Total Number Of Mast Cells Research Articles

Relationship between mast cells and E-cadherin in odontogenic keratocysts and radicular cysts.

This study aimed to evaluate tryptase and E-cadherin protein expression in odontogenic keratocysts (OKCs) and radicular cysts (RCs) and their relationship with lesion size. Thirty OKC and 30 RC cases were analyzed by immunohistochemistry. Tryptase expression was quantitatively assessed using the quantification of mast cells, and expression of E-cadherin was semi-quantitatively analyzed estimating the proportion of positive cells: 1 = less than 25% of immunopositive cells; 2 = 26 to 50% of immunopositive cells; 3 = 51 to 75% of immunopositive cells; 4 = more than 75% of immunopositive cells. Data on cystic lesion sizes were obtained from patients' clinical files, based on previous radiographic exams, and the lesions were categorized into three groups: group 1 (< 2 to 2cm); group 2 (> 2 to 4cm), and group 3 (> 4cm). Higher mast cell means were found for RCs, with the predominance of degranulated mast cells in both OKCs and RCs (p = 0.082). Concerning the epithelial component, a higher concentration of degranulated mast cells was detected in RCs (p = 0.000). Regarding connective tissue, degranulated mast cells were more evident in OKCs (p = 0.762). A negative correlation was observed between E-cadherin expression and total number of mast cells (p = 0.011), degranulated mast cells (p = 0.040), and degranulated mast cells in both superficial (p = 0.035) and deep connective tissues (p = 0.009). Concerning lesion size, a negative correlation with total number of mast cells (p = 0.016) and number of degranulated mast cells (p = 0.049) was observed, both in the epithelial components. Herein, the larger the lesion size, the lower the number of degranulated mast cells in the epithelium (r = - 0.271; p = 0.49), suggesting that these cells play a role in the initial cystic expansion phase. The higher expression of tryptase in degranulated mast cells was linked to a lower expression of E-cadherin, which may be related to a change in the epithelial permeability in these lesions, contributing to increased cystic content and lesion growth. Evidence of the relationship between mast cells and E-cadherin in the growth of odontogenic cysts was studied.

Mast Cell Expression in Heart Transplant Acute Cellular Rejection (ACR): A Retrospective Single Institution Analysis

Purpose Heart transplant patients require close follow-up with endomyocardial biopsies, which is the gold standard. Acute cellular rejection (ACR) in endomyocardial biopsies is graded using ISHLT criteria (1990, 2005). The role of mast cells is not very well studied in ACR; results of experimental murine models are ambiguous. To our knowledge, there are no studies specifically analyzing mast cells in ACR for human cardiac transplantation. In our study, we aimed to show whether or not mast cell infiltrates can be used to differentiate low from high grade ACR. Methods This single-institution retrospective study included 42 cases of grade 2/1R (ISHLT 1990/2005) and higher grades of ACR between 2/2016 and 9/2018. 8 cases of ISHLT grade 0 were also examined to serve as a control set. All cases were divided into 3 groups (Table). Mast cells were identified and counted using CD117 immunohistochemistry at 400x magnification. Total mast cell count per biopsy as well as average number of mast cell per fragment (defined by 2mm square) were evaluated. ANOVA and post hoc analysis were performed. Results Biopsies with any ACR showed statistically higher mast cells when compared to negative biopsies. A one way between subjects ANOVA of the three groups was performed and showed a statistically significant difference (p=0.0007). Post hoc analysis utilizing the Tukey-Kramer test revealed a statistically significant difference between grades 3a/3b and grade 0 (q=5.81) and grade 2 and grade 0 (q=3.73). Although grades 3a/3b showed higher average and total number of mast cells when compared to grade 2 ACR, this was not statistically significant. Conclusion Our results show that the total and average number of mast cells per fragment in higher grades of ACR (3a,3b, 2) are significantly higher than grade 0 ACR. The average number of mast cells between grades 3a/3b and grade 2 was not statistically significant. Overall, these results show that mast cells may play an active role in higher stages of acute cellular rejection.

