DigitalUM :: Browsing by Subject "Mast cells"

Browsing by Subject "Mast cells"

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Open Access
Alterations in the dynamics of inflammation, proliferation and apoptosis in subcutaneous implants of lupus-prone mice
(Murcia: F. Hernández, 2011) Campos, Paula P.; Vasconcelos, Anilton C.; Ferreira, Mônica A.N.D.; Andrade, Silvia P.
Wound repair is a complex process that involves inflammation, proliferation, extracellular matrix deposition/remodeling and apoptosis. Autoimmune diseases profoundly affect the healing process. We have used histological parameters to characterize the recruitment of mast cells and the proliferative activity and apoptosis in the fibrovascular tissue induced by subcutaneous polyether-polyurethane sponge implants in lupus-prone New Zealand White (NZW) and in control Balb/c mouse strains at days 10 and 21 post implantation. Fibrovascular tissue infiltration (hematoxylin and eosin staining), mast cell number (Dominici staining) and cellular proliferation (AgNOR staining) peaked early (day 10) but collagen deposition (picrosirius red staining) and apoptosis remained high in implants of NZW mice during the experimental period. In contrast, implants of Balb/c animals showed a progressive increase in mast cell recruitment and cellular proliferation but apoptosis fell from day 10 to 21 postimplantation. This divergent response early mast cells recruitment, excessive collagen deposition and disturbed removal of apoptotic cells from the site of injury in NZW mice implies that the genotype trait of NZW mice is a determining factor in abnormal healing response.
Open Access
Characterization of a monoclonal antibody recognizing mast cells
(Murcia : F. Hernández, 1997) Oliveira-Nogueira, T. de; Aubin, J.E.
Immunohistochemical screening for monoclonal antibodies prepared by immunization of mice with a rat osteoblastic cell population led to identification of one antibody that reacted against a small population of cells present in the soft connective tissue compartment of 21 days fetal rat calvaria. The morphology of the cells and the immunohistochemical staining characteristics (a distinct intracellular granular pattern) suggested that the antibody might be reacting specifically against mast cells. We used combined histochemistry and immunohistochemistry to further characterize this antibody, designated RCJ102. Cryosections containing calvaria bone, soft connective tissues and skin were prepared from the top of the head of 21 days fetal rats, and from adult rats cryosections of lung, muscle, adipose tissue and small intestine were prepared. Some sections were labelled by indirect immunofluorescence with RCJ102; corresponding sections were labelled histochemically with toluidine blue. There was a direct correspondence between mast cells identified histochemically and cells labelling with RCJ102 in al1 tissues except intestine, in which the mast cell detectable by histochemistry were not labelled by RCJ102. These results suggest that the RCJ102 antibody will be a valuable new reagent for further elucidation of the heterogeneity described between connective tissue and intestinal mucosal mast cells.
Open Access
Colocalization of tumor necrosis factor-alpha and nitric oxide-synthase immunoreactivity in mast cell granules of nasal mucosa
(Murcia : F. Hernández, 1998) Bacci, S.; Rucci, L.; Riccardi-Arbi, R.; Borghi-Cirri, M.B.
We have demonstrated, with immunohistochemical techniques, the colocalization of tumour necrosis factor-a (TNFa) with a constitutive neuronal isoform of nitric oxide-synthase (NOS) in granules of the majority (52.77%) of the mast cells (MCs) of healthy human nasal mucosa. Very few cells were positive for NOS alone (2.54%). Some cells were positive for TNFa alone (16.73%) or negative for both antigens (18%). Since dim degranulation occurs in MCs of healthy nasal mucosa at any time, we propose that low concentrations of TNFa and NOS secreted by these cells are involved not only in the regulation of homeostasis of normal human nasal mucosa, but also in the survival and function of MCs themselves.
