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At least 1,423 records · Page 79Linked to original sources
PubMed2000

Persistent anaphylactic reaction after induction with thiopentone and cisatracurium.

A 6-year-old boy presented for surgery for phimosis. The anaesthetic technique included intravenous induction with thiopentone and neuromuscular blockade with cisatracurium. Severe persistent bronchospasm and central cyanosis followed the administration of these drugs. A continuous i.v. infusion of epinephrine at 0.2 microg. kg(-1) x min(-1) was necessary to break the severe refractory bronchial hyperresponsiveness. There was no previous exposure to anaesthetic drugs and no definite family history of allergy. Through increased serum eosinophil cationic protein, tryptase and histamine levels and IgE levels specific to cisatracurium, we demonstrated an IgE-mediated anaphylactic reaction to cisatracurium in the child's first exposure to this new neuromuscular blocking agent. Anaphylactic reactions to new anaesthetic drugs may be challenging to recognize and treat during general anaesthesia in children. The pathogenesis, diagnosis and management of life threatening persistent allergic reactions to intravenous anaesthetics are discussed.

Adrenergic Agonists↗
PubMed2002

A long-term coculture model for the study of mast cell-keratinocyte interactions.

Physiologic and pathologic events associated with cutaneous differentiation and repair are the result of a concerted action of various types of resident tissue cells. In vitro models simulating this complex in vivo situation are therefore needed to clarify the specific contribution and relevant interaction of, for example, dermal mast cells with other major cutaneous cells. The aim of this study was to establish a long-term coculture model that includes dermal mast cells, dermal fibroblasts, and keratinocytes in a human skin equivalent organotypic setting. Normal dermal mast cells and fibroblasts (1:4) were enclosed in collagen gel and normal keratinocytes were grown on top with exposure to the air interface. Under these conditions, mast cell integrity and functionality was preserved even after 4 wk of culture, as shown by electron microscopy and immunohistochemistry using antibodies against the mast-cell-specific granule enzyme tryptase and the receptors for stem cell factor and IgE. Mast cells also released histamine on stimulation with anti-IgE, and on ultrastructure were found to degranulate, with decrease of granule matrix density and formation of cell-cell contacts with fibroblasts. After 2 wk of culture, keratinocytes had formed an epidermis-like multilayer and were able to proliferate and differentiate, as shown by bromodeoxyuridine incorporation of basal cells and immunohistochemical staining for transglutaminase and cytokeratins 1 and 10. The model presented here thus provides a potentially relevant tool to further clarify the interaction of dermal mast cells with major other skin cells and their contribution to cutaneous physiology, repair processes, and pathology.

Cell Communication↗
PubMed2001

Role of stem cell factor and mast cells in the progression of chronic glomerulonephritides.

BACKGROUND: Mast cells (MCs) have been implicated in the pathogenesis of atherosclerosis and tissue fibrosis. However, the role of MC in the development of renal fibrosis has not been fully elucidated. Stem cell factor (SCF; the ligand for MC c-kit receptor) is thought to attract and activate MCs. METHODS: The intensity of MC infiltration and SCF expression in renal biopsies from 56 patients with different forms of primary and secondary glomerulonephritis and five controls were investigated by immunohistochemistry, using a monoclonal anti-human MC tryptase antibody and a polyclonal antihuman SCF antibody. RESULTS: A large number of MCs were detected in the renal interstitium of the diseased kidneys. Immunostainable SCF was detected in tubular as well as interstitial cells. MC infiltration was significantly higher in glomerulonephritis (16.9 +/- 10.2 cells/field) compared with controls (2.8 +/- 2.1 cells/field, P = 0.03). Similarly, immunostainable SCF was 0.6 +/- 0.3% for controls and 3.3 +/- 2.1% in the glomerulonephritis group (P = 0.02). MC infiltration was highly correlated with SCF expression in diseased kidneys (r = 0.93, P = 0.0001). Double immunostain showed them to colocalize in some interstitial cells. Analysis of MC proliferation [proliferating cell nuclear antigen (PCNA) positivity] and apoptosis (in situ end labeling of DNA) showed these cells to be terminally differentiated. Both MCs and SCF were correlated with interstitial fibrosis (R = 0.71 for MC and R = 0.62 for SCF, P = 0.0001) and interstitial alpha-smooth muscle actin (R = 0.69 for MC and R = 0.60 for SCF P = 0.0001). Using regression analysis, the number of MC infiltration was found to be a very powerful determinant of interstitial fibrosis in the glomerulonephritis group (R2 = 91.4%). CONCLUSION: MCs as an infiltrating hematopoietic cell and its growth factor (SCF) seem to be up-regulated in glomerulonephritis, and may play a role in the development of renal fibrosis.