Spinal Cord Glycine Transporter 2 Mediates Bilateral ST35 Acupoints Sensitization in Rats with Knee Osteoarthritis.

The concept of “acupoint sensitization” refers to the functional status of acupoint switches from silent to active under pathological conditions. In clinic, acupoint sensitization provides important guidance for acupoints selection in different diseases. However, the mechanism behind this phenomenon remains unclear. We generated a model of knee osteoarthritis (KOA) by intra-articular injection of monosodium iodoacetate (MIA) into the left knee of rats. The paw withdrawal mechanical threshold (PWMT) and the total number of mast cells as well as mast cell degranulation rate (MCDR) of acupoint tissue were used to test whether the acupoints were sensitized. The results showed that KOA resulted in a reduced mechanical threshold and elevated total number of mast cell as well as mast cell degranulation rate at bilateral ST35 (Dubi) but not GB37 (Guangming) or nonacupoint area. The acupoint sensitization was accompanied by upregulation of glycine transporter 2 (GlyT2) and reduction of extracellular glycine levels in the bilateral dorsal horns of the spinal cord at L3-5. Selective inhibition of GlyT2 or intrathecal administration of glycine attenuated ST35 acupoint sensitization. The sensitization of bilateral ST35 was blocked after intraspinal GlyT2 short hairpin (sh) RNA (GlyT2-shRNA) microinjection to specifically downregulate GlyT2 expression in the left side (ipsilateral) L3-5 spinal cord dorsal horn before MIA injection. Moreover, electroacupuncture (EA) stimulation at ST35 ameliorated articular pathological lesions and improved KOA-related pain behaviors. GlyT2-shRNA injection reversed EA-induced pain relief but not EA-induced reduction of joint lesions. Overall, this study demonstrated that spinal GlyT2, especially elevated GlyT2 expression in the ipsilateral dorsal horn of the spinal cord, is a crucial mediator of ST35 acupoint sensitization in KOA rats.

Skin Mast Cell Promotion in Random Skin Flaps in Rats using Bone Marrow Mesenchymal Stem Cells and Amniotic Membrane

Background:Skin flap procedures are employed in plastic surgery, but failure can lead to necrosis of the flap. Studies have used bone marrow mesenchymal stem cells (BM-MSCs) to improve flap viability. BM-MSCs and acellular amniotic membrane (AAM) have been introduced as alternatives. The objective of this study was to evaluate the effect of BM-MSCs and AAM on mast cells of random skin flaps (RSF) in rats.Methods:RSFs (80 × 30 mm) were created on 40 rats that were randomly assigned to one of four groups, including (I) AAM, (II) BM-MSCs, (III) BM-MSCs/AAM, and (IV) saline (control). Transplantation was carried out during the procedure (zero day). Flap necrosis was observed on day 7, and skin samples were collected from the transition line of the flap to evaluate the total number and types of mast cells. The development and the total number of mast cells were related to the development of capillaries.Results:The results of one-way ANOVA indicated that there was no statistically significant difference between the mean numbers of mast cell types for different study groups. However, the difference between the total number of mast cells in the study groups was statistically significant (p = 0.001).Conclusion:The present study suggests that the use of AAM/BM-MSCs can improve the total number of mast cells and accelerate the growth of capillaries at the transient site in RSFs in rats.

Uncontrolled asthmatics have increased FceRI+ and TGF-β-positive MCTC mast cells and collagen VI in the alveolar parenchyma.

