Mast Cell Counts Research Articles

Pterjium nüksünde mast hücresinin rolü

Purpose: To investigate the role in pterygium recurrence of mast cell, which is known to play a role in inflammatory and immunological events, we aimed to determine the mast cell number in primary and recurrent pterygium tissue samples and to determine its relationship with angiogenesis.Materials and Methods: The study included 61 patients with pterygium who underwent primary pterygium excision with a bare sclera technique, but recurrent after a while. Primary and recurrent pterygium tissue samples of the same patient were examined histopathologically. The mean mast cell count was calculated by counting from 3 different areas under light microscope at 400 x magnification. In addition, the number of vessels was scored at 200x magnification.Results: 34 of the patients were male and 27 were female. The mean age was 57.02 ± 7.96. The mean mast cell count was 8.46±2.52 in the primary pterygium tissue and 14.07±3.05 in the recurrent pterygium tissue. The mean vascular count was 12.90 ± 3.17 in primary pterygium tissue and 16.21 ± 2.24 in recurrent pterygium. Statistical analysis revealed a significant increase in the number of mast cells and vascular number in the recurrent pterygium. Mast cell number and vascularity were correlated in primary pterygium and recurrent pterygium tissue samples.Conclusion: Increased mast cell in pterygium tissue may play an important role in the recurrence of pterygium. Determining mast cell count in preventing pterygium recurrence may be important.

Correlation of pterygium severity with IQ-domain GTPase-activating protein 1 (IQGAP1) and mast cells

IQ-domain GTPase-activating protein 1 (IQGAP1) is a multidomain scaffold protein that is involved in cytoskeleton dynamics and tumor metastasis. Although the role of IQGAP1 in various cancers had been reported, the function of IQGAP1 in pterygium has not been studied. In this study, surgically excised pterygium and control conjunctival tissue from cataract patients were analysed by immunohistochemistry, confocal microscopy, and Western blot for IQGAP1 expression, mast cell counts, and microvascular count. Pterygium was clinically divided into mild and severe types according to Tan's classification and Kim's criteria based on translucency and vascularity of the tissue. Greater clinical severity of pterygium was associated with higher expression of IQGAP1 expression. Compared to normal conjunctival tissue, severe pterygium had significantly higher IQGAP1 expression (P = 0.005), which strongly correlated to the number of microvessels (P = 0.003) and mast cells (P = 0.01). Confocal microscopy revealed IQGAP1 colocalization with mast cell and CD31. IQGAP1 expression was higher in the pterygium body compared to the head. In conclusion, the level of IQGAP1 expression was found to be correlated to the clinical severity of pterygium. Mast cells were identified in pterygium and is suspected to be involved in promoting fibrovascular invasion.

Study of mast cells in appendicitis: possible significance

Background: To study the mean mast cell count per square mm field in different layers of appendix and to correlate the relationship of these with progression of disease and extent of fibrosis. Also to study the possible significance of mast cell counts with different histological changes and relation with clinical presentation. Material and Methods: A total of 120 cases of appendix comprised of 20 cases of normal appendix which served as the control and 100 cases of appendicitis in different phase of evolution of the disease were studied for mast cell counts and its significance was assessed in correlation with the histopathological diagnosis as per the evolution of the disease. Results: Mast cell counts in submucosa were always higher then in mucosa or in muscular propria both in normal and in pathological appendicitis. The increased mast cell count in the mucosal layer was statistically significant in organizing phase than in chronic appendicitis. Submucosal mast cell count did not show any statistically significant difference between different stages of appendicitis and normal appendicitis. The mast cell count in muscularis propria showed statistically significant increase in chronic appendicitis as well as in early acute phase. In appendicitis with grade 2,3 and 4 histology, the total mean mast cell count/sq mm was much higher than in range in grade 1 and grade 5. Conclusion: In acute phase of inflammation there is decrease in the mast cell. In chronic phase of inflammation there is increase in the mast cell counts. A significant increase of mast cells in muscularis propria during early acute phase of appendicitis which was observed in present study has not been described in literature. This finding needs further evaluation to explain the role of mast cells in the development of early acute inflammatory response.

