Histochemical comparison of vertebrate mast cells

Chiu, Herbert; Lagunoff, David

doi:10.1007/bf01004972

Cited by 67 publications

(21 citation statements)

References 39 publications

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“…There is uncertainty as to whether or not the mast cells function as a storage site for histamine in fish (Ellis 1982), despite the fact that several previous studies have conclusively demonstrated that most tissues of fish (lungfish is a n exception) contain very low levels of histamine (Reite 1965, 1969a, b, Takaya 1969, Chiu & Lagunoff 1972, Lorenz et al 1973. By comparing 2 tissues, rainbow trout swimbladder and hamster cheek pouch, both rich in mast cells, the former tissue showed histamine levels of 0.2 to 0.5 pg g-', while the levels of the latter were 19.8 to 30.5 pg g-' (Reite 1969a).…”

Section: Discussionmentioning

confidence: 99%

Mast cells in the swimbladder of Atlantic salmon Salmo salar:histochemistry and responses to compound 48/80 and formalin-inactivated Aeromonas salmonicida

Reite¹,

Evensen²

1994

Dis. Aquat. Org.

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Observations were made on t~s s u e spreads from the swimbladder of the Atlantlc salmon Salmo salar The t~ssues were f~x e d In ethyl alcohol and stalned with alcoholic thionin All preparations showed numerous tlssue mast cells The dlstr~bution of the mast cells resembled thelr distribution In mammalian tissues, with a concentration In the vlclnity of the vascular network Mast cell degranulatlon could be demonstrated at 2 h after lntrapentoneal ~nlectlons of compound 48/80, but In fish kllled at 24 and 48 h, no signs of degranulatlon were found Intrapentoneal injections of formalln-inactivated Aeromonas salmonloda subsp s a l m o n~a d a produced a n inflammatory reactlon and degranulatlon of the mast cells of the swlmbladder

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Section: Discussionmentioning

confidence: 99%

Mast cells in the swimbladder of Atlantic salmon Salmo salar:histochemistry and responses to compound 48/80 and formalin-inactivated Aeromonas salmonicida

Reite¹,

Evensen²

1994

Dis. Aquat. Org.

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“…Widely distributed in vertebrates, mast cells are found at the interface between the organism and its environment (i.e., skin, respiratory system, and gastrointestinal tract) and in connective tissues, especially in vicinity to blood vessels ( 41 ). To recognize and eliminate pathogens, mast cells possess a multitude of receptor systems and are capable of releasing mediators with antimicrobial, vasoactive, enzymatic, anticoagulant, and pro-infl ammatory properties ( 17 ).…”

Section: Discussionmentioning

confidence: 99%

Mast cells, macrophages, and crown-like structures distinguish subcutaneous from visceral fat in mice

Altintas

Azad

Nayer

et al. 2011

Journal of Lipid Research

167

163

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This article is available online at http://www.jlr.org is of grave consequence to human health. In fact, cardiovascular diseases, mostly as a result of long-standing metabolic dysregulations, are the leading cause of morbidity and mortality in many parts of the world.The pathogenesis of obesity-linked insulin resistance is only partially understood. Accumulating evidence has revealed a strong association between obesity-linked insulin resistance and infl ammation ( 2 ). Tumor necrosis factor-a (TNF-a ), a prototypical pro-infl ammatory cytokine, was upregulated in the epididymal fat of obese rodents, and neutralization of TNF-a ameliorated insulin resistance ( 3 ). Moreover, obese mice lacking TNF-a demonstrated improved insulin sensitivity ( 4 ). In addition, increased numbers of macrophages and their transcripts were reported in the epididymal fat of genetically and dietinduced obese (DIO) mice ( 5, 6 ). These adipose tissue macrophages (ATM) were found scattered between adipocytes (herein referred to as solitary ATM ) or forming clusters around adipocytes. Based on ultrastructural and immunohistochemical alterations, it was argued that most ATM in obese mice and humans surround dead adipocytes, forming so-called crown-like structures (CLS) ( 7 ). Subsequently, we reported that CLS were distributed differentially in abdominal fat depots of DIO mice ( 8 ). Consistent with our fi ndings, it was recently reported that CLS were also more prevalent in visceral than subcutaneous fat of leptin-defi cient ob/ob and leptin receptor-defi cient db/db mice ( 9 ).Although macrophages are critical in innate and adaptive immunity, most immune responses are the result of interplay between multiple cell types and mediators of the immune system ( 10 ). Therefore, it comes as no surprise to learn that regulatory T cells ( 11 ), CD8+ effector T cells Over the past several decades a steady increase in the prevalence of obesity across the continents, especially in the US, has been observed ( 1 ). Increased caloric intake, mostly due to consumption of a high-fat diet, and decreased physical activity seem to be major contributors. Insulin resistance, hypertension, and dyslipidemia often accompany obesity. The constellation, referred to as metabolic syndrome, This work was supported by generous funds from the Katz Family Foundation.