Asthma has been associated with increased collagen deposition in both conducting airways and alveolar parenchyma. Mast cells (MCs) are key effector cells in asthma and have the ability to affect collagen synthesis. However, the link between clinical control and changes in bronchial and alveolar MC phenotypes and specific collagens in controlled and uncontrolled asthma remains unknown. To investigate MC phenotypes in correlation with deposition of specific collagen subtypes in patients with controlled and uncontrolled asthma as well as to healthy controls. The tissue expression of IgE+ , FcεRI+ and TGF-β+ MCs, as well as immunoreactivity of collagen I, III and VI, was assessed using immunohistochemistry on bronchial and transbronchial biopsies from controlled asthmatics (n=9), uncontrolled asthmatics (n=16) and healthy controls (n=8). In the alveolar parenchyma, the total number of MCs, as well as the number of FcεRI+ MCs and pro-fibrotic TGF-β+ MCTC, was significantly increased in uncontrolled asthma compared to both controlled asthma and healthy controls. The proportion of TGF-β+ MCTC correlated positively to an increased immunoreactivity of alveolar collagen VI but not collagen I and III. Collagen VI was increased in the alveolar parenchyma of uncontrolled asthmatics compared to controlled asthmatics. Controlled asthmatics had an increased deposition of alveolar collagen I. In bronchi, the immunoreactivity of collagen I was increased in both controlled and uncontrolled asthmatics while collagen III was increased only in controlled asthmatics. Patients with uncontrolled atopic asthma have an altered pro-fibrotic MCTC phenotype in the alveolar parenchyma that is associated with alveolar collagen VI. The present data thus support distal lung mast cell and matrix changes as histopathological features of asthma that may be of particular clinical relevance in patients who have remaining symptoms despite conventional inhaler therapy.

Mast cell inhibition as a therapeutic approach in fibrodysplasia ossificans progressiva (FOP).

Episodic flare-ups of fibrodysplasia ossificans progressiva (FOP) are characterized clinically by severe, often posttraumatic, connective tissue swelling and intramuscular edema, followed histologically by an intense and highly angiogenic fibroproliferative reaction. This early inflammatory and angiogenic fibroproliferative response is accompanied by the presence of abundant mast cells far in excess of other reported myopathies. Using an injury-induced, constitutively-active transgenic mouse model of FOP we show that mast cell inhibition by cromolyn, but not aprepitant, results in a dramatic reduction of heterotopic ossification. Cromolyn, but not aprepitant, significantly decreases the total number of mast cells in FOP lesions. Furthermore, cromolyn specifically diminishes the number of degranulating and resting degranulated mast cells in pre-osseous lesions. This work demonstrates that consideration of FOP as a type of localized mastocytosis may offer new therapeutic interventions for treatment of this devastating condition.

Siramesine causes preferential apoptosis of mast cells in skin biopsies from psoriatic lesions.

Skin mast cells are implicated as detrimental effector cells in various inflammatory skin diseases such as contact eczema, atopic dermatitis and psoriasis. Selective reduction of cutaneous mast cells, e.g. by inducing targeted apoptosis, might prove a rational and efficient therapeutic strategy in dermatoses negatively influenced by mast cells. The objective of the present study was to evaluate whether a lysosomotropic agent such as siramesine can cause apoptosis of mast cells present in psoriatic lesions. Punch biopsies were obtained from lesional and uninvolved skin in 25 patients with chronic plaque psoriasis. After incubation with siramesine, the number of tryptase-positive mast cells and their expression of interleukin (IL)-6 and IL-17 was analysed. Skin biopsies were digested to allow flow cytometric analysis of the drug's effect on cutaneous fibroblasts and keratinocytes. Siramesine caused a profound reduction in the total number of mast cells in both lesional and uninvolved psoriatic skin biopsies without affecting the gross morphology of the tissue. The drug reduced the density of IL-6- and IL-17-positive mast cells, and showed antiproliferative effects on epidermal keratinocytes but had no apparent cytotoxic effect on keratinocytes or dermal fibroblasts. Considering the pathophysiology of psoriasis, the effects of siramesine on cutaneous mast cells may prove favourable from the therapeutic aspect. The results encourage further studies to assess the usefulness of siramesine and other lysosomotropic agents in the treatment of cutaneous mastocytoses and inflammatory skin diseases aggravated by dermal mast cells.

Effects of Nigella sativa seeds and certain species of fungi extracts on number and activation of dural mast cells in rats.