Adolescent↗
PubMed2001

Mast cell chymase expression and mast cell phenotypes in human rejected kidneys.

BACKGROUND: Mast cells (MCs) are known to participate in various types of chronic disease, but their role in chronic renal rejection is poorly understood. Recently, distinct phenotypes of MCs have been described in humans by the demonstration of one protease, chymase. Hence, we questioned whether chymase in MCs could play a role in the pathogenesis of renal rejection in humans. METHODS: We investigated MC chymase expression and MC phenotypes, using immunohistochemical single- and double-staining techniques, in nephrectomy (N = 13) and biopsy (N = 8) specimens of human rejected kidneys. Tissue chymase levels were determined by enzymatic assay for chymase activity. We also examined the association between MC chymase expression and the degree of interstitial fibrosis in these renal allografts. RESULTS: Based on chymase positivity, rejected kidneys were divided into two groups, a chymase-negative [Chy(-)] group and a chymase-positive [Chy(+)] group. Quantitative analysis showed that the number of chymase-positive MCs and tissue chymase levels were significantly higher in the Chy(+) group than in the Chy(-) group. Furthermore, the interstitial fibrotic area in the Chy(+) group was significantly larger than that in the Chy(-) group. Immunodouble staining analysis also demonstrated that a new MC phenotype, positive for chymase but negative for tryptase, was present in the human rejected kidney. CONCLUSIONS: These results show that increased expression of chymase in MCs is related to the severity of interstitial fibrosis in human rejected kidneys.

Adolescent↗
PubMed1999

Mast cell density and subtypes in the skin of dogs with atopic dermatitis.

Skin biopsies from seven dogs with atopic dermatitis and 13 dogs with no clinical or histological evidence of skin diseases were examined. The study of the atopic dogs included 11 biopsy samples of nonlesional skin and 15 samples of lesional skin. One section of each tissue sample was stained with haematoxylin and eosin and another with toluidine blue to demonstrate the sulphated acid glycosaminoglycans in mast cell (MC) granules. To investigate MC subtypes, the MC-specific proteases tryptase and chymase were examined by a double enzyme-immunohistochemical staining technique. With the double labelling technique a significantly lower mast cell density was demonstrated in lesional (P = 0.0023) and nonlesional (P = 0.0004) skin samples of the atopic dogs than in the skin of control dogs. In the dermis of control dogs, a median mast cell density of 31.2 MC/mm2 was detected with the toluidine blue staining method and of 27.5 MC/mm2 with the double labelling technique. In lesional dermis of atopic dogs 29.8 MC/mm2 were seen with toluidine blue while only 12.4 MC/mm2 were stained with the double labelling method (P = 0.0027). A similar difference was observed in nonlesional dermis samples, in which a mast cell density of 23.3 MC/mm2 was detected with toluidine blue but only 6.4 MC/mm2 with the double labelling method (P = 0.0127). The data provide evidence that mast cell granule heterogeneity exists in the dog and suggests that degranulation occurs selectively, depending on the pathological condition of the canine skin. Further investigations on the pathophysiological role of mast cell subtypes may help to elucidate the pathogenesis of atopic dermatitis.

Animals↗
PubMed2003

Gastric mucosal mast cells are increased in Helicobacter pylori-negative functional dyspepsia.

