existence of interindividual susceptibility to ingested histamine.
- 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 (123 words)
Histamine intolerance, also referred to as enteral histaminosis or sensitivity to dietary histamine, is a disorder associated with an impaired ability to metabolize ingested histamine that was described at the beginning of the 21st century. Although interest in histamine intolerance has considerably grown in recent years, more scientific evidence is still required to help define, diagnose and clinically manage this condition. This article will provide an updated review on histamine intolerance, mainly focusing on its etiology and the existing diagnostic and treatment strategies. In this work, a glance on histamine intoxication will also be provided, as well as the analysis of some uncertainties historically associated to histamine intoxication outbreaks that may be better explained by the existence of interindividual susceptibility to ingested histamine.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32824107 · DOI · PMC7463562
Histaminylation alters collagen matrix mechanics and attenuates cardiac fibrosis post-myocardial infarction via mechanotransduction signaling axis [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Histaminylation is a newly discovered monoaminylation catalyzed by transglutaminase 2 (TGM2), and its role in myocardial fibrosis has not yet been elucidated.
- Closing excerpt
- This study also highlights a novel role of histamine in maintaining stress environment mechanical stability.
- 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 (245 words)
Histaminylation is a newly discovered monoaminylation catalyzed by transglutaminase 2 (TGM2), and its role in myocardial fibrosis has not yet been elucidated. Here, we identified histaminylation in cardiac type I collagen isolated from mice 7 days after acute myocardial infarction (AMI) by mass spectrometry. Using histamine-deficient Hdc-/- mice, we demonstrated an increase in TGM2-mediated γ-glutamyl-ε-lysine crosslinks and a higher myocardial Young's modulus in the scar region of Hdc-/- mice than in wild-type controls, indicating that histaminylation might restrain the role of TGM2 in cardiac fibrogenesis after AMI. Furthermore, we reconstituted an in vitro crosslinking system, yielding unmodified collagen and histaminylated collagen. The results of mechanical indentation and electron microscopy demonstrated that histaminylation could reduce crosslink formation, lower matrix stiffness, and alter viscoelasticity. Subsequently, primary murine cardiac fibroblasts were cultured under cyclic stretch with TGF-β on different substrates, and the results revealed that histaminylated collagen strongly attenuated TGF-β-induced fibroblast-to-myofibroblast transition and reduced focal adhesion assembly. Mechanically, integrated single-cell and bulk RNA-seq analyses indicated that the PIEZO1/ITGB1 mechanotransduction axis was upregulated and mediated downstream signal transduction in the infarcted hearts of Hdc-/- mice. Finally, local delivery of a histamine-releasing hydrogel to Hdc-/- mice after AMI could significantly reinstate collagen histaminylation and reduce crosslink abundance and cardiac dysfunction. Collectively, these data reveal that collagen histaminylation limits TGM2-dependent crosslinking, softens the extracellular matrix, and inhibits the PIEZO1/ITGB1 axis, thereby mitigating myocardial fibrosis after AMI. This study also highlights a novel role of histamine in maintaining stress environment mechanical stability.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42270610 · DOI · PMC13254370
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 Histamine in the nervous system [5]
- Research article The role of histamine and the tuberomamillary nucleus in the nervous system [6]
- Research article Histamine and histamine intolerance [7]
- Research article International Union of Basic and Clinical Pharmacology. XCVIII. Histamine Receptors [8]
- Research article Advances in H1-antihistamines [9]
- Research article Histamine and H1-antihistamines: celebrating a century of progress [10]
References
- Thangam EB, Jemima EA, Singh H, Baig MS, Khan M, Khan M, et al.. The Role of Histamine and Histamine Receptors in Mast Cell-Mediated Allergy and Inflammation: The Hunt for New Therapeutic Targets. . 2018. PMID 30150993 · DOI · PMC6099187
- Branco ACCC, Yoshikawa FSY, Pietrobon AJ, Sato MN. Role of Histamine in Modulating the Immune Response and Inflammation. . 2018. PMID 30224900 · DOI · PMC6129797
- Comas-Basté O, Sánchez-Pérez S, Veciana-Nogués MT, Latorre-Moratalla M, Vidal-Carou MDC. Histamine Intolerance: The Current State of the Art. . 2020. PMID 32824107 · DOI · PMC7463562
- Zhu J, Sun D, Zeng G, Wu K, Yang X, Zhu X, et al.. Histaminylation alters collagen matrix mechanics and attenuates cardiac fibrosis post-myocardial infarction via mechanotransduction signaling axis. . 2026. PMID 42270610 · DOI · PMC13254370
- Haas HL, Sergeeva OA, Selbach O. Histamine in the nervous system. Physiol Rev. 2008. PMID 18626069 · DOI
- Haas H, Panula P. The role of histamine and the tuberomamillary nucleus in the nervous system. Nat Rev Neurosci. 2003. PMID 12563283 · DOI
- Maintz L, Novak N. Histamine and histamine intolerance. Am J Clin Nutr. 2007. PMID 17490952 · DOI
- Panula P, Chazot PL, Cowart M, Gutzmer R, Leurs R, Liu WL, et al.. International Union of Basic and Clinical Pharmacology. XCVIII. Histamine Receptors. Pharmacol Rev. 2015. PMID 26084539 · DOI · PMC4485016
- Simons FE. Advances in H1-antihistamines. N Engl J Med. 2004. PMID 15548781 · DOI
- Simons FE, Simons KJ. Histamine and H1-antihistamines: celebrating a century of progress. J Allergy Clin Immunol. 2011. PMID 22035879 · 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.