In this study, we aimed to investigate the effects of Nigella sativa seeds and certain species of fungi extracts on the number and degranulation states of dural mast cells in rats. Rats were fed ad libitum with normal tap water or tap water with extract of N. sativa seed, Ramaria condensata, Lactarius salmonicolor, Lactarius piperatus, and Tricholoma terreum for 3 days. Mast cells in dura mater were counted and evaluated in terms of granulation and degranulation states. Compound 48/80, a mast cell degranulating agent, and T. terreum significantly increased the percent of degranulated mast cells in dura mater, respectively (p < 0.01 and p < 0.05). Moreover, T. terreum causes a significant increase in the total number of mast cells (p < 0.05). N. sativa significantly inhibited mast cell degranulation induced by both the compound 48/80 and T. terreum (p < 0.05), and significantly decreased the mast cell numbers increased by T. terreum (p < 0.05). Our results suggested that T. terreum following ingestion can contribute to headaches like migraine via dural mast cell degranulation and N. sativa may be able to exert analgesic and anti-inflammatory effects by stabilizing dural mast cells. However, investigation is needed to determine the ingredients of N. sativa that may be responsible for these beneficial effects.

Serum tryptase levels in melanoma patients: case-control study and review of the literature.

Serum tryptase results from the constant release of the enzyme from mast cells and serum tryptase levels are commonly considered to be related to the total number of mast cells. They are increased in several malignancies, as pancreatic carcinoma, angiosarcoma, hepatic carcinoma and proliferative and/or non-proliferative hematological disorders. Contrariwise, it has been reported that the number of tryptase- and chymase-positive mast cells was lower in deeply invasive melanoma compared to in-situ melanoma and dysplastic nevi. Considering the underlying pathophysiological linkages between mast cells and melanocytes and that serum tryptase is related to angiogenesis, tissue-degrading proprieties and metastatization, we have decided to evaluate serum tryptase levels in melanoma patients and in a healthy control. We performed a case-control study evaluating serum tryptase in melanoma and in healthy group. Starting from an initial general analysis, we have performed a sub-analysis for each sample. In general population serum tryptase was statistically higher in elderly patients. Generally, in melanoma patients, median serum tryptase was in lower normal range. We found a decreasing of serum tryptase levels from the healthy control to thin (≤1.00 mm Breslow thickness), reaching the lowest levels in thicker melanoma (≥1.01 mm Breslow thickness), in ulcerated and metastatic melanoma. Tryptase may have a protective role in melanoma or in the early stage of the tumorigenesis. Serum tryptase is an easy and useful biomarker to better investigate melanoma biology.

Low Intratumoral Mast Cells Are Associated With a Higher Risk of Prostate Cancer Recurrence.

Mast cells are of interest in prostate cancer because they possess both pro- and anti-tumorigenic properties and are present in the tumor microenvironment. We studied the association of mast cell count and densities with prostate cancer recurrence using tissue microarrays (TMAs) for 462 men who recurred (cases) and 462 controls that were matched to the cases nested in a cohort of radical prostatectomy patients. Dual-immunostaining for mast cell tryptase and epithelial cytokeratin-8 and whole slide image analysis were used to assess total mast cell number, mast cell density (mast cell number/tissue area), and mast cell number per epithelial or stromal area in TMA spots containing tumor (up to 4 per man). We used conditional logistic regression to estimate the odds ratio (OR) and 95% confidence interval of recurrence for the mean, minimum, and maximum mast cell parameters in tumor tissue among each man's TMA spots. After taking into account matching factors of age, race, Gleason sum, and pathologic stage, higher minimum mast cell density in the tumor (comparing highest to lowest quartiles: OR = 0.58, 95% CI 0.40-0.86; P-trend = 0.004) was associated with a lower risk of recurrence. Patterns for mast cell number and ratio of mast cell number to epithelial or stromal area were similar to those for mast cell density. Our results suggest that intratumoral mast cells may be protective against prostate cancer recurrence and could potentially serve as a prognostic biomarker after prostatectomy. Prostate 77: 412-424, 2017. © 2016 Wiley Periodicals, Inc.

