Mast Cell Density Research Articles

The Neuroimmune Basis of Acupuncture: Correlation of Cutaneous Mast Cell Distribution with Acupuncture Systems in Human.

The hypothesis that cutaneous mast cells (MCs) are responsible for skin phenomena in acupuncture was proposed 40 years ago, but very little is known about the correlation of MC distribution with acupuncture systems in human. The aim of this study is to quantify cutaneous mast cells at different body sites and compare them with the distributions of classical acupuncture points and micro-acupuncture systems. Skin biopsies from dermatological practice were evaluated under microscope with H&E or CD117 stains. Dermal MCs were counted and expressed as MCs per high power field. Densities of classical acupuncture points at different body sites were also calculated and expressed as points per dm2. MC densities at special sites of the body were compared with micro-acupuncture systems. After examining 285 skin biopsies, MC enriched special sites (MESS) were found at peripheral parts of the body and around orifices of body surfaces. Comparative mapping showed that patterns of MC distribution are highly correlated with the distributions of classic acupuncture points in 14 classic acupuncture meridians, with the exception of the trunk areas. Mapping also revealed that all micro-acupuncture systems were established at MESS, including ear, scalp, hand, foot, eye, face, and umbilicus. The conclusion is that the densities of cutaneous MCs are highly correlated with classical acupuncture points and micro-acupuncture systems. These findings provide tissue evidence of neuroimmune basis of acupuncture and suggest that MC is a tissue target for acupuncture stimulation and may serve as a tissue marker for acupuncture points.

Mast Cells as an Indicator and Prognostic Marker in Molecular Subtypes of Breast Cancer.

Mast cells (MCs) represent the most controversial non-malignant element of the tumor microenvironment. Our aim was to study how MCs density and distribution (intratumoral-MCit versus peritumoral-MCpt) relate to tumor grade and molecular subtypes. MCs tryptase immunohistochemistry was performed on 80 cases of breast carcinomas. For Luminal A tumors, a partial correlation was detected between MCit and progesterone receptor (PR) (p=0.005). Luminal B tumors showed a significant correlation between MCpt and age (p=0.009), estrogen receptor (ER) (p=0.017) and PR (p=0.035). MCit and MCpt were strongly interrelated in this subtype (p=0.002) and in triple-negative breast cancers (p=0.002). In HER2 subtype, MCpt tumors were significantly correlated with HER2 (p=0.044). In G2 tumors, MCpt correlated with ER (p=0.015) and PR (p=0.038) while in G3 tumors ER correlated with both MCit (p=0.009) and MCpt (p=0.000487) tumors. MCs dynamics are strongly influenced by hormone receptors and HER2 status. MCit increased in aggressive tumor types and is a worse prognostic factor.

Mast cells induce epithelial-to-mesenchymal transition and migration in non-small cell lung cancer through IL-8/Wnt/β-catenin pathway.

Background: In the various cancer, mast cells (MCs) infiltration is correlated with a worse prognosis. There is an increasing evidence that MCs and their mediators are participated in remodeling of the tumor microenvironment and facilitate tumor growth, epithelial-to-mesenchymal transition (EMT) and metastasis.Methods: The transwell was conducted to evaluate the correlations between MCs and non-small cell lung cancer (NSCLC) cells in vitro. The RNA interference of β-catenin was performed to further explore the signaling pathway. Lung adenocarcinoma cell line A549 and human MC (HMC-1) were subcutaneously injected into BALB/c nude mice. The conventional experiment methods (such as quantitative RT-PCR Western Blot, Immunofluorescence, and ELISA) were used in the present study.Results: We found that high density of MCs in NSCLC correlates with worse prognosis. The NSCLC cells could release CCL5 and recruit MCs to the tumor microenvironment. Then, we explored that HMC-1 transplantation accelerated the growth of A549 cell in nude mice. Moreover, the MCs-derived factors were responsible for tumor growth. When NSCLC cells were activated, MCs produced various factors that induced EMT and migration. We also identified that CXCL8/interleukin (IL)-8 served as the major modulator containing in the activated MC conditioned medium. Furthermore, MCs and exogenous IL-8 promoted β-catenin phosphorylation in NSCLC cells. Inhibiting the Wnt/β-catenin pathway by RNA interference could revert EMT and migration of NSCLC.Conclusions: Our study suggests that MCs are recruited into NSCLC microenvironment and improve the EMT and migration of cancer cells, thereby accelerating the growth of NSCLC.