Safety and efficacy of a new micronized formulation of the ALIAmide palmitoylglucosamine in preclinical models of inflammation and osteoarthritis pain

BackgroundOsteoarthritis is increasingly recognized as the result of a complex interplay between inflammation, chrondrodegeneration, and pain. Joint mast cells are considered to play a key role in orchestrating this detrimental triad. ALIAmides down-modulate mast cells and more generally hyperactive cells. Here we investigated the safety and effectiveness of the ALIAmide N-palmitoyl-d-glucosamine (PGA) in inflammation and osteoarthritis pain.MethodsAcute toxicity of micronized PGA (m-PGA) was assessed in rats following OECD Guideline No.425. PGA and m-PGA (30 mg/kg and 100 mg/kg) were orally administered to carrageenan (CAR)-injected rats. Dexamethasone 0.1 mg/kg was used as reference. Paw edema and thermal hyperalgesia were measured up to 6 h post-injection, when also myeloperoxidase activity and histological inflammation score were assessed. Rats subjected to intra-articular injection of sodium monoiodoacetate (MIA) were treated three times per week for 21 days with PGA or m-PGA (30 mg/kg). Mechanical allodynia and motor function were evaluated at different post-injection time points. Joint histological and radiographic damage was scored, articular mast cells were counted, and macrophages were immunohistochemically investigated. Levels of TNF-α, IL-1β, NGF, and MMP-1, MMP-3, and MMP-9 were measured in serum using commercial colorimetric ELISA kits. One- or two-way ANOVA followed by a Bonferroni post hoc test for multiple comparisons was used.ResultsAcute oral toxicity of m-PGA resulted in LD50 values in excess of 2000 mg/kg. A single oral administration of PGA and m-PGA significantly reduced CAR-induced inflammatory signs (edema, inflammatory infiltrate, and hyperalgesia), and m-PGA also reduced the histological score. Micronized PGA resulted in a superior activity to PGA on MIA-induced mechanical allodynia, locomotor disability, and histologic and radiographic damage. The MIA-induced increase in mast cell count and serum level of the investigated markers was also counteracted by PGA and to a significantly greater extent by m-PGA.ConclusionsThe results of the present study showed that PGA is endorsed with anti-inflammatory, pain-relieving, and joint-protective effects. Moreover, it proved that particle size reduction greatly enhances the activity of PGA, particularly on joint pain and disability. Given these results, m-PGA could be considered a valuable option in the management of osteoarthritis.

Bronchoalveolar lavage fluid cytokine, cytology and IgE allergen in horses with equine asthma

The pathophysiology of equine asthma (EA) is still not fully described, but the involvement of an allergic reaction is strongly suspected. This theory has led to the use of allergen-specific immunoglobulin (Ig)E tests to support a diagnosis of asthma. The objective of this descriptive study was to evaluate the correlation between four subgroups of EA (mastocytic mild equine asthma [MEA], neutrophilic MEA, mixed MEA, and severe equine asthma [SEA]), allergen specific IgE (measured in both serum and BALF) and mRNA expression of selected genes in bronchoalveolar lavage fluid (BALF). Serum and BALF were collected from 64 horses with a history of lower airway problems with or without poor performance. Differential cell counts from BALF were used to assign horses to one of four groups (mastocytic MEA; neutrophilic MEA, mixed MEA, and SEA). The expression of messenger RNA (mRNA) coding for IL4, IL5, IL8, IL10, TGFB, TNFA, toll-like receptor (TLR)4, IL1RA, IL1B, matrix metalloproteinase 8 (MMP8), TLR9, chemokine ligand 5 (CCL5) and cluster of differentiation (CD)14 in BALF were measured using reverse transcriptase (RT) quantitative PCR (qPCR). Allergen-specific IgE was measured in serum and BALF using an allergen-specific IgE ELISA test with the screening panel: house mites, storage mites, mould and pollen. As expected, the BALF neutrophil differential count correlated with mRNA expression of MMP-8 (r = 0.611, p < 0.001), TLR-4 (r = 0.540, p < 0.001), IL-1RA (r = 0.490, p < 0.001), IL-1β (r = 0.463, p < 0.001) and IL-8 (r = 0.302, p = 0.015). Cytokine expression of IL-1β (p = 0.014), MMP8 (p = 0.028) and IL-1RA (p = 0.037) was significantly higher in the SEA group compared to the MEA subgroups. The BALF mast cell count was correlated with allergen-specific IgE for insects (r = 0.370, p = 0.002) and pollen (r = 0.313, p = 0.011). Eosinophils in BALF were correlated with BALF mRNA expression of IL-4 (r = 0.340, p = 0.006) together with a significant correlation between BALF eosinophils and allergen-specific IgE for mites (r = 0.930, p < 0.001) and pollen in BALF (r = 0.837, p < 0.001). No correlation was found between allergen-specific IgE in serum and BALF for any of the allergen in the screening panel. Based on these results from allergen-specific IgE in horses with EA is not found in systemic circulation, and only the mastocytic and mixed subgroups of horses with EA had allergen-specific IgE in BALF. Further studies are needed to clarify the relationships identified here.