BACKGROUND & AIMS: Mast cells might be involved in pathogenesis of functional dyspepsia because they can release a wide range of potent mediators, capable of altering gastric nerve and muscle function. This study aimed to determine whether mast cell numbers were increased in the gastric mucosa of patients with functional dyspepsia compared to control subjects. METHODS: Biopsy samples were taken from the antrum and corpus of 111 patients: 20 asymptomatic control subjects, 62 patients with Rome criteria functional dyspepsia (33 Helicobacter pylori positive, 29 H. pylori negative), and 29 inflammatory control subjects (H. pylori positive). Mast cells were detected immunohistochemically by using a mouse monoclonal antibody specific for tryptase. Quantification was performed with light microscopy, and results were expressed as mast cells/mm(2) +/- standard error of mean. RESULTS: Mast cells were significantly increased in H. pylori negative functional dyspepsia samples compared to normal control samples in the antrum (230.1 +/- 11.3 vs. 94.8 +/- 8.4, P < 0.001) and corpus (264.1 +/- 27.1 vs. 123.9 +/- 11.5, P = 0.001). Mast cells were also significantly increased in the antrum of patients with H. pylori positive functional dyspepsia compared to asymptomatic control subjects (166.5 +/- 17.0 vs. 94.8 +/- 8.4, P < 0.03). However, there was no significant difference between mast cell numbers in patients with H. pylori positive functional dyspepsia compared to inflammatory control subjects. CONCLUSIONS: Mast cells are increased in functional dyspepsia, independently of inflammation. This might contribute to the pathogenesis of functional dyspepsia by altering signaling in the brain-gut axis.

Adolescent↗
PubMed2001

Studies on the mechanism of edematous changes at the endometrial stroma for implantation.

The endometrium undergoes edematous changes during the implantation period. Many factors may be involved in these biochemical reactions. We investigated the localization of inducible NO synthase (iNOS), interleukin-8 (IL-8), mast cell tryptase, neutrophil elastase, type III collagen, and CD44 in human endometrium. Immunohistochemical staining was performed by the labeled streptavidin-biotin method. iNOS was stained in the entire endometrial tissue from the midproliferative phase. The IL-8-positive cells, mast cells, and neutrophil elastase in the stroma increased toward the early to midsecretory phase. Type III collagen was arranged regularly in the stromal extracellular matrix during the proliferative phase; however, it was dissected during the secretory phase. CD44 was detected around stromal cells in the midsecretory phase. From these results, we propose the following mechanism. Initially, iNOS, expressed by the entire endometrial tissues from the midproliferative phase, catalyzes the production of NO. NO stimulates cells, supposed to be mast cells, to produce IL-8, which lets neutrophils migrate into the stroma. Neutrophils secrete elastase, which degrades type III collagen, generating spaces in the stroma. Hyaluronic acid adheres to CD44 around the stromal cells and retains water intermolecularly, finally forming the edematous matrix.

Adult↗
PubMed1995

[Allergic and pseudo-allergic reactions in anesthesia. II: Symptoms, diagnosis, therapy, prevention].

In this article we present the symptomatic features and discuss relevant diagnostic and therapeutic aspects of anaphylactoid reactions. In addition we give practical advice as to how to avoid and manage allergic or pseudoallergic reactions during anaesthesia. Measurements of serum tryptase-levels and of methylhistamine in urine have been introduced in clinical diagnostic routine. Skin tests and determination of specific antibodies are essential to identify responsible substances. Preventive measures like careful premedication, calm atmosphere, slow injection of drugs, the use of diluted solutions, and the use of drugs with a low potential for anaphylactoid reactions are important. Substances like inhalation anaesthetics, propofol, etomidate, ketamine, midazolam, fentanyl, alfentanil and bupivacain without epinephrine should be used.

Anesthesia, General↗
PubMed2000

Basophil and eosinophil accumulation and mast cell degranulation in the nasal mucosa of patients with hay fever after local allergen provocation.

BACKGROUND: Basophils and mast cells have certain similarities and are believed to be important in upper and lower respiratory allergy. OBJECTIVE: We sought to apply immunohistology to investigate the distribution and numbers of mast cells and basophils in the nasal mucosa after allergen provocation. METHODS: Allergen challenge with grass pollen was performed in 9 patients with seasonal allergic rhinitis out of the hay fever season. Nasal biopsy specimens were taken before and approximately 1 hour, 24 hours, and 1 week after intranasal allergen provocation. We determined relative numbers and their phenotypic characteristics by using mAbs specific for tryptase, chymase, IgE, eosinophils (BMK-13), and a new mAb against basophils (BB1) by using immunohistochemistry in frozen sections. RESULTS: In the nasal mucosa at baseline, practically no basophils were found in the epithelium. A significant increase in numbers was found in the epithelium and lamina propria of the nasal mucosa in the early phase as early as 1 hour after allergen provocation. At 24 hours and 1 week after allergen provocation, a significant increase in basophil numbers was found in the lamina propria only. The proportion of mast cells staining for chymase in the lamina propria decreased from a median of 38% (range, 0%-82%) to 14% (range, 0%-78%) within 1 hour of allergen provocation. The proportion of mast cells staining for chymase increased from 1% (range, 0%-86%) at baseline to 21% (range, 3%-85%) within 1 hour of allergen provocation. One week after provocation, mast cells returned to baseline numbers. A definite tissue eosinophilia was observed after allergen provocation. CONCLUSION: Basophil numbers are increased in the epithelium and lamina propria of the nasal mucosa of subjects with rhinitis after allergen challenge, with influx already apparent at 1 hour. Moreover, changes in mast cell percentages and numbers were observed within 1 hour of allergen provocation.