A STUDY ON THE MAST CELLS DENSITY IN THE WHOLE WALL OF INTRAPULMONARY BRONCHI AND BRONCHIOLES IN RATS OF DIFFERENT AGE USING TOLUIDINE BLUE STAINING

The contentious information concerning mast cells distribution in intrapulmonary airways in normal rat lung gave us a reason to perform this study. The aim of our study is to present the mast cells density in the whole wall of large-, small bronchi and bronchioles in rats of three different age groups in terms of the clinical significance. Mature and immature male Wistar rats were used. Sections from both left and right lung were stained with Toluidine blue. Distribution of mast cells was specified for the whole wall of intrapulmonary large-, small bronchi and bronchioles. The number of mast cells per airways` wall was compared between pulmonary lobes and different age groups. In conclusion, the topographic and age dependent differences in mast cell distribution found in this study implement the information about mast cell localization and help to elucidate the role of these cells in maintaining of lung homeostasis as well as the data can be used as referent values.

Immunohistochemical analysis of lymphatic vessel density and mast cells in oral tongue squamous cell carcinoma

The aim of this study was to analyze lymphangiogenesis and the presence of mast cells in oral tongue squamous cell carcinoma (OTSCC), correlating the findings with clinicopathological parameters (clinical stage, tumor size, nodal metastasis, histological grade of malignancy, local recurrence, and clinical outcome). Fifty-six cases of primary OTSCC were selected. Lymphatic vessels and mast cells were identified by immunostaining with anti-podoplanin (D2-40) and anti-tryptase antibody, respectively. Lymphatic vessel density (LVD) and mast cell density (MCD) were determined in the intratumoral and peritumoral areas. Intratumoral LVD was higher in advanced clinical stages (III/IV) when compared to early-stage (p = 0.017) and in metastatic cases compared to non-metastatic tumors (p = 0.013). Peritumoral LVD and intratumoral or peritumoral MCD did not differ significantly according to the clinicopathological parameters of OTSCCs (p > 0.05). No significant correlations between LVD and MCD were observed at the intratumoral (r = −0.014; p = 0.918) or peritumoral level (r = 0.156; p = 0.251). Our findings suggest that intratumoral lymphatic vessels, compared to peritumoral lymphatic vessels, appear to be more related to the progression of OTSCC. MCD alone does not seem to be determinant for lymphangiogenesis or for the biological behavior of OTSCC, indicating multiple pro- and antitumor effects of these inflammatory cells.

Functional Inhibitory Siglec-6 Is Upregulated in Human Colorectal Cancer-Associated Mast Cells.