Evaluation of Mast Cell Distribution in Oral Lichen Planus and Lichenoid Lesions by Immunohistochemical and Histochemical Analysis

The histopathological assessment of Oral Lichen Planus (OLP) and oral lichenoid lesions is relatively subjective. The distinguishing criteria established by WHO effectively reproducible when all selection criteria were fulfilling but sometimes fail to provide a reliable diagnosis. The aim of the present study was to evaluate mast cell counts and their distribution among OLP and lichenoid lesions. The density and localization of mast cells was examined in 22 patients with a diagnosis of OLP (11 patients) or oral lichenoid reactions (11 patients) by c-kit/CD117 immunohistochemical and toluidine blue histochemical staining. Data were analyzed using either the Kruskal-Wallis or Mann-Whitney U tests. No significant difference in the total number of mast cells was observed between the two groups (P = 0.599); however, a significant difference was observed in mast cell counts between reticular and junctional zones (P<0.05). The findings of the present study suggest that mast cells play a key role in the pathogenesis of oral inflammation; however, the ability of mast cell measurements to reliably differentiate between lichen planus and other lichenoid mimickers was limited as the number of mast cells was found to be increased in both the conditions.

Abstract C73: A relationship between mast cells and the racial disparity of prostate cancer

Abstract Prostate cancer afflicts African American men to a greater degree than European American men, with a 60% greater incidence and 2-3 times greater mortality. In addition, studies have shown that the incidence rate of distant metastasis is 4 times greater in African American men than in European American men, consistent with the notion that prostate cancer is more aggressive in African Americans. Of interest, African American men are also significantly more likely to present with inflammation in benign prostate biopsies, and studies have shown higher expression of a number of inflammatory markers in prostate cancer tissue from African Americans compared to European Americans. One immune cell type of particular interest in the context of prostate cancer are mast cells, which have the potential to play a number of roles in cancer, and have also been shown to increase in number in prostate cancer versus benign regions of the prostate. In the present study, immunohistochemistry (IHC) was used to directly visualize and localize mast cells in the prostate microenvironment of African American and European American men in a tissue microarray (TMA) containing tumor and benign tissues from 75 African American and 75 European American prostate cancer patients matched on tumor grade and stage. Automated counting of mast cell numbers as well as the calculation of mast cell-to-epithelial ratio (MC/Ep) and mast cell numbers per total tissue area (density) was aided by novel digital image analysis using a software framework integrating whole slide imaging, virtual microscopy, and ImageJ based analysis algorithms. Key results to date include the finding that mast cell density in prostate tumor tissues of African American men is significantly lower than that of Caucasian Americans (p &amp;lt; 0.0001). This same trend was observed for total mast cell numbers and MC/Ep (p=0.001). These results suggest the intriguing possibility that a decrease in tumor-infiltrating mast cells may contribute to the racial disparity observed in association with prostate cancer and additional studies are underway to determine the biological function of mast cells in the prostate tumor microenvironment. Citation Format: Heidi A. Hempel, Ibrahim Kulac, Nathan S. Cuka, Toby C. Cornish, Angelo M. De Marzo, Karen S. Sfanos. A relationship between mast cells and the racial disparity of prostate cancer. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr C73.

Thymol accelerates the recovery of the skeletal muscle of mice injured with cardiotoxin.

The aim of this study was to investigate the preventive effect of thymol in in vivo muscle inflammation and regeneration on cardiotoxin-induced injury. Mice were pretreated (p.o.) with thymol (10-100 mg/kg), and after 1 h, cardiotoxin (25 μM, 40 μl) was administrated into the gastrocnemius muscle. The quantification of the areas of inflammation and regeneration of muscle tissue (3, 7 and 10 days) in HE-stained slides as well as the count of total mast cells and different phenotypes of mast cells were made. Sirius red staining was used to analyse total collagen expression. The pretreatment with thymol significantly reduced the area of inflammation (30 and 100 mg/kg) and increased the area of regeneration (100 mg/kg) 3 days after the cardiotoxin injection. Thymol at 30 and 100 mg/kg increased the area of collagen in 3 days and also decreased this area in 7 and 10 days, compared to the injured group. The pretreatment with thymol did not affect the number of total mast cells; however, it was able to change the number of mucosal mast cells within 10 days. This study suggests that thymol ameliorates inflammatory response and accelerates regeneration in cardiotoxin-induced muscle injury.