Open Access
Density and migration of mast cells in lip squamous cell carcinoma and actinic cheilitis
(Murcia : F. Hernández, 2009) Lago Costa, Nádia; Ferreira Oton-Leite1, Angélica; Peixoto Cheim-Júnior, Adonai; Gonçalves Alencar, Rita de Cássia; Jabur Bitta, Glória Oton; Aparecida Silva, Tarcília; Carvalho Batista, Aline
Mast cells (MCs) display a diversity of roles that may contribute to the stromal microenvironment alterations during tumor progression. The aim of this study was to investigate MC populations expressing tryptase and c-kit in lip squamous cell carcinoma (lip SCC) (n=37), actinic cheilitis (AC) (n=15) and normal lip mucosa (control) (n=6), as well as their relationship with microscopic parameters (collagen degeneration, elastin changes, angiogenesis and proliferative index). Tryptase, c-kit, CD31 and Ki-67 expressions were analyzed by means of immunohistochemistry and collagen and elastic fibers were visualized with Picrosirus and Verhoeff’s stain, respectively. The numbers of tryptase+ MC were significantly higher in lip SCC when compared with control (P=0.01), while a similar density of these cells was observed in AC and lip SCC (P=0.09). The density of c-kit+ MC was similar in all groups examined (P=0.65). MC migration (ckit+/Tryptase+ relationship) was 69% in lip SCC, 60% in AC and 100% in control. The number of CD31+ blood vessels was significantly higher in the lip SCC when compared with control and AC (P<0.01). The increase of MCs and angiogenesis in lip SCC may reflect an important modification in the tumor microenvironment during squamous photocarcinogenesis.
Open Access
Do mast cells affect villous architecture? Facts and conjectures
(Murcia : F. Hernández, 2005) Crivellato, E.; Finato, N.; Ribatti, Doménico; Beltrami, C.A.
In adult life, the architecture of the intestinal villus is maintained by a complex series of epithelialstromal interactions that involve different types of fixed and mobile cells located in the intestinal mucosa. Mast cells (MC) are normal constituents of the small bowel mucosa where they reside in the villous and pericryptal lamina propria as well as within the columnar epithelial cell layer. Besides being involved in numerous immune and inflammatory reactions in the context of both innate and acquired host defence, MC are known to exert important non-immunological functions like wound repair, extracellular matrix remodelling, angiogenesis and neurotrophism as well as modulation of fibroblast, epithelial cell and smooth muscle cell activity. These pleiotropic functions put MC in a central, strategic position to organize tissue defence, restore tissue damage and maintain tissue homeostasis. This review summarizes the most recent advances concerning the functional anatomy of the crypt-villus unit and discusses the way intestinal MC might become part of the instructive circuits that ultimately lead to the maintenance of a proper villous shape.
Open Access
In-situ analysis of mast cells and dendritic cells in coronary atherosclerosis in chronic kidney disease (CKD)
(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Wachter, D.L.; Neureiter, Daniel; Câmpean, V.; Hilgers, K.F.; Büttner Herold, M.; Daniel, C.; Benz, K.; Amann, K.
Aims. Mast cells (MC) and dendritic cells (DC) have immune modulatory function and can influence T-cell activity. Both cell types have been found in atherosclerotic plaques and are thought to play an important role for plaque stability. Compared to matched segments of the non-renal population, patients with chronic kidney disease (CKD) show a more pronounced and more aggressive course of atherosclerosis with higher plaque calcification and significantly higher complication rates. It was the aim of this study to analyze the number and localization of MCs and DCs, macrophages, T- and B-cells as well as the expression of markers of inflammation such as CRP and NFκΒ in calcified and non-calcified atherosclerotic plaques of patients with CKD and control patients. Methods. Fifty coronary atherosclerotic plaques from patients with endstage CKD (CKD, n=25) and control (n=25) patients were categorized according to the Stary classification and investigated using immunohistochemistry (markers for MC, DC, T, B, macrophage and NFκΒ). Expression was analyzed separately for the complete plaque area as well as for the different plaque subregions and correlations were analyzed. Results. We found only very few DCs and MCs per lesion area with slightly increased numbers in calcified plaques. MCs per plaque area were significantly more frequent in CKD than in control patients and this was independent of plaque calcification. MCs were most frequently found in the shoulder and basis of the plaque. DCs per plaque area were significantly less in calcified plaques of CKD compared to control patients. In control, but not in CKD patients, DCs were significantly more frequent in calcified than in non-calcified plaques. Within the plaques, DCs were similarly distributed between all 4 subregions. Conclusions. Coronary atherosclerotic plaques of CKD patients showed a significantly higher number of MCs whereas DCs were less frequent compared to control patients particularly if plaques were calcified. These findings might indicate a potential proinflammatory role of MCs, but not of DCs in atherosclerotic lesions of CKD patients, adding another characteristic of advanced atherosclerosis in these patients.