Adult↗
PubMed1995

Conditioned media from a cell strain derived from a patient with mastocytosis induces preferential development of cells that possess high affinity IgE receptors and the granule protease phenotype of mature cutaneous mast cells.

We have demonstrated for the first time that a conditioned medium from a human cell strain can induce morphologically mature mast cells that express Fc epsilon RI and three mast cell-specific proteases from normal bone marrow progenitor cells. In contrast, recombinant human Kit ligand induced the differentiation of mast cells that were tryptase-positive but negative for chymase, carboxypeptidase, and Fc epsilon RI. This data indicates that factors other than Kit ligand are critical for inducing the differentiation and maturation of mast cells in the human. The HBM-M cell was originally derived from a patient with mastocytosis. As mastocytosis is thought to represent a reactive hyperplasia rather than a mast cell malignancy, the factor secreted by the HBM-M cell strain could well be responsible for the mast cell hyperplasia seen in some patients with mastocytosis.

Base Sequence↗
PubMed1999

Generation of catalytically active granzyme K from Escherichia coli inclusion bodies and identification of efficient granzyme K inhibitors in human plasma.

Granzymes are granule-stored lymphocyte serine proteases that are implicated in T- and natural killer cell-mediated cytotoxic defense reactions after target cell recognition. A fifth human granzyme (granzyme 3, lymphocyte tryptase-2), renamed as granzyme K (gene name GZMK), has recently been cloned from lymphocyte tissue. For its further characterization we successfully generated catalytically active enzyme in milligram quantities per liter of Escherichia coli culture. The natural proform of granzyme K with the amino-terminal propeptide Met-Glu was expressed as inclusion bodies and converted to its active enzyme by cathepsin C after refolding of precursor molecules. Recombinant granzyme K cleaves synthetic thiobenzyl ester substrates after Lys and Arg with k(cat)/K(m) values of 3.7 x 10(4) and 4.4 x 10(4) M(-1) s(-1), respectively. Granzyme K activity was shown to be inhibited by the synthetic compounds Phe-Pro-Arg-chloromethyl ketone, phenylmethylsulfonyl fluoride, PefablocSC, and benzamidine, by the Kunitz-type inhibitor aprotinin and by human blood plasma. The plasma-derived inter-alpha-trypsin inhibitor complex, its bikunin subunit, and the second carboxyl-terminal Kunitz-type domain of bikunin were identified as genuine physiologic inhibitors with K(i) values of 64, 50, and 22 nM, respectively. Inter-alpha-trypsin inhibitor and free bikunin have the potential to neutralize extracellular granzyme K activity after T cell degranulation and may thus control unspecific damage of bystander cells at sites of inflammatory reactions.

Alpha-Globulins↗
PubMed2005

Chemerin activation by serine proteases of the coagulation, fibrinolytic, and inflammatory cascades.

Proteases function at every level in host defense, from regulating vascular hemostasis and inflammation to mobilizing the "rapid responder" leukocytes of the immune system by regulating the activities of various chemoattractants. Recent studies implicate proteolysis in the activation of a ubiquitous plasma chemoattractant, chemerin, a ligand for the G-protein-coupled receptor CMKLR1 present on plasmacytoid dendritic cells and macrophages. To define the pathophysiologic triggers of chemerin activity, we evaluated the ability of serum- and inflammation-associated proteases to cleave chemerin and stimulate CMKLR1-mediated chemotaxis. We showed that serine proteases factor XIIa and plasmin of the coagulation and fibrinolytic cascades, elastase and cathepsin G released from activated neutrophil granules and mast cell tryptase are all potent activators of chemerin. Activation results from cleavage of the labile carboxyl terminus of the chemoattractant at any of several different sites. Activation of chemerin by the serine protease cascades that trigger rapid defenses in the body may direct CMKLR1-positive plasmacytoid dendritic cell and tissue macrophage recruitment to sterile sites of tissue damage, as well as trafficking to sites of infectious and allergic inflammation.