Chronic infection with the protozoan Toxoplasma gondii prevents the development of experimental atopic dermatitis in mice

BackgroundSupporting the hypothesis thatT. gondii infection protects against allergy in humans we previously demonstrated that this infection can modulate not only the susceptibility to develop respiratory allergies in mice but also suppresses allergic responses at systemic level. This latter finding suggests that T. gondii infection could prevent the onset of other allergic diseases, such as atopic dermatitis. At present, few studies have investigated the modulation of atopic dermatitis by parasite infections. ObjectiveHere, we sought to investigate whether chronic infection with T. gondii is capable of modulating the development of atopic dermatitis. MethodsChronically infected mice were sensitized by repeated epicutaneous ovalbumin administration. Skin histopathology, humoral response, cytokine production and innate type-II lymphoid cells (ILC2) were assessed. ResultsA marked reduction in epidermal thickness and dermal inflammatory infiltrate along with a reduction in mast cell count was observed in infected mice compared to non-infected mice. These results correlated with a diminished TH2 and TH1 allergen specific response. Reduced type-II IL-4 and IL-5 cytokines were already detected during the first 24 h of allergen sensitization in splenocytes and draining lymph nodes from infected mice. Moreover, this reduced type-II profile in chronically infected animals correlated with diminished ILC2 number in draining lymph nodes. ConclusionChronic infection withT. gondii prevents the development of atopic dermatitis. The diminished susceptibility seems to result from changes in type-II innate immune response that may lead to the induction of a deficient TH2 response and consequently to a lower susceptibility to develop atopic dermatitis.

Overexpression of fractalkine and its histopathological characteristics in primary pterygium.

This study aimed to evaluate the differences in the expressions of fractalkine in normal bulbar conjunctiva and primary pterygium tissues. The study included 48 patients who had been operated on for primary pterygium. Histopathologically, the presence of epithelial atypia, epithelial hyperplasia, goblet cell hyperplasia, epithelial lymphocytic exocytosis, stromal inflammation, mast cell count, and stromal vascularity were evaluated in the primary pterygium tissues. An immunohistochemical fractalkine stain was applied to the primary pterygium tissue samples and normal bulbar conjunctival tissue samples. Primary pterygium and normal bulbar conjunctival tissue samples were histopathologically analyzed. Epithelial atypia, epithelial hyperplasia, epithelial lymphocytic exocytosis, stromal inflammation, stromal vascularity, and mast cell count were found to be significantly higher in the primary pterygium (p = 0.001, p = 0.002, p = 0.024, p = 0.007, p = 0.024, and p = 0.013, respectively). When evaluated in terms of fractalkine expression, the epithelial, vascular endothelial, and inflammatory cells were significantly higher in the primary pterygium (p ≤ 0.001, p = 0.002, p = 0.001, respectively). Moreover, compared to the normal bulbar conjunctiva, Ki-67 expression was significantly higher in the primary pterygium tissue samples. Fractalkine might play a key role in the etiopathogenesis of pterygium. Fractalkine may be important in developing new treatment approaches.

Impact of Photobiomodulation and Condition Medium on Mast Cell Counts, Degranulation, and Wound Strength in Infected Skin Wound Healing of Diabetic Rats.