Open Access
Lipopolysaccharide induces the early enhancement of mice colonic mucosal paracellular permeability mainly mediated by mast cells
(Universidad de Murcia. Departamento de Biología Celular e Histología, 2019) Sun, Tingyi; Wang, Yaxi; Hu, Shilong; Sun, Haimei; Yang, Shu; Wu, Bo; Ji, Fengqing; Zhou, Deshan
The alteration of intestinal mucosal barrier is considered to be the central pathophysiological process in response to gastrointestinal infections, and mucosal microstructural damage is a major factor for enhancing epithelial permeability in persistent bacterial infections. However, the mechanism involved in hyperpermeability in the early stage of acute bacterial infections is not fully understood. In the present study, fluorescein isothiocyanate-dextran across and transepithelial resistance measured in Ussing chambers were used to assess the intestinal paracellular permeability. Mast cell activation was evaluated by western blotting for the presence of tryptase released from mast cells. Serum levels of interleukin-6 were evaluated using enzymelinked immunosorbent assay. Our results indicated that mast cells played a pivotal role in colonic mucosal hyperpermeability in wild type mice treated with lipopolysaccharide (LPS) for 2 h. And the effect of LPS was mainly dependent on mast cell degranulation, while no change in permeability was observed in the mast celldeficient mice (Wads-/- ) after LPS administration. No obvious changes of the mucosal structure including histomorphological architecture and expression of intercellular junction proteins were obtained in either wild type or Wads-/- mice after LPS stimulation by hematoxylin and eosin staining, immunofluorescence staining and western blot analysis. Furthermore, the selfrenewal of intestinal epithelia, detected by using proliferation marker 5’-bromo-2’-deoxyuridine, was not involved in increased permeability. Collectively, activation of mast cells induced by LPS mediated intestinal hyperpermeability in the initial stage, and played a crucial role in barrier dysfunction rather than mucosal microstructural damage in acute enterogenous bacterial infection.
Open Access
Mast cell chymase: an indispensable instrument in the pathological symphony of idiopathic pulmonary fibrosis?
(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2013) Kosanovic, Djuro; Daha, Bhola Kumar; Wygrecka, Malgorzata; Reiss, Irwin; Günther, Andreas; Ghofrani, Ardeschir; Weissmann, , Norbert; Grimminger, Friedrich; Seeger, Werner; Schermuly, Ralph Theo; Banat, Gamal-Andre
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and fatal lung disease with no known etiology and treatment options. The hallmarks of the histopathology, which is characteristic of usual interstitial pneumonia (UIP) pattern, include interstitial fibrosis, honeycomb changes and fibroblast foci that develop owing to fibroblast proliferation and excessive matrix deposition. Although the complete pathomechanism is not yet understood, several molecular culprits, including transforming growth factor (TGF)-ß, Angiotensin (Ang) II, endothelin (ET)-1, matrix metalloproteinases (MMPs) and cytokines have been identified. IPF is increasingly believed to be an epithelial-driven disease; however, the literature does support an implication of altered immune response and inflammatory processes in the onset or progression of the disease. Mast cells (MCs) are multifunctional tissue resident cells involved in the inflammatory and immune response. An increasing body of evidence suggests a role of MCs and their mediator chymase in the pathology of IPF. With regard to the underlying mechanisms, it is conceivable that MC chymase may function via activation or processing of factors such as proteases, cytokines and growth factors. In this review, we will discuss how MC chymase is linked to and can potentially contribute to the development of IPF. Moreover, the findings from animal model studies will be discussed to highlight the chymase inhibitors as a promising strategy for the treatment of pulmonary fibrosis.
