Histamine metabolism and transport are deranged in human keratinocytes in oral lichen planus

Abstract

HOKs are histamine-producing cells. They release histamine via OCT3 channels in concentrations too low to activate the classical low-affinity H R and H R, but high enough to stimulate the high-affinity H R in autocrine and paracrine modes. The substantially deranged histamine metabolism and transport in OLP could, in part, contribute to the disease pathogenesis.

Role of the high mobility group box 1 signalling axes via the receptor for advanced glycation end‐products and toll‐like receptor‐4 in the immunopathology of oral lichen planus: a potential drug target?

“…In OLP, HMGB1 expression was noticeably increased. Such a dramatic change could be attributed to certain exogenous OLP‐relevant stimuli of HMGB1, such as bacterial lipopolysaccharide, or by endogenous cytokines, such as TNF‐ α and interferon‐gamma (IFN‐ γ ) . High mobility group box 1‐carrying DNA breaks could passively leak out from the damaged basal keratinocytes in OLP.…”

Histamine H4 receptor signalling in tongue cancer and its potential role in oral carcinogenesis - a short report

“…Environmental factors can also affect histamine metabolism. Previously, we have already shown that oral microbiota, via bacterial lipopolysaccharides (LPS), can affect HDC levels and stimulate the release of histamine from oral epithelial cells [13]. The present study was undertaken to characterize H 4 R in oral epithelial dysplasia (OED), OTSCC tissue samples and in two OTSCC-derived cell lines.…”

“…It is noteworthy that many cancer-derived cell lines and primary human neoplasias exhibit deranged levels of histamine and its synthesizing enzyme, L-histidine decarboxylase (HDC) [6,[10][11][12]. Recently, we reported that oral keratinocytes can synthesize and release histamine, in a biphasic manner, to regulate diverse responses in the oral mucosa [13]. We also showed that histamine metabolism is deranged in oral lichen planus (OLP), which is regarded as a potentially malignant lesion.…”

Extracellular interleukin‐17F has a protective effect in oral tongue squamous cell carcinoma

“…23 However, our findings in the present study suggest a nonsignificant correlation between the morphometrical distribution of the total inflammatory cells and the clinical status of patients with all-stages of oral tongue SCC. 30 In conclusion, extracellular mast cell-derived IL-17F has a protective role in oral tongue SCC. These molecules are released extracellularly either within minutes of activation (acute phase of disease) or over hours or even days (delayed or chronic phase).…”

“…Histamine remains inactive inside the granules of mast cells until its release upon degranulation to the oral mucosal environment. 30 In conclusion, extracellular mast cell-derived IL-17F has a protective role in oral tongue SCC. It also could separate high-risk from low-risk patients with early-stage oral tongue SCC.…”