Background: Numerous people suffer from diabetes mellitus (DM) and resultant diabetic foot ulcers (DFU), which lack effective treatment. Photobiomodulation (PBM) has accelerated wound healing in diabetic animals and patients in some studies. However, there is scant information on the number and activation state of skin mast cells (MCs) in PBM-treated diabetic wounds. Objective: We intend to assess the influence of the number of MCs and degranulation in the remodeling step of an infected wound model on wound strength and its microbial flora in a type 1 DM (T1DM) rat model by administration of PBM, condition medium (CM) derived from human bone marrow mesenchymal stem cells (hBMMSCs), and the combination of PBM+CM. Methods: We prepared CM by culturing hBMMSCs. T1DM was induced in 72 rats and, after 1 month, we created one excisional wound in each rat. All wounds were infected with methicillin-resistant Staphylococcus aureus (MRSA). We divided the rats into four groups: (n = 18): (i) control; (ii) PBM; (iii) CM, and (iv) PBM+CM. On days 4, 7, and 15, we conducted microbiological, tensiometrical, and stereological analyses. The type of MCs (T1MCs, T2MCs, or T3MCs) and total number of MCs (TOMCs) were counted by light microscopy. Results: On day 15, the PBM+CM, PBM, and CM groups had significantly increased wound strength compared with the control group. There was a significant decrease in colony-forming units (CFU) at all time points in the PBM+CM and PBM groups. The PBM+CM and PBM groups had more stable MCs (T1MCs), less significant degranulated MCs (T2MCs), less significant disintegrated MCs (T3MCs), and less significant TOMCs compared with the control group at all time points. Conclusions: PBM+CM and PBM treatments significantly increased the healing process in an ischemic and MRSA-infected wound model of T1DM rats. PBM+CM and PBM significantly decreased both TOMCs and their degranulation, and significantly decreased CFU.

1244 Symptomatic Patients Suspected of Eosinophilic Gastritis and/or Enteritis Have Elevated Mucosal Mast Cell Counts Without Eosinophilia: A New Diagnostic Entity?

INTRODUCTION: Eosinophilic gastrointestinal diseases (EGIDs) are a set of inflammatory diseases subclassified according to the site(s) of abnormal accumulation of eosinophils (eos) in the gastrointestinal (GI) tract such as eosinophilic esophagitis (EoE), gastroenteritis (EGE), and colitis. These conditions often decrease quality of life due to debilitating symptoms. While the pathogenesis of EGIDs is primarily thought to be driven by eos, there is increasing evidence for the involvement of mast cells (MCs). AIM: To characterize symptomatic patients (pts) with suspected EG/EGE who did not meet histopathologic entry criteria for mucosal eosinophilia for a Phase 2 randomized, double-blind, placebo-controlled study of AK002, an anti-Siglec-8 antibody. METHODS: To undergo screening endoscopy for this study, pts were required to report an average symptom score ≥3 (0 to 10 scale) for abdominal pain, nausea, and/or diarrhea on a daily patient-reported outcome questionnaire for ≥2 weeks and have no other known cause for GI symptoms. During the screening endoscopy, biopsies were systematically obtained from the stomach and duodenum, and read by a single pathologist. Eos counts (eos/hpf; hpf area = 0.237 mm2) were assessed on H&amp;E slides. To quantify MCs, immunohistochemistry for tryptase was performed. We quantified eos and MCs in the stomach and duodenum. Histopathologic entry criteria for the randomized study was ≥30 eos/hpf in 5 hpfs in the stomach (EG) and/or ≥30 eos/hpf in 3 hpfs in the duodenum (EGE). A literature review was conducted to determine normal MC counts in the GI tract. RESULTS: Eighty-eight pts underwent screening endoscopy based upon suspected EG/EGE and active symptoms, and 72 pts met histopathologic eos criteria. All pts whose eos did not meet entry criteria (n = 16) were found to have elevated MC counts (Figure 1; reported normal range = 12-19 MCs/hpf). In these pts, the mean gastric eos count was 6 eos/hpf in 5 hpfs and mean duodenal eos count was 15 eos/hpf in 3 hpfs. In contrast, these pts exhibited a mean gastric MC count of 47 MC/hpf in 5 hpfs and a mean duodenal MC count of 49 MC/hpf in 3 hpfs. Almost all symptomatic pts screened (87/88; 99%) had elevated MC counts. CONCLUSION: Data from this large randomized EG/EGE study showed that symptomatic pts with suspected EG/EGE had increased mucosal MCs with or without mucosal eosinophilia. These data suggest that MCs may play a role in pts with suspected EG/EGE and raise the possibility of a unique clinical presentation driven by MCs.