Open Access
Mast cell granule composition and tissue location - a close correlation
(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2000) Beil, W. J.; Schulz, M.; Wefelmeyer, U.
This review provides a survey on mast cell heterogeneity, with aspects differing in humans and rodents or which are subject of conflicting evidence being discussed in greater detail. Mast cell subsets have been first defined in rats by their fixation and dyebinding properties, and detailed studies in humans and pigs reveal very similar observations. The dye-binding properties of rat mast cell subsets are causally related to the absence or presence of heparin in their granules. In humans, this relation has not been shown. Rodent mast cell subsets store different chymase-isoforms. In contrast, just a single chymase has been defined in humans, and mast cells are classified by the presence or relative absence of this chymase. Different investigators find quite different proportions of chymase-positive to chymase-negative mast cells. Tryptase(s) are found in most or every human mast cell, but in rodents, they have hitherto been essentially localised to mast cells in connective tissues. Human mast cell subsets may also be defined by their expression of receptors such as CSaR and possibly the B-chemokine receptor CCR3; the CCR3 expression seems to be related to the human mast cell chymase expression. Ultrastructural studies are helpful to distinguish human mast cell subsets, and allow to distinguish between chronic and acute activation. The phenotypical characteristics may change in association with inflammation or other disease processes. Studies in humans and pigs show changed dye-binding and fixation properties of the granules. Experimental rodent infection models reveal similar changes of chymase isoform expression. Human lung mast cells have been reported to strongly upregulate their chymase content in pulmonary vascular disease. This line of evidence can explain some inconsistent information on mast cell heterogeneity and may help to understand the physiological role of mast cells.
Open Access
Mast cells and wound healing: Still an open question
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Fernández Guarino, Montserrat; Bacci, Stefano
Open Access
Pathomechanism of entrapment neuropathy in diabetic and nondiabetic rats reared in wire cages
(Murcia : F. Hernández, 2008) Nishimura, Toshico; Hirata, Hitoshi; Tsujil, Masaya; Iida, Ryu; Hoki, Yoko; Iino, Takahiro; Ogawa, Satoru; Uchida, Atsumasa
To examine the pathomechanism of entrapment neuropathy associated with diabetes with special emphasis on the roles of mast cells and Tenascin- C using a rat model of Streptozotocin-induced diabetes. The roles of mast cells and Tenascin-C in development of tarsal tunnel syndrome were analyzed electrophysiologically and histologically in 20 male Ws/Ws-/-rats (mast cell deficient) and 20 of their male wild type counterparts (12-16 weeks old; 250-300g). Rats were assigned randomly to one of the following three groups; diabetic group and nondiabetic group reared in cages with a wire grid flooring; non-diabetic group in cages with sawdust covered plastic flooring. No significant role for mast cells in entrapment neuropathy was found in the rats with streptozotocin-induced diabetes. Distal latency was prolonged in diabetic rats compared with nondiabetic rats, and positively correlated with increases in blood glucose levels. Tenascin-C expression levels in the endoneurium at the tarsal tunnel in diabetic rats were found to be correlated with distal latency. The anti-alpha-smooth muscle actin (a-SMA) positive myofibroblast was scattered in nerve fascicles overexpressing Tenascin-C. It seems likely that Tenascin-C expressing myofibroblasts constrict axons by inducing collagen contraction of the endoneurium. Our data indicate that metabolic and phenotypic abnormalities of endoneurium and perineurum lie behind the vulnerability of diabetic patients to entrapment neuropathy.
