Role of histamine in the development of neurogenic inflammation of rat oral mucosa

1991 ◽  
Vol 32 (3-4) ◽  
pp. 229-236 ◽  
Author(s):  
A. Györfi ◽  
Á. Fazekas ◽  
E. Pósch ◽  
F. Irmes ◽  
L. Rosivall
Keyword(s):  
Oral Mucosa ◽  
Neurogenic Inflammation

Role of substance P (SP) in development of symptoms of neurogenic inflammation in the oral mucosa of the rat

1993 ◽  
Vol 28 (3) ◽  
pp. 191-196 ◽  
Author(s):  
A. Gyorfi ◽  
A. Fazekas ◽  
F. Irmes ◽  
G. Jakab ◽  
T. Suto ◽  
...  
Keyword(s):  
Substance P ◽  
Oral Mucosa ◽  
Neurogenic Inflammation

scholarly journals Immune Tolerance in the Oral Mucosa

2021 ◽  
Vol 22 (22) ◽  
pp. 12149
Author(s):  
Hector F. Pelaez-Prestel ◽  
Jose L. Sanchez-Trincado ◽  
Esther M. Lafuente ◽  
Pedro A. Reche
Keyword(s):  
Epithelial Cells ◽  
Oral Mucosa ◽  
Immune Cells ◽  
Commensal Bacteria ◽  
First Line ◽  
Innate And Adaptive Immunity ◽  
Oral Epithelial Cells ◽  
A Site ◽  
Oral Epithelial

The oral mucosa is a site of intense immune activity, where a large variety of immune cells meet to provide a first line of defense against pathogenic organisms. Interestingly, the oral mucosa is exposed to a plethora of antigens from food and commensal bacteria that must be tolerated. The mechanisms that enable this tolerance are not yet fully defined. Many works have focused on active immune mechanisms involving dendritic and regulatory T cells. However, epithelial cells also make a major contribution to tolerance by influencing both innate and adaptive immunity. Therefore, the tolerogenic mechanisms concurring in the oral mucosa are intertwined. Here, we review them systematically, paying special attention to the role of oral epithelial cells.

scholarly journals A critical role of AREG for bleomycin-induced skin fibrosis

2021 ◽  
Author(s):  
Mary Yinghua Zhang ◽  
Shuyi Fang ◽  
Hongyu Gao ◽  
Xiaoli Zhang ◽  
Dongsheng Gu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Oral Mucosa ◽  
Healing Process ◽  
Critical Role ◽  
Skin Fibrosis ◽  
Wound Healing Process ◽  
Organ Function ◽  
Signaling Axis

ABSTRACTWe report our discovery of an important player in the development of skin fibrosis, a hallmark of scleroderma. Scleroderma is a fibrotic disease, affecting 70,000 to 150,000 Americans. Fibrosis is a pathological wound healing process that produces an excessive extracellular matrix to interfere with normal organ function. Fibrosis contributes to nearly half of human mortality. Scleroderma has heterogeneous phenotypes, unpredictable outcomes, no validated biomarkers, and no effective treatment. Thus, strategies to slow down scleroderma progression represent an urgent medical need. While a pathological wound healing process like fibrosis leaves scars and weakens organ function, oral mucosa wound healing is a scarless process. After re-analyses of gene expression datasets from oral mucosa wound healing and skin fibrosis, we discovered that several pathways constitutively activated in skin fibrosis are transiently induced during oral mucosa wound healing process, particularly the amphiregulin (Areg) gene. Areg expression is upregulated ~10 folds 24hrs after oral mucosa wound but reduced to the basal level 3 days later. During bleomycin-induced skin fibrosis, a commonly used mouse model for skin fibrosis, Areg is up-regulated throughout the fibrogenesis and is associated with elevated cell proliferation in the dermis. To demonstrate the role of Areg for skin fibrosis, we used mice with Areg knockout, and found that Areg deficiency essentially prevents bleomycin-induced skin fibrosis. We further determined that bleomycin-induced cell proliferation in the dermis was not observed in the Areg null mice. Furthermore, we found that inhibiting MEK, a downstream signaling effector of Areg, by selumetinib also effectively blocked bleomycin-based skin fibrosis model. Based on these results, we concluded that the Areg-EGFR-MEK signaling axis is critical for skin fibrosis development. Blocking this signaling axis may be effective in treating scleroderma.