Study of mast cell and eosinophil count in surgically resected appendix

Introduction: Appendix is a normal true diverticulum of the caecum that is prone to acute and chronic inflammation. Mast cells are present in chronic inflammatory reactions and they secrete cytokines that promote inflammation. Eosinophils are abundant in immune reactions mediated by IgE and in parasitic infection. Objective: To evaluate mast cell and eosinophil count variation in appendicitis and to suggest their possible role in pathogenesis of appendicitis. Materials and Methods: It is a two-year prospective study done on 470 resected specimens of appendices received for histopathology. Results: Mast cells and eosinophils were present in all the appendicular lesions studied. Mean mast cell count was highest in chronic appendicitis and lowest in acute appendicitis. Mucosa of chronic appendicitis showed highest count, lowest was seen in the muscularis propria of acute appendicitis compared to normal / unremarkable appendix taken as controls. Correlation between mast cell density, fibrosis and neural ganglia hypertrophy was seen in chronic appendicitis. Mean eosinophil count was highest in acute suppurative appendicitis and lowest in chronic appendicitis, with highest count in the mucosa of acute suppurative appendicitis and lowest in the muscularis propria of chronic appendicitis. Conclusion: The presence of mast cells and eosinophils in cases of appendicitis supports the allergic theory of appendicitis in which the Type I hypersensitivity reaction leads to recruitment of eosinophils and discharge of primary and secondary mediators of inflammation by degranulation of mast cells which play a role in pathogenesis of appendicitis.

Increased number of mast cells in the bone marrow of chronic myeloid leukemia may herald the pending myeloid transformation—the mast cell is an indicator of myeloid transformation

Background: Tumor cells are surrounded by many inflammatory cells, including mast cells (MCs), which can secrete several classic proangiogenic factors, resulting in endothelial cell proliferation and angiogenesis. However, the researches of the number of MC and microvessel density (MVD) in the bone marrow in chronic myeloid leukemia (CML) are rare. In this study, we aimed to investigate the relationship between tryptase-positive MCs and MVD in the different phases of CML. Methods: Bone marrow samples of 61 patients with CML and 20 healthy donors were collected from 2007 to 2017. Antibodies against the endothelial cell marker CD34 and against tryptase were used in immunohistochemistry. The diagnosis and counting of tryptase-positive MC and microvessel in bone marrow was at ×400 magnification. Results: MVD in CML group was higher than which in the control group, and the blast phase (BP) group had a higher MVD than which in chronic phase (CP) group (P Conclusions: The number of MCs and MVD might be markers for the outcome of patients with CML in the Chinese population.

Mast cells are increased in the small intestinal mucosa of patients with irritable bowel syndrome: A systematic review and meta‐analysis

Colonic mast cells have been proposed to be related to the pathophysiology of irritable bowel syndrome (IBS). Whether mast cell counts are altered in the small intestine, a less-explored region in patients with IBS is not completely clear. PubMed and EMBASE were searched for case-control studies on mast cell count/density in the small intestine of patients with IBS vs controls through February 2019. Mast cell counts were separately analyzed in the duodenum, jejunum, and ileum. Data were pooled using the standardized mean difference (SMD) method. When zero was not within the 95% confidence interval (CI), the SMD was considered significant. Data from 344 patients with IBS and 229 healthy controls from three studies in the duodenum, six in the jejunum, and five in the ileum were pooled in this meta-analysis. The number of mast cells was significantly higher in the ileum (SMD: 1.78 [95% CI: 0.89, 2.66]) of patients with IBS. Mast cell counts were not significantly different in the duodenum (SMD:0.81 [-0.06, 1.67]) or the jejunum (SMD:0.58 [-0.03, 1.19]) of patients with IBS vs healthy controls. Mast cells are increased in the small intestine of IBS vs controls, mainly in the ileum. Future studies should address whether such findings are IBS subtype or gender-dependent. Methodological variations, single-center bias, and the limited number of studies included in this meta-analysis may affect the final results.