Open Access
Reorganization of the subplasmalemmal cytoskeleton in association with exocytosis in rat mast cells
(Murcia : F. Hernández, 1989) Holm Nielsen, E.; Braun, K.; Johansen, T.
The subplasmalernmal cytoskeleton in mast cells has been studied by scanning electron microscopy of the internal side of the plasma membrane. Rearrangement of the dense subplasmalemmal network of actin filaments took place following cell activation by compound 48/80 and secretion of histamine. The rearrangement was a withdrawal of the subplasmalemmal cytoskeleton from the exocytotic sites and the development of bare, filament-free areas around the sites. In calciumdepleted mast cells we demonstrated a dense network that was difficult to break. Activation of the calciumdepleted cells by compound 48/80 did not induce rearrangement of the network, and in parallel there was no secretion of histamine.
Open Access
Ri bonuclease-gold labels proteoglycancontaining cytoplasmic granules and ribonucleic acid-containing organelles - A survey
(Murcia : F. Hernández, 1999) Dvorak, A. M.; Morgan, E.S.
An enzyme-affinity-gold method to detect RNA in routinely prepared ultrastructural samples is based on the affinity of the gold-coupled enzyme, ribonuclease, for its substrate, RNA. High concentrations of a known inhibitor of RNase, heparin, are uniquely located in human mast cell granules. Specific labeling for the presence of heparin in these structures was determined using the RNase-gold (R-G) reagent based on the RNase inhibitor property of heparin. This property was used to probe for the presence of proteoglycans (PG) known to be present in a wide variety of ultrastructural samples, none of which contain heparin. In addition to known subcellular sites of RNA, the R-G reagent was shown to bind to PG-rich cytoplasmic granules in a wide variety of leukocytes and secretory cells of epithelial, endocrine, and neuroendocrine origin. This newly recognized property was used to image the changing distribution of labeled PGs during cellular maturation, secretion, and recovery from secretion of secretory cells in vivo, ex vivo, in vitro and in isolated, biochemically defined guinea pig basophil granule preparations.
Open Access
RNA is closely associated with human mast cell lipid bodies
(Murcia : F. Hernández, 2003) Dvorak, A. M.; Morgan, E.S.; Weller, P.F.
Both novel and multiple ultrastructural studies based on different principles show relationships of cytoplasmic lipid bodies and ribonucleic acid (RNA) of potential importance to RNA metabolism in human mast cells. The methods include general ultrastructural morphological observations, imaging of RNA with an EDTA regressive stain, imaging of the incorporation of radio labeled uridine by ultrastructural autoradiography, postembedding immunogold labeling of uridine, ribosomes and small nuclear ribonuclear proteins and ultrastructural in situ hybridization detection of poly(A)- positive messenger RNA. Altogether these studies implicate human mast cell lipid bodies in RNA metabolism and are analogous to earlier similar studies which showed that human mast cell granules also curtain RNA.
Open Access
The mast cell: an active participant or an innocent bystander?