Mast cells (MC) accumulate in colorectal cancer (CRC) and the relationship between MC density and cancer progression has been well recognized. MC can be either pro-tumor or anti-tumor players, depending on the local factors present in the tumor microenvironment. Upon malignant transformation, cancer cells express high levels of sialic acids on cell membrane or by secretion. Siglecs are a family of immunoglobulin-like receptors that bind sialic acids and each subtype has a distinct pattern of expression on immune cells. Among them, Siglec-6 is expressed predominately by MC. However, the function of Siglec-6 in MC is largely unexplored and whether it is expressed by CRC-associated MC remains unknown. In this study, we explored the function of Siglec-6 in CD34+ derived human MC. MC activation was initiated by IgE crosslinking with or without preincubation of anti-Siglec-6 Ab. Siglec-6 engagement significantly attenuated IgE-dependent MC degranulation as measured by ß-hexosaminidase release and CD63 expression. Interestingly, the production of GM-CSF was also shown reduced upon Siglec-6 engagement. To mimic the milieu of CRC, we cultured primary human MC with colon cancer cells or under hypoxia and Siglec-6 was then measured on these conditioned MC. Coculture with colon cancer cells (HT29 and Caco2) induced upregulation of Siglec-6 on MC. In comparison, normal colon cells (CCD841) had no effect. Also, a time-dependent increase of Siglec-6 by MC was observed under 1% O2. Immunohistochemistry of CRC tissue showed expression of Siglec-6 by MC in submucosa. Lectin immunochemistry revealed the presence of actual ligands for Siglec-6 in human CRC tissues. Together, our findings illustrate that Siglec-6 is a functionally inhibitory receptor on MC and suggest that Siglec-6 expression may be relevant for MC activity in the tumor microenvironment of CRC.

The role of inflammation in irritable bowel syndrome (IBS).

Irritable bowel syndrome (IBS) is a complex, functional gastrointestinal disorder characterized by chronic abdominal pain or discomfort and altered bowel habits. Despite the global prevalence and disease burden of IBS, its underlying pathophysiology remains unclear. Inflammation may play a pathogenic role in IBS. Studies have highlighted the persistence of mucosal inflammation at the microscopic and molecular level in IBS, with increased recruitment of enteroendocrine cells. Substantial overlaps between IBS and inflammatory bowel disease have also been reported. This review thus aimed to discuss the body of evidence pertaining to the presence of mucosal inflammation in IBS, its putative role in the disease process of IBS, and its clinical relevance. Increased mast cell density and activity in the gut may correlate with symptoms of visceral hypersensitivity. As evidenced by patients who develop postinfectious IBS, infective gastroenteritis could cause systemic inflammation and altered microbiome diversity, which in turn perpetuates a cycle of chronic, low-grade, subclinical inflammation. Apart from mucosal inflammation, neuroinflammation is probably involved in the pathophysiology of IBS via the “gut–brain” axis, resulting in altered neuroendocrine pathways and glucocorticoid receptor genes. This gives rise to an overall proinflammatory phenotype and dysregulated hypothalamic–pituitary–adrenal axis and serotonergic (5-HT) functioning, which could, at least in part, account for the symptoms of IBS. Although a definite and reproducible pattern of immune response has yet to be recognized, further research into anti-inflammatories may be of clinical value.

Low tumor infiltrating mast cell density confers prognostic benefit and reflects immunoactivation in colorectal cancer.

The role of mast cells (MCs) in colorectal cancer (CRC) progression was controversial. Thus, our study was designed to evaluate the prognostic value of MCs as well as their correlation with immune microenvironment. A retrospective cohort of CRC patients of stages I-IV was enrolled in our study. Consecutive patients (854) were divided into training set (427 patients) and validation set (427 patients) randomly. The findings were further validated in a GEO cohort, GSE39582 (556 patients). The mast cell density (MCD) was measured by immunohistochemical staining of tryptase or by CIBERSORT algorithm. Low MCD predicted prolonged overall survival (OS) in training and validation set. Moreover, MCD was identified as an independent prognostic indicator in both sets. Better stratification for CRC prognosis can be achieved by building a MCD based nomogram. The prognostic role of MCD was further validated in GSE39582. In addition, MCD predicted improved survival in stages II and III CRC patients receiving adjuvant chemotherapy (ACT). Multiple immune pathways were enriched in low MCD group while cytokines/chemokines promoting anti-tumor immunity were highly expressed in such group. Furthermore, MCD was negatively correlated with CD8+ T cells infiltration. In conclusion, MCD was identified as an independent prognostic factor, as well as a potential biomarker for ACT benefit in stages II and III CRC. Better stratification of CRC prognosis could be achieved by building a MCD based nomogram. Moreover, immunoactivation in low MCD tumors may contributed to improved prognosis.