Increased number of mast cells in the bone marrow of chronic myeloid leukemia may herald the pending myeloid transformation-the mast cell is an indicator of myeloid transformation.

BackgroundTumor cells are surrounded by many inflammatory cells, including mast cells (MCs), which can secrete several classic proangiogenic factors, resulting in endothelial cell proliferation and angiogenesis. However, the researches of the number of MC and microvessel density (MVD) in the bone marrow in chronic myeloid leukemia (CML) are rare. In this study, we aimed to investigate the relationship between tryptase-positive MCs and MVD in the different phases of CML.MethodsBone marrow samples of 61 patients with CML and 20 healthy donors were collected from 2007 to 2017. Antibodies against the endothelial cell marker CD34 and against tryptase were used in immunohistochemistry. The diagnosis and counting of tryptase-positive MC and microvessel in bone marrow was at ×400 magnification.ResultsMVD in CML group was higher than which in the control group, and the blast phase (BP) group had a higher MVD than which in chronic phase (CP) group (P<0.05). The number of MCs in three groups of CML was higher than which in control group, and the number of MCs in AMLT group was highest (P<0.05). Patients with a lower grade of tryptase-positive MCs in CP group survived longer OS and PFS (P<0.05).ConclusionsThe number of MCs and MVD might be markers for the outcome of patients with CML in the Chinese population.

Endoglin is Highly Expressed in Human Mast Cells.

Endoglin, known to be expressed in proliferating vessels, is of worth when evaluating microvessel density as a prognostic factor in many types of malignancies, including some subtypes of leukemia cells. In childhood acute lymphoblastic leukemia, endoglin is associated with adverse outcome. In bone marrow, endoglin identifies the repopulating hematopoietic stem cells. Mast cells are a component of normal tissue and play an important role in the regulation of several processes, including inflammation and neoplasia. The aim of this study was to evaluate the use of endoglin as a biological marker of mast cells compared with the gold standard stains. We studied 15 specimens of neurofibroma, 9 of mastocytosis, and 6 of fibrous scar tissue through immunohistochemistry (for endoglin and mast cell tryptase) and histochemical staining using toluidine blue. Quantitative analysis of the cells was performed by counting 5 hotspots. The validity of endoglin as a mast cell marker was assessed by intraclass correlation coefficient. The Kruskal-Wallis test was used to compare mast cell count for each marker. A strong endoglin expression was found in the cytoplasmic granules of mast cells within the 3 groups. Similar results were observed with mast cell tryptase as well as toluidine blue. The intraclass correlation coefficient revealed that endoglin is a highly reliable biomarker of mast cells when compared with mast cell tryptase and toluidine blue. In conclusion, endoglin may assist in the diagnosis and pathogenesis study of various processes associated with mast cells. An endoglin-neutralizing treatment for solid cancers and leukemia could also affect mastocytes and the immunologic system.

Comparison of mast cell counts between the patients with moderate and severe periodontitis.

Background The role of mast cells in periodontal tissue degradation has been established. These cells can be efficient in the etiology of periodontitis by participating in gingival homeostasis and releasing cytokines and enzymes, resulting in connective tissue matrix breakdown. Therefore, the aim of this study was to compare the mast cell counts between patients with moderate and severe periodontitis. Methods This case‒control study was performed on 15 subjects with severe periodontitis and 15 subjects with moderate periodontitis, who needed periodontal surgical treatment. Incisional biopsies were provided during periodontal surgery. Afterward, the mean counts of mast cells were determined after toluidine blue staining of the samples. Finally, data were analyzed with SPSS. Results The results of this study showed that mast cell counts in severe periodontitis cases were lower than those in moderate periodontitis. However, there were no statistically significant differences between the two groups (P=0.611). In addition, the mean mast cell counts in males and females did not show a statistically significant difference (P=0.231), although the count was higher in female subjects. Conclusion Based on the results, no statistically significant differences were found in mast cell counts between subjects with severe periodontitis and those with moderate periodontitis.