(Murcia : F. Hernández, 2004) Crivellato, E.; Beltrami, C.A.; Mallardi, F.; Ribatti, Doménico
Mast cells (MC) are phylogenetically old cells which are distributed throughout the human organism and, on the whole, occupy roughly the volume of the spleen. MC have long been recognized as key cells of type I hypersensitivity reactions. Several lines of evidence, however, indicate that they not only express critical effector functions in classic IgE-associated allergic disorders, but also play important roles in host defence against parasites, bacteria and perhaps even viruses. Indeed, it is now clear that MC can contribute to host defence in the context of either acquired or innate immune responses through the release of a myriad of pro-inflammatory and immunoregulatory molecules and the expression of a wide spectrum of surface receptors for cytokines and chemokines. Moreover, there is growing evidence that MC exert distinct nonimmunological functions, playing a relevant role in tissue homeostasis, remodeling and fibrosis as well as in the processes of tissue angiogenesis. In this review, we provide a small insight into the biology of human MC and their potential implications in clinical pathology
Open Access
The morphofunctional pattern of neuronal biogenic amines in postpartum involution period - in vivo study
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Gu, Hao; Dindyaev, Sergey V.; Beeraka, Narasimha M.; Kasatkin, Denis V.; Mikhaylenko, Elizaveta V.; Liu, Junqi; Kirkland, Cecil Eric; Aliev, Gjumrakch; Somasundaram, Siva G.; Muresanu, Cristian; Fan, Ruitai
Postpartum uterine diseases are associated with significant imbalance in the levels of biogenic amines (BAs) in rat uterus. Mast cells (MCs) are the main suppliers of BAs such as serotonin, catecholamines, and histamine in uterus. There is limited evidence of the BA-positive elements involved in the physiological regulation of uterus during postpartum involution. The aim of present study is to determine the concentration and distribution of biogenic amines (BAs) such as histamine, serotonin, and catecholamines in the uterine endometrium, myometrium, and peritoneal fluid (PF) during the postpartum uterine involution. A total of 110 nulliparous outbred female nonpregnant Wistar rats of mature age were divided into eleven groups (n=10 per group) according to days of postpartum involution. Tissue specimens of uterine segments, PF were prepared. Serotonin, catecholamines, and histamine concentrations were examined by fluorescence-histochemical techniques. The fluorescence of the BA-positive elements was detected and analyzed by microspectrofluorimetry. Results were analyzed using the KruskalWallis chi-squared test and pairwise Mann-WhitneyWilcoxon tests with "Benjamini-Hochberg correction" in R 3.6.3. Mast cells in uterine segments, PF exhibited characteristic yellowish-green fluorescence. The highest MCs number was reported in corpus uteri on the 15th day of postpartum involution. Serotonin, catecholamines, and histamine levels were significantly higher in BA-positive elements in the initial days. BA content was dynamic and relies on the time elapsed after parturition. There was statistically significant difference in the levels of BAs in the cornu and cervix uteri. A single morphofunctional complex of BA supply was noticed in the reproductive system of the rats. The coupled interactions of intra- and extra-organic BA-positive elements was associated with anabolic/catabolic equilibrium in uterus through the metabolism of serotonin, catecholamines, and histamine during postpartum involution.
Open Access
Ultrastructural changes in bones of the senescence-accelerated mouse (SAMP6): a murine model for senile osteoporosis
(Murcia : F. Hernández, 2004) chen, H.; Shoumura, S.; Emura, S.
SAMP6, a substrain of senescenceaccelerated mice, was developed as an animal model for senile osteoporosis. In the present study, we investigated the bone morphology, together with serum calcium and bone mineral density (BMD) in SAMP6 and agematched normal mice SAMR1. We did not find any significant differences between SAMR1 and SAMP6 at 1 month of age with regard to the serum compositions and bone morphology. As compared with SAMR1, BMD, the femoral weight, femoral calcium and phosphorus levels were significantly reduced in SAMP6 at 2 and 5 months of age. The number of osteoblasts in trabecular bones was also significantly reduced. Swollen mitochondria and myelin-like structures were found in osteoblasts and osteocytes of SAMP6 mice at 2 and 5 months of age. There was a greater proportion of resting surface and less forming surface in the femoral endosteal surfaces of SAMP6 mice. The amount of trabecular bone in the lumbar vertebra and the distal metaphysis of the femur was reduced. The number of the mast cells in bone marrow of the tibia significantly increased in SAMP6 mice. These findings indicate that the lower bone mass in SAMP6 was due to the reduction in osteoblast formation and suggested that mast cells in bone marrows play a role in the pathogenesis of senile osteoporosis.

Browsing by Subject "Mast cells"

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