Beta-adrenergic and prostanoid inhibition of canine fundic mucosal mast cells

Soll, Andrew H.; Toomey, Mary

doi:10.1152/ajpgi.1989.256.4.g727

Cited by 7 publications

(5 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In studies describing an inhibitory effect for PGE 2 on histamine release, mast cells were preincubated with PGE 2 for Ն5 min before the addition of the other stimuli (19,21); whereas, in experiments where PGE 2 potentiated mast cell degranulation, concurrent activation with PGE 2 and the secretagogue was employed (12,18, and this study). Cyclic AMP has been implicated as the second messenger mediating PGE 2 -directed inhibition of degranulation (21,45,46). Conversely, increased Ca 2ϩ rather than cAMP was implicated in a study where degranulation was potentiated by PGE 2 (12), and these observations are not surprising considering the absolute requirement for increased intracellular Ca 2ϩ in the induction of mast cell degranulation (47).…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E2 Selectively Enhances the IgE-Mediated Production of IL-6 and Granulocyte-Macrophage Colony-Stimulating Factor by Mast Cells Through an EP1/EP3-Dependent Mechanism

Gomi

Zhu

Marshall

2000

The Journal of Immunology

View full text Add to dashboard Cite

PGE2 is an endogenously synthesized inflammatory mediator that is over-produced in chronic inflammatory disorders such as allergic asthma. In this study, we investigated the regulatory effects of PGE2 on mast cell degranulation and the production of cytokines relevant to allergic disease. Murine bone marrow-derived mast cells (BMMC) were treated with PGE2 alone or in the context of IgE-mediated activation. PGE2 treatment alone specifically enhanced IL-6 production, and neither induced nor inhibited degranulation and the release of other mast cell cytokines, including IL-4, IL-10, IFN-γ, and GM-CSF. IgE/Ag-mediated activation of BMMC induced the secretion of IL-4, IL-6, and GM-CSF, and concurrent PGE2 stimulation synergistically increased mast cell degranulation and IL-6 and GM-CSF, but not IL-4, production. A similar potentiation of degranulation and IL-6 production by PGE2, in the context of IgE-directed activation, was observed in the well-established IL-3-dependent murine mast cell line, MC/9. RT-PCR analysis of unstimulated MC/9 cells revealed the expression of EP1, EP3, and EP4 PGE receptor subtypes, including a novel splice variant of the EP1 receptor. Pharmacological studies using PGE receptor subtype-selective analogs showed that the potentiation of IgE/Ag-induced degranulation and IL-6 production by PGE2 is mediated through EP1 and/or EP3 receptors. Our results suggest that PGE2 may profoundly alter the nature of the mast cell degranulation and cytokine responses at sites of allergic inflammation through an EP1/EP3-dependent mechanism.

show abstract

Section: Discussionmentioning

confidence: 99%

Prostaglandin E2 Selectively Enhances the IgE-Mediated Production of IL-6 and Granulocyte-Macrophage Colony-Stimulating Factor by Mast Cells Through an EP1/EP3-Dependent Mechanism

Gomi

Zhu

Marshall

2000

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…Consistent with earlier data on human mast cells reported by Cohan et al , 189 we did not observe a biologically significant effect of the corticosteroid dexamethasone on histamine release from canine skin mast cells 171 . In contrast, salbutamol, a β 2 ‐receptor agonist, exerted a weak inhibitory effect on IgE‐dependent histamine release from isolated canine cutaneous mast cells 183 and human cutaneous mast cells, 177 suggesting that a functional β ‐adrenergic receptor is coupled to mast cell populations 190 . This inhibitory effect was particularly obvious when lung mast cells, rather than those from skin, from both humans and dogs were exposed to the β 2 ‐receptor agonist 184,191 .…”

Section: Secretagogue‐induced Activation and Pharmacological Inhibitimentioning

confidence: 99%

“…171 In contrast, salbutamol, a b 2 -receptor agonist, exerted a weak inhibitory effect on IgE-dependent histamine release from isolated canine cutaneous mast cells 183 and human cutaneous mast cells, 177 suggesting that a functional badrenergic receptor is coupled to mast cell populations. 190 This inhibitory effect was particularly obvious when lung mast cells, rather than those from skin, from both humans and dogs were exposed to the b 2 -receptor agonist. 184,191 This blockade might partly account for the efficacy of such drugs in the treatment of allergic asthma.…”

Section: Drug-induced Modulation Of Canine Mast Cellsmentioning

confidence: 99%

The role of mast cells in atopy: what can we learn from canine models? A thorough review of the biology of mast cells in canine and human systems