Amino Acid Sequence↗
PubMed2002

Immunohistological analysis of mast cell numbers in the intratumoral and peritumoral regions of prostate carcinoma compared to benign prostatic hyperplasia.

Recently, some studies reported the presence of mast cells in various malignancies and their role in tumor growth. The aim of the study was to determine the utility of mast cell numbers in evaluating benign and malignant prostate lesions, and to ascertain whether there are variations in the numbers of mast cells with the Gleason grade. The relationship between mast cell numbers and patient age was also investigated. Retrospectively, 104 prostate specimens were examined for the presence of mast cells. The study group consisted of 57 benign prostatic hyperplasias and 47 prostate carcinomas. The paraffin sections were stained with anti-human mast cell tryptase immunohistologically. The numbers of positively staining cells in five high-power fields were counted, and their mean was calculated. There was no relationship found between mast cell numbers and age statistically. The mean mast cell numbers of the intratumoral region were significantly different from those of the peritumoral region (p = 0.0001). While the difference between benign hyperplasia and the intratumoral region was found to be significant (p = 0.0001), no difference between hyperplasia and the peritumoral region was noted (p = 0.762). There was no statistical difference between Gleason score groups (p = 0.452), and there was no interaction between score groups and intraperitumoral regions (p = 0.355).

Adenocarcinoma↗
PubMed2004

Mast cells induce activation of human lung fibroblasts in vitro.

Mast cells are able to induce proliferation of skin fibroblasts; however, their effect on lung fibroblasts has not been clearly established. Using in vitro cocultures of rat or human mast cells with lung fibroblasts, the authors determined whether mast cells alter proliferation, collagen synthesis, and metalloproteinase production from lung fibroblasts. Mast cells enhanced the proliferation of human fibroblasts (mean +/- SEM: 90% +/- 4.7% increase, P < .001) while inhibiting fibroblast collagen synthesis (48.1% +/- 4.2% decrease, P < .001). Histamine, but not tryptase, significantly enhanced fibroblast proliferation: 92% +/- 5.8% (P < .001) and 39.2% +/- 4.3% (P > 0.05), respectively. Rat mast cell sonicate added to lung fibroblasts induced the activation of metalloproteinase-9 while inhibiting that of metaloproteinase-2. The addition of lipopolysaccharide (LPS)-stimulated lung macrophage supernatant further enhanced the poliferative effect of mast cells on fibroblasts (by 60% +/- 7.8%, P < .001) and induced synthesis of collagen from these cells (190% +/- 28% increase versus control, P < .05). This study demonstrates that mast cells influence several aspects of lung fibroblast function in vitro.

Cell Extracts↗
PubMed2006

Upregulation of the axonal growth and the expression of substance P and its NK1 receptor in human allergic contact dermatitis.

Nerve fibers and sensory neuropeptides substance P and calcitonin gene-related peptide (CGRP) have been reported to be involved in allergic contact dermatitis (ACD). In the present study, we investigated the general innervation (using antibody against protein gene product 9.5, PGP 9.5), axonal growth (using antibody against growth associated protein, GAP-43), CGRP, and substance P with its receptor neurokinin 1 (NK1), in positive epicutaneous reactions to nickel sulphate from nickel-allergic patients, at the peak of inflammation, 72 hr after challenge with the antigen. There was an increased (p < 0.01) number of GAP-43 positive fibers in the eczematous compared with control skin, indicating an increased axonal growth already at 72 hr postchallenge. Double staining revealed a coexpression of CGRP and GAP-43 on dermal nerve fibers. There was no difference in the number of substance P and CGRP positive nerve fibers between eczematous and control skin. However, semiquantification analyses showed an increased expression of substance P positive inflammatory cells, being CD3, CD4, or CD8 positive, and NK1R positive inflammatory cells, being tryptase or CD3 positive. These results indicate a contribution of regenerating nerve fibers and substance P to the contact allergic reaction.

Axons↗
PubMed2002

Stem cell factor-induced bone marrow mast cell hyperplasia mimicking systemic mastocytosis (SM): histopathologic and morphologic evaluation with special reference to recently established SM-criteria.