Mast cell expression in oral lichen planus: A systematic review.

Lichen planus is a common chronic, inflammatory, immune-mediated mucocutaneous disorder affecting the skin and mucosa. The role of mast cells in the genesis of lichen planus has been debated. Establishing a definitive part played by mast cells and its degranulation would possibly provide a permanent, cost-effective treatment modality for oral lichen planus (OLP). This review aims to study the expression of mast cells qualitatively and quantitatively in OLP. The research questions were framed to assess the mast cell count, localization within the epithelium basement membrane zone and degranulation of mast cells. We performed a systematic search of PubMed, Medline, Cochrane and Web of Science. We found a total of 120 studies from which 12 were found suitable for the review. There is a marked increase in the number of mast cells in OLP. The mast cells were seen in increased numbers in the epithelial and connective tissue junction at areas of basement membrane disruption. There was also an increase in the degranulation of mast cells. It is evident that there is an increase in the mast cell number in lichen planus and its subsequent degranulation.

Role of hippocampal mast cells in early postoperative cognitive impairment in rats

Objective To evaluate the role of hippocampal mast cells in the early postoperative cognitive impairment in rats. Methods Eighty male Sprague-Dawley rats, aged 6-8 weeks, weighing 200-250 g, were divided into 4 groups (n=20 each) using a random number table method: normal saline control group (group C), cromolyn injected into lateral cerebral ventricle group (group L), operation group (group O), and cromolyn injected into lateral cerebral ventricle plus operation group (group LO). Cromolyn 2 μl (100 μg/ul) was intracerebroventricularly injected in L and LO groups.The equal volume of normal saline was given instead in C and O groups.Open reduction and internal fixation was performed after tibial fracture was induced 30 min later in O and LO groups.Contextual fear conditioning and Y-maze tests were performed at 1 and 3 days after operation, and the freezing time and the number of learning trails were recorded.The animals were then sacrificed, and hippocampal tissues were obtained for determination of activated mast cell count (by toluidine blue staining) and expression of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) mRNA (by polymerase chain reaction). Results Compared with group C, the number of learning trails was significantly increased, and the freezing time was shortened, the number of activated mast cells in hippocampi was increased, and the expression of IL-1β mRNA was up-regulated at 1 and 3 days after operation, and the expression of TNF-α mRNA was up-regulated at 1 day after operation in group O(P 0.05). Compared with group O, the number of learning trails was significantly decreased, and the freezing time was prolonged, the number of activated mast cells in hippocampi was decreased, and the expression of IL-1β mRNA in hippocampi was down-regulated at 1 and 3 days after operation, and the expression of TNF-α mRNA in hippocampi was down-regulated at 1 day after operation in group LO (P<0.05). Conclusion Activation of hippocampal mast cells can induce central inflammatory responses and is involved in the mechanism of early postoperative cognitive impairment in rats. Key words: Mast cell; Inflammation; Cognition disorders; Postoperative complications

First study on the effect of Asiatic honey bee (Apis cerana) venom on cutaneous, hepatic and renal rat tissues

Recently, honey bee venom has been used for medical purposes. Studying the effect of bee venom on skin, liver and kidney tissues is of importance to understanding the pathology of bee stings. Various studies have demonstrated the effects of venom extracted from Apis spp. on tissues of model animals like the rat. However, no published data are available on the effect of specific doses of Asiatic honey bee (Apis cerana) venom on different tissues. In this study, we examined effects of A. cerana venom dissolved in 0.85% NaCl at dosage of 30.0 µg/g body weight on cutaneous, hepatic and renal tissues of six male rats. This dosage was given via subcutaneous injection of 200 µl per rat compared to those of controls (n = 6) that were injected with 200 µl physiological saline solution. After 48 h, tissues were removed and processed by paraffin technique and stained with Masson’s trichrome staining, Periodic acid Schiff’s reagent and alcian blue 8GX for histological structure analyses. Venom-injected rats showed signs of tissue damage: There were greater numbers of both Kupffer cells and damaged hepatocytes compared to those of controls. Moreover, signs of renal lesions were also observed such as dispersion and retraction of glomeruli, wider Bowman’s space and injury to brush borders of proximal convoluted tubules, including damage to other tubular cells (renal tubular necrosis). Additionally, dermal mast cell counts were significantly lower than the controls. In conclusion, A. cerana venom at 30.0 µg/g body weight can cause renal lesions, hepatic injury and tissue damage to the vital organs of rats. The results of this study provide a basis for further studies on the application of A. cerana bee venom in clinical therapy.