Role of mast cells in estrogen-mediated experimental endometriosis in rats

To investigate the role of mast cells in the pathogenesis of estrogen-mediated experimental endometriosis in rats. Endometriosis model was established by transplanting autologous fragments of uterus to the inner surface of the abdominal wall in 24 un-pregnant female Sprague Dawley rats. The rats were divided randomly into three groups (n=8 in each group), and were injected with different doses of estrogen: high-dose group (200 μg·kg⁻¹·d⁻¹), low-dose group (100 μg·kg⁻¹·d⁻¹) and the control group (0 μg·kg⁻¹·d⁻¹). The ovaries were surgically removed in high-dose and low-dose groups. Four rats were sacrificed in each group at 2 and 4 weeks after surgery. Their serum estradiol levels, size of lesions, total number of mast cells and degranulations, serum TNF-α levels, expression of tryptase and NGF in tissues were analyzed and compared among groups. The mean levels of serum estradiol 2 weeks and 4 weeks after model established and serum TNF-α at 4 weeks in estrogen-treated groups were significantly higher than those in control group (all P<0.05). The mean size of endometriotic lesions in the estrogen-treated groups was also significantly larger than that in the control group 2 weeks and 4 weeks after model established (all P<0.05). Meanwhile, both at week 2 and week 4, the mean ratio of degranulation/total number of mast cells by toluidine blue staining in low-dose estrogen group was significantly higher than that in the control group (P<0.05). The expression of NGF in high-dose estrogen group was significantly higher than that in the control group at week 4(P<0.05). Estrogen can promote the growth of endometriotic lesions and may mediate the pathogenesis of endometriosis by activating mast cells, which may be associated with increasing TNF-α and NGF levels.

Sodium cromoglycate attenuates experimental endometriosis in rats by regulating mast cells

To investigate the effect of sodium cromoglycate on experimental endometriosis in rats. Endometriosis model was established in 36 unpregnant female SD rats by transplanting autologous fragments of endometrium to the inner surface of the abdominal wall. The endometriotic lesions were measured by a second laparotomy 2 weeks after surgery. Then the rats were randomly divided into four groups (n=8 in each group) to receive intraperitoneal injection of different doses of sodium cromoglycate for 2 weeks: high-dose group (20 mg·kg⁻¹·d⁻¹); low-dose group (10 mg·kg⁻¹·d⁻¹); the negative control group and the blank control group. The animals were sacrificed and the size of the lesions were measured. The endometriosis model of SD rats was identified by HE staining and immunohistochemical staining of keratin and vimentin. The total number of mast cells and their degranulation were measured by Toluidine blue staining; the concentrations of TNF-α in serum were measured by enzyme linked immunosorbent assay; the concentrations of estradiol in serum were measured by enzyme immunoassay; the expression of tryptase and nerve growth factor (NGF) were measured by immunohistochemical staining. The number of activated mast cells (MC) by Toluidine blue staining in high-dose group was significantly lower than that in negative control group (P<0.05), and its ratio of degranulation/total number of MC was significantly lower than that in negative control group or blank control group (P<0.05). The serum TNF-α levels and tryptase expression in tissues in high-dose group were significantly lower than those in negative control group or blank control group (P<0.05). However, no significant difference in the size of endometriotic lesions and expression of NGF was found among groups (P>0.05). Sodium cromoglycate can stabilize mast cells from degranulation, which may relieve the clinical symptoms of endometriosis by reducing TNF-α and tryptase levels.

A novel fungus concentration-dependent rat model for acute invasive fungal rhinosinusitis: an experimental study.