Testosterone and Mast Cell Interactions in the Development of Kidney Fibrosis after Unilateral Ureteral Obstruction in Rats.

Mast cell and testosterone interactions involved in renal fibrosis in rats subjected to unilateral ureteral obstruction (UUO) were investigated. Orchiectomized (ORX) and nonorchiectomized Wistar rats were subjected to UUO, and a nonorchiectomized group was sham-operated (control: SO). Animals from the UUO group were treated with saline or sodium cromoglycate (CG). Some ORX rats from the saline or CG groups also received testosterone propionate replacement (TR). Kidneys and blood were collected 14 d after UUO or SO. Kidney sections were stained with toluidine blue to quantify mast cells, and picrosirius red was used for collagen analysis. Immunohistochemistry for α-smooth muscle actin (α-SMA) and proliferating cell nuclear antigen (PCNA) expression was also performed. Plasma testosterone levels (PTLs) were measured. ORX decreased and TR normalized PTLs. UUO increased mast cell density in the kidney pelvis, but not in the kidney parenchyma. UUO increased mast cell degranulation, and CG or ORX inhibited this effect. TR partially reversed the effect of ORX on mast cell degranulation, and CG partially inhibited that effect of TR. UUO increased the collagen areas of the renal parenchyma, whereas CG or ORX abolished that alteration; TR reversed the effects of ORX, and CG partially inhibited that effect of TR. UUO increased tubulointerstitial α-SMA expression and PCNA-positive cells, and these changes were sensitive to ORX or CG to the same degree, while TR again reversed the effect of ORX. Renal fibrosis after UUO appears to be determined by interactions between testosterone and mast cells.

An observational study of headaches in children and adolescents with functional abdominal pain: Relationship to mucosal inflammation and gastrointestinal and somatic symptoms.

Headaches and abdominal pain are among the most common pediatric pain conditions. Mast cells have been implicated in the pathophysiology of migraines, as well as functional dyspepsia (FD) and irritable bowel syndrome (IBS). The primary aims of the current study were to assess headache prevalence in patients with FD and to assess the association between headaches and mucosal mast cells and eosinophils. An additional aim was to explore associations of headache with other symptoms.We conducted a cross-sectional retrospective chart review of 235 consecutive patients with chronic abdominal pain. All patients had completed a standardized questionnaire as part of their routine clinical evaluation. Both gastrointestinal and non-gastrointestinal somatic symptoms were included in the analysis. All patients diagnosed with FD had undergone upper endoscopy with biopsies obtained from the gastric antrum and duodenum and these specimens were utilized to assess eosinophil and mast cell densities, respectively.Overall, 86% of patients fulfilled Rome IV criteria for FD. Headache was reported by 73.8% of FD patients versus 45.2% of non-FD patients (P = .001). Duodenal mast cell densities were significantly increased in those reporting headaches. Headache was not associated with any specific gastrointestinal symptoms but was associated with a wide array of non-gastrointestinal symptoms including fatigue, dizziness, muscle pain, joint pain, and chest pain.Headaches are common in children and adolescents with abdominal pain and, utilizing Rome IV criteria, are specifically associated with FD. In patients with FD, headaches are associated with increased duodenal mast cell density and a variety of somatic symptoms, all of which are possibly the result of mast cell activation.

Histopathological changes in the gastroduodenal mucosa of children with functional dyspepsia