Abstract 1630: The utility of the online pathologist network for cancer research

Abstract Introduction: Pathologic review of tumors is critical to understand what type of cancer is present, changes in the immune microenvironment, and assess for the presence of necrosis. Simultaneously, in animals treated with immunotherapeutic agents, the assessment of the presence of abnormal inflammation and corresponding tissue damage in normal organs is of the utmost importance to measure a medication’s potential side effect profile. The current problem is that most researchers do not have the skill in interpreting histology that pathologists have, barring them from the above histologic observations. This is compounded by the fact that most pathologists have busy clinical schedules and even if they wanted to help a research study, they do not have access to researchers. Another issue is that, even if researchers and pathologists could be connected, there is the issue of compensation. If an online platform could be constructed where researchers can connect to pathologists and pathologists can connect to researchers to help them interpret their slides with equitable compensation, the quality of histologic interpretation of research materials would increase. With improved slide interpretation quality, researchers would more rapidly know which experimental paths have potential and which should be avoided based on unfavorable histology. Methods: To build this platform we used our histology business where wet tissue is converted to digital scanned slides and offered the pathologist consultation service to our customers. Researcher requests for pathology assistance were first screened by a board-certified pathologist (AB) for addressability by pathologists. When histology questions were deemed answerable by pathology, pathologists on Histowiz’s remote pathologist network reviewed the slides and generated reports in 3 days that were then sent to the researchers. Results: Between February and September 2018 there were 60 online consultations performed at HistoWiz. Nearly half (25/60) of the studies involved measuring inflammation in mouse organs. Only one study asked for tumor grading, one study asked for tumor percentage estimation, and two studies asked for tumor type identification. The remaining studies were for miscellaneous requests such as mast cell counting, GVHD measurement, coronary atherosclerosis measurement, organ damage assessment (skin: 6, small intestine: 1, lung: 3, brain: 2, cartilage: 2, liver: 2), IHC suitability assay, differences between WT and KO mice, and toxicology after chemical treatment of mice. Conclusions: It is possible to build a platform whereby pathologists assist researchers through remote review of their scanned slides. In 7 months of this service, nearly half of the researcher requests were for assessment of inappropriate inflammation. Less requested services included tumor grading, tumor percentage estimation, and tumor type identification. Note: This abstract was not presented at the meeting. Citation Format: Ke Cheng, Christoper Gibson. The utility of the online pathologist network for cancer research [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 1630.

Reaction of the Palatine Tonsillar Immunocompetent Cells to Irrigation of Crypts by Suspension of Silica Nanoparticles under Conditions of Chronic Tonsillitis.

We studied the response of neutrophils, macrophages, and mast cells to local application of silica nanoparticles (10-20 nm). Histological examination of tonsillar postoperative material from 6 patients aged 24-44 years with recurrent tonsillitis was carried out. Irrigation of the tonsillar lacunae was carried out over 5 days before bilateral tonsillectomy: on the right by Polysorb MP suspension (1 g/liter), on the left by saline. The contact of nanoparticles with the mucosa led to a decrease in the number of cells expressing myeloperoxidase (p=0.02) and an increase in the count of CD68+ cells (p=0.04); the count of mast cells remained unchanged. Local use of medical adsorbent based on silica nanoparticles induced changes in cells due to their resorption by the tissue. Positive chemotaxis of CD68+ macrophages revealed in the tonsillar lymphoid tissue attested to stimulation of non-specific immunity and inductive phase of specific immunity. The authors hypothesized that internalization of medical nanoparticles by resident phagocytes of the mucosa could support targeted biodistribution of drugs in the palatine tonsils.