BackgroundAcute invasive fungal rhinosinusitis is a lethal infectious process afflicting immunocompromised individuals. Knowledge about this disease is still limited due to the scarcity of animal models designed to study the pathogenesis of this infection. Mast cells are tissue-resident immune cells that participate in a variety of allergic and inflammatory conditions. Limited attention has been given to the role of mast cells in acute invasive fungal rhinosinusitis. Therefore, the objectives of this study were to create a rat model of acute invasive fungal rhinosinusitis based on analyzing the impact of different fungal concentrations on establishing infection, and to observe the changes of mast cells in rats with this disease.MethodsSprague–Dawley rats were divided randomly into four groups, three of which were experimental and received different concentrations of Aspergillus fumigatus inoculations, and one was a control group (D). The inoculated Aspergillus fumigatus concentrations were 5 × 107 conidia/ml in group A, 107 conidia/ml in group B, and 106 conidia/ml in group C. Before fungal inoculation, rats were immunosuppressed using cyclophosphamide and cortisone acetate, and had Merocel sponges inserted into the right nares. Hematology and histopathology investigations were then performed.ResultsAn acute invasive fungal rhinosinusitis rat model was established successfully with an incidence rate of 90% in group A, 50% in group B and 10% in group C. Aspergillus fumigatus invasion was observed in 20% of the lungs in group A, but was not seen in the remaining groups. In addition, no fungi invaded the orbital tissue, brains, livers, spleens or kidneys of any rat. Compared with the control set, the total number of mast cells in the experimental groups was not significantly increased, but mast cell degranulation, on the other hand, was only found in infected nasal cavities.ConclusionsThis investigation illustrates that various fungal concentrations have different effects on the incidence of acute invasive fungal rhinosinusitis, and it also demonstrates the feasibility of using this model to study the process of fungal rhinosinusoidal invasion. In addition, the results suggest that mast cells may play a role in the protection of sinuses against acute Aspergillus fumigatus infection and in the clearance of established hyphal masses.Electronic supplementary materialThe online version of this article (doi:10.1186/s12879-014-0713-y) contains supplementary material, which is available to authorized users.

AB0041 Number of Mast Cell Are Higher in End Stage Knee Osteoarthritis

BackgroundMast cells could be important in osteoarthritis (OA), as it is the only type of immune cell whose numbers were shown to be as high or sometimes higher compared to...

Abstract 475: Circulating Immunoglobulins Are Not Associated With Intraplaque Mast Cell Number and Other Vulnerable Plaque Characteristics in Patients With Carotid Artery Stenosis

Background: Atherosclerosis is a chronic systemic inflammatory disease in which many immune cells participate. Recently we have shown that mast cell numbers are associated with atherosclerotic plaque vulnerability and interestingly with future cardiovascular events (S. Willems et.al. 2013). The endogenous trigger that activates mast cells within the lesion remains unidentified. We hypothesized that mast cells are activated via receptors for IgG and/or IgE. In this study we aimed to establish whether specific immunoglobulin levels in plasma of atherosclerotic patients were related to intraplaque mast cell numbers. In addition, the levels were related to other vulnerable plaque characteristics and baseline clinical data. Results: Serum levels of total IgG, total IgE and oxLDL specific IgG were determined in 135 patients that underwent carotid endarterectomy. The studied patient population with a mean age of 67 and a male prevalence (71%) reflects a relatively typical population of patients with vascular occlusive diseases. The majority of patients were symptomatic (74%) as illustrated by the incidence of amaurosis fugax, a TIA or a stroke. No associations were observed between either the serum immunoglobulin levels or the total mast cell numbers in atherosclerotic plaques (total IgG vs. total mast cells r= -0,038, p=0.664) (tIgE vs total mast cells r=-0.038, p=0.664) (oxLDL-IgG vs total mast cells r=0.137 p=0.114). Furthermore, no associations were found between immunoglobulin levels and the following plaque characteristics: lipid core size, degree of calcification, number of macrophages or smooth muscle cells, amount of collagen and number of microvessels. Interestingly, we observed a negative association between statin use and total IgE (97.5 [43.1-276.8] vs. 157.3 [75.2-545.4] ng/mL, p=0.012) and statin use and oxLDL-IgG (288 [224-406] vs. 399 [282-584] mU/mL, p=0.004). Conclusions: In patients suffering from carotid artery disease, total IgG or IgE and oxLDL-IgG levels do not associate with plaque mast cell numbers or vulnerable plaque histopathological characteristics These data may indicate that other endogenous factors activate mast cells within the atherosclerotic plaque.