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“…With respect to these parameters, they are therefore closely related to primary murine mast cells. CPU cells were used for studying the transcriptional regulation o f chemokines and lymphokincs in this cell type as well as signal transduction path ways from the Fc, Rl down to the gene level [30,[32][33][34][35]. In this respect they comprise a suitable model system for investigating the involve ment of PI3-kinase in the activation of mast cells after allergic trigger ing.…”

Section: Cpu Mouse Mast Cellsmentioning

confidence: 99%

Effects of Phosphatidylinositol-3-Kinase Inhibitors on Degranulation and Gene Induction in Allergically Triggered Mouse Mast Cells

Pendl¹,

Prieschl²,

Thumb³

et al. 1997

Int Arch Allergy Immunol

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Background: Phosphatidylinositol-3-kinase (PI3-kinase) comprises an essential component in a number of signaling cascades, primarily of the growth factor type. Two specific inhibitors, wortmannin and demethoxyviridin (DMV), are widely used to block signaling via this molecule and link certain receptors to the PI3-kinase pathway Methods: We have studied the extent of involvement of PI3-kinase in signaling events by Fc_εRI in mast cells using a mouse mast cell line as a model system. This was done using β-hexosaminidase release assays, a leukotriene ELISA, transient transfections with reporter gene constructs of TNFα and MARC, and in addition a TNFα ELISA. Results: Consistent with previously published data in the rat basophilic cell line RBL-2H3, we find that wortmannin as well as DMV prevent the degranulation reaction in the mouse mast cell line CPU. DMV also inhibits the release of leukotrienes, leading to the conclusion that Fc_εRI activates PI3-kinase which then mediates these reactions. On the contrary, however, lymphokine and chemokine induction at the gene and protein level is not inhibited, suggesting that the activation of this gene set in mast cells is independent of PI3-kinase. Conclusion: PI3-kinase is activated in our mast cell model system via cross-linking of the FcεRI. This reaction is clearly necessary for the degranulation process and the release of leukotrienes. Activation of lymphokine and chemokine genes as well as secretion of their gene products are not triggered along the PI3-kinase signaling pathway. This is in agreement with our previous findings, showing that the MAP kinase pathway and Ca²⁺ influx are both involved in gene activation in this cell type.

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Histochemical comparison of vertebrate mast cells

Cited by 67 publications

References 39 publications

Mast cells in the swimbladder of Atlantic salmon Salmo salar:histochemistry and responses to compound 48/80 and formalin-inactivated Aeromonas salmonicida

Mast cells in the swimbladder of Atlantic salmon Salmo salar:histochemistry and responses to compound 48/80 and formalin-inactivated Aeromonas salmonicida

Mast cells, macrophages, and crown-like structures distinguish subcutaneous from visceral fat in mice

Effects of Phosphatidylinositol-3-Kinase Inhibitors on Degranulation and Gene Induction in Allergically Triggered Mouse Mast Cells

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