Introduction and ObjectiveFunctional dyspepsia (FD) is a functional gastrointestinal disorder that affects a significant number of children presenting with chronic abdominal pain. A high proportion of these children undergo endoscopy to obtain mucosal biopsies which, by standard criteria, generally do not identify a clear explanation for symptoms. We undertook this study of children diagnosed with FD to elucidate the histopathological changes of gastroduodenal mucosa and to describe mast cell and eosinophil densities. MethodsIn this retrospective study, we evaluated 114 FD subjects and 10 control subjects from whom gastric antral and duodenal biopsies were available as formalin-fixed paraffin embedded tissue. We reviewed the H&E stained slides and performed immunohistochemistry for tryptase, to determine eosinophil and mast cell densities, respectively. ResultsWe found that the duodenal mucosa showed no evidence of inflammation in 86% of subjects, a median peak eosinophil count of 24 and a median peak mast cell count of 22. The histopathological features of the gastric antral mucosa comprised no evidence of inflammation in 52% of subjects, mild chronic inflammation in 41% of subjects, a median peak eosinophil count of 11.5 and a median peak mast cell count of 18. ConclusionsA significant proportion of children with FD do not show chronic or active inflammation, but have increased mast cell density and eosinophil density in the stomach and duodenum mucosa. Our study adds functional dyspepsia to the list of various abnormalities that have increased gastroduodenal mucosal elevations of eosinophils and/or mast cells.

Mast Cells Density in Hyperkeratosis, Dysplastic Oral Mucosa and Oral Squamous Cell Carcinoma

Background: Mast cells normally present in small numbers in the connective tissue of all organs and release a variety of potent mediators like histamine, leukotrienes, cytokines, chymase, basic fibroblast growth factor (bFGF), tryptase and heparin through degranulation. Objectives: The aim of the present study was the assessment of mast cell density in hyperkeratosis, dysplastic oral mucosa and oral squamous cell carcinoma (OSCC).Methods: In this retrospective analytical study, paraffinized specimens from 15 cases of normal mucosa and 23 cases of well-differentiated OSCC, cases of hyperkeratosis and dysplasia were selected. Sections were stained with toluidine blue and then were counted at 400× magnification in hotspot areas under a light microscope. The results were analyzed using ANOVA. P values less than 0.05 were considered significant. Results: Mast cells density (MCD) increased in hyperkeratosis, dysplasia, and OSCC. There was not any significant correlation between mast cell density and hyperkeratosis, dysplastic mucosa and normal mucosa. There were significant differences between mast cell counts in SCC and normal mucosa. Conclusions: MCD is higher in hyperkeratosis and dysplastic oral mucosa than in normal mucosa. There were significant differences between mast cell counts in SCC and normal mucosa.

Changes of gastric mucosal mast cells in patients with functional dyspepsia after Hylicobacter pylori infection

Objective To investigate the changes of gastric mucosal mast cells in patients with functional dyspepsia (FD) after Helicobacter pylori (H.pylori) infection, and to explore the correlation between the changes and dyspeptic symptoms. Methods From November 2012 to March 2014, 32 patients with FD and 16 asymptomatic patients (control group) from Beijing Jishuitan Hospital were enrolled. H. pylori infection situation was examined. The mucosal biopsies from gastric antrum and gastric body were taken for histological examination. The mast cells of gastric mucosa were detected by immunohistochemical stain. T test was performed for statistical analysis. Results Among 32 FD patients, 17 had H. pylori infection (one with gastric body involved, two with gastric antrum involved, 14 with both gastric antrum and gastric body involved), and 15 had no H. pylori infection. Among 16 asymptomatic patients, 12 had H. pylori infection and four had no H. pylori infection. Among FD patients, the percentage of degranulated mast cells in gastric mucosa with H. pylori infection group was (61.45±24.86)%, which was higher than that without H. pylori infection group ((48.34±21.63)%), and the difference was statistically significant (t=-2.145, P=0.036). The percentage of degranulated mast cells in gastric mucosa with H. pylori infection group was (29.73±12.99)%, which was higher than that without H. pylori infection group ((20.77±10.86)%), and the difference was statistically significant (t=-2.856, P=0.006). In H. pylori infection group, the percentage of degranulated mast cells in gastric body mucosa of FD patients was (66.99±18.85)%, which was higher than that of asymptomatic patients in control group ((46.77±8.43)%), and the difference was statistically significant (t=3.642, P=0.002). The ratio of degranulated mast cells in gastric body mucosa and the density of mast cells in gastric antrum mucosa of prandial distress syndrome (PDS) patients, the density of mast cells in gastric body mucosa of epigastric pain syndrome (EPS) patients and the ratio of degranulated mast cells in gastric body mucosa and the degree of degranulation of mast cells of PDS and EPS patients were all higher than those of asymptomatic patients in control group, and the differences were statistically significant (t=2.750, 3.601, 2.799, 9.522 and 5.755, all P<0.05). Conclusions The dyspeptic symptoms of FD patients with H. pylori infection is correlated with the changes of mast cells. With the infection of H. pylori, dyspeptic symptoms of different subtypes of FD may be correlated with the changes of mast cells in different gastric region. H. pylori infection may cause the dyspeptic symptoms of FD patients by increase the number and activation of mast cells. Key words: Helicobacter pylori; Mast cells; Functional dyspepsia; Dyspeptic symptom