Circulating Immunoglobulins Are Not Associated with Intraplaque Mast Cell Number and Other Vulnerable Plaque Characteristics in Patients with Carotid Artery Stenosis

BackgroundRecently, we have shown that intraplaque mast cell numbers are associated with atherosclerotic plaque vulnerability and with future cardiovascular events, which renders inhibition of mast cell activation of interest for future therapeutic interventions. However, the endogenous triggers that activate mast cells during the progression and destabilization of atherosclerotic lesions remain unidentified. Mast cells can be activated by immunoglobulins and in the present study, we aimed to establish whether specific immunoglobulins in plasma of patients scheduled for carotid endarterectomy were related to (activated) intraplaque mast cell numbers and plasma tryptase levels. In addition, the levels were related to other vulnerable plaque characteristics and baseline clinical data.Methods and ResultsOxLDL-IgG, total IgG and total IgE levels were measured in 135 patients who underwent carotid endarterectomy. No associations were observed between the tested plasma immunoglobulin levels and total mast cell numbers in atherosclerotic plaques. Furthermore, no associations were found between IgG levels and the following plaque characteristics: lipid core size, degree of calcification, number of macrophages or smooth muscle cells, amount of collagen and number of microvessels. Interestingly, statin use was negatively associated with plasma IgE and oxLDL-IgG levels.ConclusionsIn patients suffering from carotid artery disease, total IgE, total IgG and oxLDL-IgG levels do not associate with plaque mast cell numbers or other vulnerable plaque histopathological characteristics. This study thus does not provide evidence that the immunoglobulins tested in our cohort play a role in intraplaque mast cell activation or grade of atherosclerosis.

Comparison of Mast Cells and Inflammatory Cells within Periapical Lesions and Comparison of Degranulated Mast Cells Between Fibrous and Inflamed Area in Radicular Cysts: An Immunohistochemical Study.

The role of mast cells as the key effector of allergic inflammation, anaphylactic inflammatory reactions and in the pathogenesis of chronic inflammation, is well-known. The present study is adopted to compare mast cells and inflammatory cells within periapical granuloma and cysts and localize the mast cells and quantify their number in the periapical cysts so as to propose a role of mast cells in the pathogenesis of this lesion. Biopsy specimens of 30 periapical lesions were stained with hematoxylin-eosin, and immunohistochemical Mast Cell Tryptase from Bio SB (IHC detection system kit) antibody. The tryptase positive mast cells and mononuclear inflammatory cells were counted in 10 consecutive high power fields (100X) using the binocular microscope from Motic attached to a computer with Motic Advanced Images 3.2 software. Comparative microscopic analysis indicated that periapical cyst shows more percentage of mast cells and less percentage of inflammatory cell than periapical granuloma (comparison of mean and standard deviation of total number of mast cells and inflammatory cells, mast cells 3.15±1.39 in the granuloma group and 4.43±1.91in the cyst group, inflammatory cells, 67.11±1.2 in the granuloma group and 52.66±0.8 in the cyst group). Numerous degranulated mast cells were observed in the fibrous wall than the inflammatory infiltrate of the periapical cysts. The mean and standard deviation of degranulated mast cells between the inflammatory and fibrous zone within the cyst group, being 0.95±1.10 and1.68±1.34 respectively. The values varied significantly between the two zones. The number of inflammatory cells in the cyst group is less than periapical granuloma and total number of mast cells in the cyst group is more as compared to periapical granuloma. The degranulated cells were quantified and they were higher in the fibrous area of the cysts than the inflammatory zone. This study could support the fact that the various mediators released on degranulation play a role in the connective tissue remodeling, chronicity and expansion of the periapical lesion.