The interplay between mast cells, pineal gland, and circadian rhythm: Links between histamine, melatonin, and inflammatory mediators

Abstract

Our daily rhythmicity is controlled by a circadian clock with a specific set of genes located in the suprachiasmatic nucleus in the hypothalamus. Mast cells (MCs) are major effector cells that play a protective role against pathogens and inflammation. MC distribution and activation are associated with the circadian rhythm via two major pathways, IgE/FcεRI‐ and IL‐33/ST2‐mediated signaling. Furthermore, there is a robust oscillation between clock genes and MC‐specific genes. Melatonin is a hormone derived from the amino acid tryptophan and is produced primarily in the pineal gland near the center of the brain, and histamine is a biologically active amine synthesized from the decarboxylation of the amino acid histidine by the L‐histidine decarboxylase enzyme. Melatonin and histamine are previously reported to modulate circadian rhythms by pathways incorporating various modulators in which the nuclear factor–binding near the κ light‐chain gene in B cells, NF‐κB, is the common key factor. NF‐κB interacts with the core clock genes and disrupts the production of pro‐inflammatory cytokine mediators such as IL‐6, IL‐13, and TNF‐α. Currently, there has been no study evaluating the interdependence between melatonin and histamine with respect to circadian oscillations in MCs. Accumulating evidence suggests that restoring circadian rhythms in MCs by targeting melatonin and histamine via NF‐κB may be promising therapeutic strategy for MC‐mediated inflammatory diseases. This review summarizes recent findings for circadian‐mediated MC functional roles and activation paradigms, as well as the therapeutic potentials of targeting circadian‐mediated melatonin and histamine signaling in MC‐dependent inflammatory diseases.

Increased peripheral inflammatory responses in myelin oligodendrocyte glycoprotein associated disease and aquaporin-4 antibody positive neuromyelitis optica spectrum disorder

“…Next, as endogenous IL-6 expression follows a stringent circadian rhythm ( 51 ) and therefore blood collections for IL-6 measurements at distance time points need to be synchronized, our retrospective study design did not allow this. In addition, availability of follow-up samples after approximately 6-12 months was limited hence; only 25 follow-up samples of NMOSD patients could be included.…”

Exploring the role of mast cells in the progression of liver disease

“…In addition, mast cells derived from CD34+/CD117+ hematopoietic stem cells stimulated by various stem cell factors (SCFs) and interleukins (ILs) in humans and rodents regulate the progression of liver disease ( Ma et al, 2017 ). The distribution and activation of MC are mediated by IgE/FcεRI and IL-33/ST2 signaling pathways ( Turner and Kinet, 1999 ; Liu et al, 2019 ; Pham et al, 2021 ). Upon activation, MCs secrete many peptidases and mediators, including chymase, tryptase, and histamine (HA) ( Gruber et al, 1997 ; Akers et al, 2000 ; Caughey, 2007 ).…”

Induction of Nrf2 Transctiption Factor Inhibits Formation of Ractive Oxygen and Nitrogen Species in Liver of Rats Under Modelling Metabolic Syndrome by Exposure to Round-the-Clock Lighting

“…Одним з найважливіших механізмів саморозвитку патологічних процесів при МС вважається тривала гіперактивація транскрипційних факторів (NF-κB, AP-1, STAT та ін) з подальшим збільшенням експресії генів, що кодують біосинтез низки прозапальних та прооксидантних білків [6]. Активація транскрипційних факторів, зокрема NF-κB, може бути пов'язана як з надлишком у раціоні вуглеводів та жирів («дієта західного типу») [7], так і зі змінами експресії індуцибельних генів центрального та периферичних циркадіанних осциляторів при порушенні світлового режиму [8].…”