Mora

Puigdemont

Torres

2006

British Journal of Dermatology

View full text Add to dashboard Cite

Mast cell research has largely focused on the role of these cells in the early phase of allergic reactions. However, their involvement may well extend beyond this stage, and even reach across nonallergic conditions. Mast cells from different sources have helped advance our knowledge of their biology. Although in vitro and in vivo research in this area has mainly focused on humans, such studies are limited by the extent to which cells from certain human tissues and/or human patients can be collected or studied. While rodents also provide valuable models with which to further our understanding of the behaviour of mast cells and their contribution to allergy, reported differences between human and murine mast cells, and, in some instances, the limitations of in vivo rodent models of mast cell-mediated allergic conditions, preclude their use. In this review, we introduce a relatively unknown mast cell population, that of the dog. Canine mast cells display many phenotypic and functional similarities with their human counterparts, and dogs develop spontaneous and induced allergic diseases that share clinical and pathophysiological features with the human condition. Therefore, the use of canine cells can shed light on the general role of mast cells, particularly in relation to allergic diseases given the potential of in vivo dog models within this field. Here we provide a detailed review of the data reported from in vitro and in vivo studies of canine mast cells, and compare them with results obtained in human systems. We also highlight direct evidence of the mast cell contribution to canine atopy. We conclude that the dog offers useful in vitro and in vivo models in which to investigate mast cell behaviour, and that its use should be considered when undertaking studies aimed either at elucidating the role of mast cells in health and disease, or at prescreening novel therapies prior to entry into man.

show abstract

“…Isolated fundic soma tostatin-containing D cells release somatostatin via Padrenoceptor-mediated mechanisms [24], Activation of p-adrenoceptors increases gastrin release from isolated vascularly perfused rat stomach [25] and from rat antral mucosal fragments [26], Furthermore, P-adrenoceptor ag onists have been shown to decrease the release of hista mine from isolated canine fundic mast cells [27], The presence of P-adrenoceptors on parietal cells and nonpar ietal cells may contribute to the increase or decrease in gastric acid secretion in vivo. Conflicting results on the roles of gastric P-adrenoceptors in the regulation of gastric acid secretion were therefore due probably to inhibition and stimulation of nonparietal and parietal cell functions by activation of P-adrenoceptors.…”

Section: Effects O F Noradrenaline On Carbachol-andmentioning

confidence: 99%

Roles of Adrenoceptors in Isolated Canine Parietal Cells

Yokotani

Park

DelValle³

et al. 1994

Digestion

View full text Add to dashboard Cite

Functional roles of adrenoceptors in parietal cells were pharmacologically investigated using isolated canine parietal cells. In the crude membranes obtained from preparations highly purified in parietal cells ( > 95% of purity), the specific binding of [³H]dihydroalprenolol (DHA) was observed with a Kd value of 2.9 nM and B_max of 234 fmol/mg protein, while the specific binding of [³H]prazosin and [³H]rauwolscine were not attained. Propranolol concentration-dependently reduced the specific binding of [³H]dihydroalprenolol with a K_i value of 2.6 nM. Isoproterenol concentration-dependently stimulated [¹⁴C]aminopyrine accumulation in preparations enriched in parietal cells (about 70% purity) with the maximum at 10 nM. Isoproterenol increased the content of cyclic AMP in preparations enriched in parietal cells (70%) with the maximum at 100 nM. The isoproterenol-induced stimulatory effect of [¹⁴C]aminopyrine accumulation in preparations enriched in parietal cells (70%) was completely abolished by 1 μM propranolol but not by 1 μM phentolamine. In the presence of 1 μM propranolol, 100 μM noradrenaline did not affect carbachol- and histamine-induced [¹⁴C]aminopyrine accumulation in preparations enriched in parietal cells (70%). The present study suggests that stimulation of β-adrenoceptors located on canine parietal cells evokes acid production in a cyclic-AMP-dependent manner. Furthermore, a possibility arises that canine parietal cells are not the site of action of α-adrenoceptors in mediating inhibition of gastric acid secretion.

show abstract

Beta-adrenergic and prostanoid inhibition of canine fundic mucosal mast cells

Cited by 7 publications

References 0 publications

Prostaglandin E2 Selectively Enhances the IgE-Mediated Production of IL-6 and Granulocyte-Macrophage Colony-Stimulating Factor by Mast Cells Through an EP1/EP3-Dependent Mechanism

Prostaglandin E2 Selectively Enhances the IgE-Mediated Production of IL-6 and Granulocyte-Macrophage Colony-Stimulating Factor by Mast Cells Through an EP1/EP3-Dependent Mechanism

The role of mast cells in atopy: what can we learn from canine models? A thorough review of the biology of mast cells in canine and human systems

Roles of Adrenoceptors in Isolated Canine Parietal Cells

Contact Info

Product

Resources

About