scholarly journals Role of apoptosis in erosive and reticular oral lichen planus exhibiting variable epithelial thickness

2008 ◽  
Vol 19 (3) ◽  
pp. 179-185 ◽  
Author(s):  
Juliana M. Caldeira Brant ◽  
Anilton C. Vasconcelos ◽  
Luciana V. Rodrigues
Keyword(s):  
Lichen Planus ◽  
Oral Mucosa ◽  
Oral Lichen Planus ◽  
Chronic Inflammatory Disease ◽  
Mechanical Trauma ◽  
Epithelial Thickness ◽  
Healthy Mucosa ◽  
Toxic Agents ◽  
Oral Lichen

Oral lichen planus (OLP) is a chronic inflammatory disease with different clinical types. Reticular and erosive forms are the most common. Although the cause of OLP remains speculative, many findings suggest auto-immune involvement, mediated by T lymphocytes against the basal keratinocytes. Inflammation, mechanical trauma or toxic agents can affect the epithelial homeostasia. Increased apoptosis may cause a decrease in epithelial thickness reflecting in the activity of the lesion. The objective of this study was to evaluate the occurrence of apoptosis and epithelial thickness in reticular and erosive forms of OLP. 15 samples of OLP each type (reticular and erosive) plus 10 of healthy mucosa were collected and processed. After morphometry, the apoptotic index and epitelial thickness were obtained. TUNEL and M30 CytoDEATH immunohistochemical assay were used to validate the morphologic criteria used. Apoptosis in the erosive OLP was significantly more intense than in the reticular type and both forms of OLP presented more apoptosis than the healthy oral mucosa. Healthy oral mucosa was thicker than both OLP forms and thicker in OLP reticular form than in the erosive one. The clinical differences between reticular and erosive forms of OLP are related to variations in epithelial thickness and in intensity of apoptosis.

528 THE ROLE OF NATURAL COMPOUND D161 IN NEUROGENIC INFLAMMATION

2009 ◽  
Vol 13 (S1) ◽  
Author(s):  
A.R. Lupu ◽  
L. Cremer ◽  
F. Kerek ◽  
A. Calugaru ◽  
N.S. Barzu ◽  
...  
Keyword(s):  
Natural Compound ◽  
Neurogenic Inflammation

scholarly journals Porphyromonas gingivalis Impairs Oral Epithelial Barrier through Targeting GRHL2

2019 ◽  
Vol 98 (10) ◽  
pp. 1150-1158 ◽  
Author(s):  
W. Chen ◽  
A. Alshaikh ◽  
S. Kim ◽  
J. Kim ◽  
C. Chun ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Oral Mucosa ◽  
Porphyromonas Gingivalis ◽  
Oral Bacteria ◽  
Conditional Knockout ◽  
Epithelial Barrier ◽  
Wild Type ◽  
Oral Epithelial ◽  
Junction Proteins