Dermal nerve fibre and mast cell density, and proximity of mast cells to nerve fibres in the skin of patients with complex regional pain syndrome.

An interaction between cutaneous nerves and mast cells may contribute to pain in complex regional pain syndrome (CRPS). To explore this, we investigated the density of dermal nerve fibres, and the density and proximity of mast cells to nerve fibres, in skin biopsies obtained from the affected and unaffected limbs of 57 patients with CRPS and 28 site-matched healthy controls. The percentage of the dermis stained by the pan-neuronal marker protein gene-product 9.5 was lower in the affected limb of patients than in controls (0.12 ± 0.01% vs 0.22 ± 0.04%, P < 0.05), indicating a reduction in dermal nerve fibre density. This parameter did not correlate with CRPS duration. However, it was lower in the affected than unaffected limb of patients with warm CRPS. Dermal mast cell numbers were similar in patients and controls, but the percentage of mast cells less than 5 µm from nerve fibres was significantly lower in the affected and unaffected limbs of patients than in controls (16.8 ± 1.7%, 16.5 ± 1.7%, and 31.4 ± 2.3% respectively, P < 0.05). We confirm previous findings of a mild neuropathy in CRPS. Our findings suggest that this either develops very early after injury or precedes CRPS onset. Loss of dermal nerve fibres in CRPS might result in loss of chemotactic signals, thus halting mast cell migration toward surviving nerve fibres. Failure of normal nerve fibre-mast cell interactions could contribute to the pathophysiology of CRPS.

Mast Cells Density in Hyperkeratosis, Dysplastic Oral Mucosa and Oral Squamous Cell Carcinoma

Mast Cells Density in Hyperkeratosis, Dysplastic Oral Mucosa and Oral Squamous Cell Carcinoma

Cutaneous somatic and autonomic nerve TDP-43 deposition in amyotrophic lateral sclerosis.

To evaluate the involvement of the sensory and autonomic nervous system in amyotrophic lateral sclerosis (ALS) and to determine whether TDP-43/pTDP-43 deposits in skin nerve fibers signify a valuable biomarker for ALS. Eighteen patients with ALS and 18 age- and sex-matched control subjects underwent physical examinations, in addition to donating skin biopsies from the distal leg. The density of epidermal, Meissner's corpuscle (MC), sudomotor, and pilomotor nerve fibers were measured. Confocal microscopy was used to determine the cutaneous somatic and autonomic nerve fiber density and TDP-43/pTDP-43 deposition. Intraepidermal nerve fiber density (IENFD) was reduced in individuals with ALS (P < 0.001). MC density (MCD) (P = 0.001), sweat gland nerve fiber density (SGNFD) (P < 0.001), and pilomotor nerve fiber density (PNFD) (P < 0.001) were all reduced in ALS patients. The SGNFD correlated with the small-fiber neuropathy Symptoms Inventory Questionnaire (SFN-SIQ), VAS and age. The SFN-SIQ was higher in ALS with sensory symptoms than without sensory symptoms (P = 0.000). Furthermore, the SFN-SIQ was higher in ALS with autonomic symptoms than without autonomic symptoms (P = 0.002). SFN-SIQ was higher in ALS patients that were pTDP-43 positive than pTDP-43 negative (P = 0.04), respectively. We established in the peripheral nervous system that higher SFN-SIQ and VAS was involved in ALS, indicating the loss of SGNF. The deposition of TDP-43/pTDP-43 in ALS nerve fibers may indicate an important role in the underlying pathogenesis of ALS. This observation might be used as a potential biomarker for diagnosing ALS.