Although systemic mastocytosis (SM) is a well-defined hematologic neoplasm, it is sometimes difficult to discriminate between SM and a reactive mast cell (MC) hyperplasia. We describe a patient with aplastic anemia who was treated with recombinant stem cell factor (SCF). In response to SCF, the patient showed transient hematologic improvement and developed a marked increase in MC as well as a transient increase in serum tryptase. Histologic and immunohistochemical examination revealed a huge increase in MC in the bone marrow with focal infiltrates similar to SM. However, most of the SM-criteria were not met: First, MC showed normal cytomorphological characteristics without significant atypias (no cytoplasmic extensions, no oval nuclei, no hypogranulated cytoplasm). Furthermore, bone marrow MC were CD2- and CD25-negative and did not exhibit the C-KIT 2468 A-->T mutation (Asp-816-Val). After discontinuation of SCF the MC hyperplasia resolved confirming its reactive nature. Based on our case and similar cases mimicking mastocytosis, it seems of importance to apply recently established SM criteria in order to discriminate between reactive MC hyperplasia and true mastocytosis with certainty.

Anemia, Aplastic↗
PubMed1997

Secretory granule proteases in rat mast cells. Cloning of 10 different serine proteases and a carboxypeptidase A from various rat mast cell populations.

Two of the major rat mast cell proteases, rat mast cell protease 1 (RMCP-1) and RMCP-2, have for many years served as important phenotypic markers for studies of various aspects of mast cell (MC) biology. However, except for these proteases only fragmentary information has been available on the structure and complexity of proteases expressed by different subpopulations of rat MCs. To address these questions, cDNA libraries were constructed from freshly isolated rat peritoneal MCs and from the rat mucosal MC line RBL-1. cDNA clones for 10 different serine proteases (RMCP-1-10), and the MC carboxypeptidase A were isolated and characterized. Six of these proteases have not been isolated previously. Based on their protease content, three separate subpopulations of MCs were identified. Connective tissue MCs (CTMCs) from the ear and peritoneum express the chymases RMCP-1 and -5, the tryptases RMCP-6, and -7 and the carboxypeptidase A. However, based on a large difference in the level of expression of RMCP-7, CTMCs of these two organs may be regarded as two separate subpopulations. RMCP-2 and the three closely related proteases of the RMCP-8 subfamily were identified as the major mucosal MC proteases in rat. In contrast to what has been reported for human MCs, no expression of cathepsin G or cathepsin G-like proteases was detected in any of the rat MC populations. To determine mRNA frequencies for the various proteases expressed by normal tissue MCs, an unamplified peritoneal MC cDNA library was screened with a panel of mono-specific cDNA probes. These results showed that peritoneal MCs are highly specialized effector cells with mRNA frequencies for the major proteases in the range of several percent of the total mRNA pool.

Amino Acid Sequence↗
PubMed2002

Regulation of eosinophil-active cytokine production from human cord blood-derived mast cells.

Human mast cells are multifunctional tissue-dwelling cells that play a crucial role in eosinophil-dependent disorders, such as asthma and parasitic diseases, by the secretion of eosinophil-active mediators. Mast cell-derived cytokines, generated in response to cross-linking of the high-affinity IgE receptor, can regulate eosinophil activation, survival, and chemotaxis. In this study, mast cells generated from human cord blood progenitors (stem cells) were studied for eosinophil-active inflammatory cytokine expression. Cord blood-derived mast cells (CBDMC) expressed typical intracellular scroll granules and microvilli-like structures on their cell surfaces, demonstrated the presence of tryptase, and elaborated prostaglandin D2 (PGD2) after cross-linkage of the high-affinity receptor for IgE (FcepsilonRI). CBDMC expressed tumor necrosis factor-alpha (TNF-alpha) and the eosinophil-active growth factors, interleukin-5 (IL-5) and granulocyte-macrophage colony-stimulating factor (GM-CSF) after activation. (IL-1beta greatly enhanced IgE-dependent production of these cytokines in response to FcepsilonRI cross-linkage, suggesting a role for bystander/phagocytic cells in modulating mast cell function. In contrast, interferon-alpha (IFN-alpha) inhibited IL-5 and GM-CSF generation, and the glucocorticoid, dexamethasone (Dex), inhibited production of IL-5 and GM-CSF from CBDMC. A macrophage-mast cell-eosinophil axis may exist in vivo that may be susceptible to pharmacologic manipulation.

Cells, Cultured↗