Oral mucosa provides the first line of defense against a diverse array of environmental and microbial irritants by forming the barrier of epithelial cells interconnected by multiprotein tight junctions (TJ), adherens junctions, desmosomes, and gap junction complexes. Grainyhead-like 2 (GRHL2), an epithelial-specific transcription factor, may play a role in the formation of the mucosal epithelial barrier, as it regulates the expression of the junction proteins. The current study investigated the role of GRHL2 in the Porphyromonas gingivalis ( Pg)–induced impairment of epithelial barrier functions. Exposure of human oral keratinocytes (HOK-16B and OKF6 cells) to Pg or Pg-derived lipopolysaccharides ( Pg LPSs) led to rapid loss of endogenous GRHL2 and the junction proteins (e.g., zonula occludens, E-cadherin, claudins, and occludin). GRHL2 directly regulated the expression levels of the junction proteins and the epithelial permeability for small molecules (e.g., dextrans and Pg bacteria). To explore the functional role of GRHL2 in oral mucosal barrier, we used a Grhl2 conditional knockout (KO) mouse model, which allows for epithelial tissue-specific Grhl2 KO in an inducible manner. Grhl2 KO impaired the expression of the junction proteins at the junctional epithelium and increased the alveolar bone loss in the ligature-induced periodontitis model. Fluorescence in situ hybridization revealed increased epithelial penetration of oral bacteria in Grhl2 KO mice compared with the wild-type mice. Also, blood loadings of oral bacteria (e.g., Bacteroides, Bacillus, Firmicutes, β- proteobacteria, and Spirochetes) were significantly elevated in Grhl2 KO mice compared to the wild-type littermates. These data indicate that Pg bacteria may enhance paracellular penetration through oral mucosa in part by targeting the expression of GRHL2 in the oral epithelial cells, which then impairs the epithelial barrier by inhibition of junction protein expression, resulting in increased alveolar tissue destruction and systemic bacteremia.

scholarly journals Videocapillaroscopy of the Oral Mucosa in Patients with Diabetic Foot: Possible Diagnostic Role of Microangiopathic Damage?

2020 ◽  
Vol 9 (11) ◽  
pp. 3641
Author(s):  
Giuseppe A. Scardina ◽  
Giovanni Guercio ◽  
Cesare F. Valenti ◽  
Domenico Tegolo ◽  
Pietro Messina
Keyword(s):  
Clinical Diagnosis ◽  
Oral Mucosa ◽  
Lower Limb ◽  
Diabetic Foot ◽  
Average Length ◽  
T Test ◽  
Control Group ◽  
Anova Test ◽  
Diagnostic Role

Introduction: Diabetic foot represents one of the most serious and expensive complications of diabetes and is subject to a high percentage of amputations that are almost always preceded by ulcers ascribable to neuropathy and/or vasculopathy. Videocapillaroscopy (VCS) can be a valuable aid in order to uncover morpho-structural anomalies in the vascular bed, both at the level of the oral mucosa and at the level of the terminal vessels of the lower limb. Materials and methods: Sixty subjects divided into 4 groups were enrolled: 15 healthy subjects; 15 patients with diabetes for more than 10 years without ulcerative foot lesions; 15 patients with neuropathic diabetic foot (clinical diagnosis, MDNS); 15 patients with ischemic diabetic foot (clinical diagnosis, ABI, lower limb doppler). A complete videocapillaroscopic mapping of the oral mucosa was carried out on each patient. The areas investigated were: labial mucosa, the retro-commissural region of the buccal mucosa, and the vestibular masticatory mucosa (II and V sextant). Results: The analysis of the morphological and densitometric characteristics of the capillaries revealed the following: a significant reduction in capillary density in neuropathic (mean ± SD 7.32 ± 2.1) and ischemic patients (mean ± SD 4.32 ± 3.2) compared to the control group of patients (both diabetic mean ± SD 12.98 ± 3.1 and healthy mean ± SD 19.04 ± 3.16) (ANOVA test and Bonferroni t test p < 0.05); a reduction in the average length of the capillaries and a significant increase in tortuosity (ANOVA test and Bonferroni t test p < 0.05). In the neuropathic patients, a recurrent capillaroscopic pattern that we defined as “sun” was found, with capillaries arranged radially around an avascular area. Conclusions: The data obtained from this preliminary study suggest a potential diagnostic role of oral capillaroscopy in the early and subclinical identification of microangiopathic damage in patients with diabetic foot.

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