Sa1161 - Mast Cell Density is Increased in Children with Eosinophilic Esophagitis Who have Persistent Symptoms, Endoscopic Findings, or Epithelial Abnormalities Despite Low Eosinophil Counts after Treatment

Sa1161 - Mast Cell Density is Increased in Children with Eosinophilic Esophagitis Who have Persistent Symptoms, Endoscopic Findings, or Epithelial Abnormalities Despite Low Eosinophil Counts after Treatment

Neurokinin A augments SynCAM expression and IL-10 release from mast cells

Abstract Cutaneous mast cells (MCs) initiate innate and adaptive immune responses. In the skin, MCs reside proximal to peripheral nerve fibers, forming a functional synapse mediated, in part, by Synaptic Cell Adhesion Molecule (SynCAM). Within the synapse, MC function is likely affected by the release of soluble neuropeptides. We and others have demonstrated that the immune functions of MCs are affected by the neuropeptides from the tachykinin family. Substance P promotes MC-inflammatory functions, whereas the role of neurokinin A (NKA) in MC biology is hereto unknown. In this study, the capacity for NKA to regulate MC stasis and IgE-initiated MC activation was evaluated. In bone marrow derived (BM) MCs, NKA increased expression of SynCAM, but not expression of other cell adhesion molecules, such as ICAM or NCAM. In IgE-activated MCs, NKA did not affect SynCAM expression. However, NKA promoted IL-10 secretion resulting in the inhibition of IgE-initiated STAT5 phosphorylation and nuclear localization, leading to the inhibition of type 2 cytokine release. STAT5 phosphorylation was restored in NKA treated BMMCs by neutralizing IL-10. In vivo, intradermal administration of NKA increased the density of MCs in the skin. In spite of this increase in MCs, NKA reduced IgE-initiated passive cutaneous anaphylaxis. Our data indicates that NKA strengthens the formation of the MC-neuron synapse and down-regulates MC pro-inflammatory functions.

Correlation of elevated mast cell and micro-vessel densities with lymph node metastasis in oral squamous cell carcinoma

Correlation of elevated mast cell and micro-vessel densities with lymph node metastasis in oral squamous cell carcinoma

Expression and clinical significance of periostin in oral lichen planus.

Oral lichen planus (OLP) is a chronic inflammatory lesion involving the oral mucosa, which has a high likelihood of progressing to cancer. The present study investigated the periostin expression in the mucosa and serum of patients with OLP and its correlation with serum cytokines. A total of 117 patients with OLP and 110 healthy controls were included in the study. The protein expression of periostin were measured in the OLP and normal oral mucosa by immunohistochemistry. ELISA was performed to measure the serum levels of periostin, tumour necrosis factor-α (TNF-α), interleukin (IL)-6, interferon-γ (IFN-γ), IL-4 and thymic stromal lymphopoietin (TSLP). Compared with the control group the OLP group had a significantly increased number of cases with high periostin expression in the oral mucosa and a significantly increased serum periostin level (P<0.05). Among all 117 OLP subjects, high periostin expression was associated with higher serum IL-6, TNF-α, TSLP and tissue mast cell density. High periostin expression was also significantly associated with a lower IFN-γ/IL-4 ratio (P<0.05). The present study concluded that periostin expression was increased in the oral mucosa and serum of patients with OLP and was associated with inflammatory response, T helper 2 cytokine-predominant immune imbalance, increased mast cell count and TSLP. The modulation of periostin may represent an attractive novel therapeutic target.