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Background
Histamine is one of the major mediators involved in immune response and inflammation. As an inflammatory biogenic monoamine, it is widely distributed in various tissues of the human body and mediates a wide range of pathophysiological effects, including metamorphosis, gastrointestinal response, cell proliferation and differentiation, and immune response. It is synthesized from L-histidine by histidine decarboxylase catalysis, and later stored in cellular cytoplasmic vesicles or granules, where it acts as a mediator or neurotransmitter that binds to specific subtypes of receptors and thus exerts its biologically active effects.
Histamine receptors can be classified into four subtypes, all of which are members of the class A G-protein-coupled receptor family and regulate downstream signaling pathways by recruiting specific G proteins through histamine activation. In numerous diseases, different histamine receptors express different patterns and functions and produce different biological effects, suggesting that histamine and its receptors play a key role in various types of diseases. For example, H1 receptors play a very important role in mediating the development of allergic inflammation, including promoting dendritic cell maturation and regulating the balance between Th1/Th2 cells. H1 antihistamines act as inverse agonists to exert antihistamine effects, which directly inhibit calcium channels to suppress the release of inflammatory mediators from mast cells and basophils. It can also inhibit the expression of cell adhesion molecules by down-regulating the expression of NF-κB activated by H1 receptors, while reducing the production of some pro-inflammatory cytokines.
Figure 1. The location of histamine receptors in the human body (Source: Smolinska S, et al. 2022)
Histamine and its various subtypes of receptors are also expressed on tumors in a variety of cell types and are involved in tumor development, affecting tumor proliferation, migration, and invasion. There is increasing evidence that histamine is associated with many tumor cell motility, but numerous controversies remain regarding the different effects of histamine on tumor cells, such as promotion or inhibition of tumorigenesis and development. Some researchers have found that histamine can exacerbate the development of allergic inflammation and the process of angiogenesis and tissue fibrosis through H4R and H2R, respectively, altering the tumor microenvironment, which in turn may induce tumorigenesis. However, it has also been found that histamine can inhibit monocyte macrophage-induced reactive oxygen species production and release by inhibiting the activity of NADPH oxidase in myeloid cells, maintain the functional roles of T-lymphocytes and NK-cells, and enhance immune regulation, which in turn kills NK-cell-sensitive tumor cells, and improves patients' overall survival and progression-free survival.
References
1. Smolinska S, et al. Histamine: A Mediator of Intestinal Disorders-A Review. Metabolites. 2022 Sep 23;12(10):895.
2. Panula P. Histamine receptors, agonists, and antagonists in health and disease. Handb Clin Neurol. 2021;180:377-387.
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References
Thermal Hyperalgesia and Mechanical Allodynia Elicited by Histamine and Non-histaminergic Itch Mediators: Respective Involvement of TRPV1 and TRPA1
Acute itch is elicited by histamine, as well as non-histaminergic itch mediators including chloroquine, BAM8-22 and Ser-Leu-Ile-Gly-Arg-Leu (SLIGRL). When injected intradermally, histamine binds to histamine H1 and H4 receptors that activate transient receptor potential vanilloid 1 (TRPV1) to depolarize pruriceptors. Chloroquine, BAM8-22, and SLIGRL, respectively, bind to Mas-related G-protein-coupled receptors MrgprA3, MrgprC11, and MrgprC11/PAR2 that in turn activate transient receptor potential ankyrin 1 (TRPA1). In this study we tested if histamine, chloroquine, BAM8-22 and SLIGRL elicit thermal hyperalgesia and mechanical allodynia in adult male mice. We measured the latency of hindpaw withdrawal from a noxious heat stimulus, and the threshold for hindpaw withdrawal from a von Frey mechanical stimulus. Intraplantar injection of histamine resulted in significant thermal hyperalgesia (p < 0.001) and mechanical allodynia (p < 0.001) ipsilaterally that persisted for 1 h. Pretreatment with the TRPV1 antagonist AMG-517 (10 or 20 mu g), but not the TRPA1 antagonist HC-030031 (50 or 100 mu g), significantly attenuated the magnitude and time course of thermal hyperalgesia and mechanical allodynia elicited by histamine (p < 0.001 for both), indicating that these effects are mediated by TRPV1. In contrast, pretreatment with the TRPA1 antagonist significantly reduced thermal hyperalgesia and mechanical allodynia elicited by chloroquine (p < 0.001 for both), BAM-822 (p < 0.01, p < 0.001, respectively) and SLGRL (p < 0.05, p < 0.001, respectively), indicating that effects elicited by these non-histaminergic itch mediators require TRPA1. TRPV1 and TRPA1 channel inhibitors thus may have potential use in reducing hyperalgesia and allodynia associated with histaminergic and non-histaminergic itch, respectively. (C) 2020 IBRO. Published by Elsevier Ltd. All rights reserved.
Between two stools? Pharmacologists nominated for Nobel prizes in "physiology or medicine" and "chemistry" 1901-1950 with a focus on John Jacob Abel (1857-1938)
Since the early stages of its academic professionalization, pharmacology has been an interdisciplinary field strongly influenced by the natural sciences. Using the Nobel Prize as a lens to study the history of pharmacology, this article analyzes nominations of pharmacologists for two Nobel Prize categories, namely "chemistry" and "physiology or medicine" from 1901 to 1950. Who were they? Why were they proposed, and what do the Nobel dossiers say about excellence in pharmacology and research trends? This paper highlights the evaluation of "shortlisted" candidates, i.e., those candidates who were of particular interest for the members of the Nobel Committee in physiology or medicine. We focus on the US scholar John Jacob Abel (1857-1938), repeatedly referred to as the "Founder of American Pharmacology." Nominated 17 times in both categories, Abel was praised by his nominators for both basic research as well as for his influential positions as editor and his work as chair at Johns Hopkins University. The Abel nominations were evaluated for the Nobel Committee in chemistry by the Swedish professor of chemistry and pharmaceutics Einar Hammarsten (1889-1968), particularly interested in Abel's work on hormones in the adrenal glands and in the pituitary gland. Eventually, Hammarsten did not view Abel's work prizeworthy, partly because other scholars had done-according to Hammarsten-more important discoveries in the same fields. In conclusion, analyses of Nobel Prize nominations help us to better understand various meanings of excellence in pharmacology during the twentieth century and beyond.
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Figure 1. The location of histamine receptors in the human body
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