Histamine release from canine lung and liver mast cells induced by radiographic contrast media

Ennis, Madeleine; Amon, E.U.; Lorenz, W.

doi:10.1007/bf02222210

Cited by 26 publications

(10 citation statements)

References 5 publications

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“…However, although the source of histamine is generally associated with circulating basophils and tissue-associated mast cells, there exists a great deal of diversity with respect to the sensitivity of basophil and mast cell populations [20]. The diversity is further c o mpounded by reported species differences in the sensitivity of the various cell types [21][22][23]. Keeping this diversity in mind, the present studies have examined the histamine-releasing potential of the glycopeptide antibiotic, vancomycin, in two cell types; the rat peritoneal mast cell and the rat basophilic cell line, RBL-1.…”

Section: Discussionmentioning

confidence: 97%

Vancomycin-induced release of histamine from rat peritoneal mast cells and a rat basophil cell line (RBL-1)

et al. 1991

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Rapid intravenous administration of the glycopeptide antibiotic, vancomycin, may cause a hypotensive reaction which can usually be prevented by infusing vancomycin in dilute solutions. The release of histamine from circulating cells such as basophils and tissue mast cells has been implicated in hypotensive reactions since the effects can be prevented by antihistamine pretreatment. The direct effects of vancomycin on histamine release were therefore investigated in rat peritoneal mast cells and rat leukemic basophils (RBL-1 cells). Suspension cultures of mast cells or RBL-1 cells were exposed to vancomycin for 30-60 minutes at concentrations comparable to those infused clinically (2.28 or 4.56 mg/ml). Vancomycin induced a time- and dose-dependent release of histamine into the culture media from both cell types. The reference degranulating agent, Compound 48/80 (CP 48/80), was also shown to induce histamine release from mast cells and RBL-1 cells. Mast cells were significantly more sensitive to vancomycin and CP 48/80 than RBL-1 cells and, unlike RBL-1 cells, were responsive to the inhibitory effects of cromolyn sodium on histamine release. Cromolyn sodium did not inhibit vancomycin-induced histamine release in RBL-1 or mast cells. Morphologically, mast cells exposed to either vancomycin or CP 48/80 exhibited dose-related degranulation. On the other hand, treatment-related degranulation effects of either vancomycin or CP 48/80 on RBL-1 cells could not be reliably distinguished from controls by qualitative evaluation. Based upon these findings it is concluded that mast cells may represent a more useful model to evaluate the potential of investigational agents to release histamine and to study mechanisms of histamine release than RBL-1 cells.

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Section: Discussionmentioning

confidence: 97%

Vancomycin-induced release of histamine from rat peritoneal mast cells and a rat basophil cell line (RBL-1)

et al. 1991

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“…Dogs are probably an ideal model for in vivo studies not only by virtue of their size but also because of their similarity to man with respect to allergic reactions and histamine release [17,18]. However, it is necessary to pay attention to their relevance to human responses, since a species-difference Fig.…”

Section: Discussionmentioning

confidence: 99%

Flush induced by fluoroquinolones in canine skin

Kurata¹,

Kasuga²,

Nanba³

et al. 1995

Inflamm Res

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The flush induced by two fluoroquinolone antibacterial agents, balofloxacin and ofloxacin, was studied in beagle dogs. Intradermal injection of the fluoroquinolones at concentrations above 10(-5) M produced a localized flushed area. The flush responses to fluoroquinolones were inhibited by co-administration with H2-antagonist(s) (ranitidine or cimetidine), but not with H1-antagonist(s) (mepyramine or chlorpheniramine). Similar inhibitory effects of these H2-antagonists were observed for the response to histamine. The flush responses to fluoroquinolones were inhibited by a local pretreatment with compound 48/80 administered to deplete the local stores of mast cell-bound histamine. When the fluoroquinolones were orally administered at a dose of 400 mg/kg, the concentration of histamine in plasma was increased, being accompanied by systemic erythema. These results indicate that the flush induced by fluoroquinolones is mediated by histamine release from canine cutaneous mast cells and H2-receptor stimulation.

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“…Accordingly, mast cell number appears to be tightly correlated with organ‐associated tryptase levels in dogs, 91 and the highest concentration of this marker has been found in the gut. Canine mast cells are also located in the skin, 92 the airways, 93,94 the bone marrow where they originate, 95,96 the gastrointestinal tract, 97,98 the testes, 99,100 the heart, 101 the brain 102 and the liver 103,104 . Because of the incidence of canine dermal allergic diseases, skin mast cells have been the focus of most studies on canine mast cell biology.…”

Section: The Canine Mast Cell Population: a Human‐like Distribution Amentioning

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

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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.

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Histamine release from canine lung and liver mast cells induced by radiographic contrast media

Cited by 26 publications

References 5 publications

Vancomycin-induced release of histamine from rat peritoneal mast cells and a rat basophil cell line (RBL-1)

Vancomycin-induced release of histamine from rat peritoneal mast cells and a rat basophil cell line (RBL-1)

Flush induced by fluoroquinolones in canine skin

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

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