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Mast cells secretion

The regulation of mast-cell activity by biologically active peptides is an area of research, the rapid growth of which has been sparked in part by this intense interest in the interactions between neural, endocrine and immune systems [4, 26, 41] and in part by the recognition that activation of mast-cell secretion as a purely allergic IgE-dependent event is undoubtedly too restrictive. The involvement of the mast cell in the inflammatory response, for example, has for years been suspected to involve a number of non-immunologic, IgE-inde-pendent factors [24,42], Direct evidence for peptide involvement, however, has... [Pg.145]

In order to influence mast-cell function, peptides must be made available at sites very near to tissue mast cells. One means of accomplishing this is by specific peptidergic innervation. This would not necessarily require a classical synaptic morphology, but only the termination of nerves within the vicinity of mast cells [1,3]. Modulation of mast-cell secretion by peptides of neural origin is particularly attractive, for it would allow for a restricted, localized expression of peptide action in specific target tissues because of the selective distribution of each peptide within particular neurones. Moreover, this could be further modified and restricted by differing mast cell specificities. (Heterogeneity of mast cell responsiveness to peptide stimulation has been well documented [52, 53 ].) The result would permit a well-localized tissue response without systemic manifestation [3]. [Pg.147]

An interaction between neuronal stimulation and mast-cell secretion has been considered for sometime in neurogenic inflammation [59, 60]. Here, it is speculated that injury to the skin elicits a characteristic reaction beginning with a local reddening at the site of injury which then rapidly spreads out for several... [Pg.148]

The number of peptides that have been shown to stimulate mast-cell secretion is impressive (Table 4.1) and it is obvious that the potential for regulation of... [Pg.149]

Somatostatin (SOM), initially identified by its ability to inhibit the release of growth hormone, is known to have inhibitory effects on a variety of cells [ 109], In mast cells and in basophils, SOM, like NT, has inhibitory as well as stimulatory effects depending on the concentration used. At high concentrations (> 10 8 M), SOM is a powerful stimulus of peritoneal mast-cell secretion (from both normal and athymic rats) and resembles other non-immunologic secretagogues such as compound 48/80, SP and NT in that it triggers a rapid exocytosis that is primarily dependent on cellular Ca [ 110,111], A similar effect is seen in vivo when injected into skin or skin blisters at high concentrations (> 10-8 M), SOM causes a rapid, dose-dependent release of histamine [88, 112] but when used at concentrations lower than those which elicit a secretory... [Pg.157]

In their initial studies on the effects of vasoactive peptides on mast-cell secretion, Johnson and Erdos [31] concluded that the ability of peptides to elicit a secretory response from mast cells depended upon the number of basic groups a peptide contained, and not on the structure of the N-terminal or C-terminal amino acids per se. They found, for example, that Polistes kinin, with... [Pg.171]

It is, however, uncertain whether the above sequence of reactions accompanies peptide stimulation of mast-cell secretion. It is known that changes in the levels of key PI cycle intermediates accompany stimulation of mast cells by antigen or by compound 48/80 [207, 208]. Besides, there is now evidence for... [Pg.179]

Lagunoff, D., Membrane Fusion During Mast Cell Secretion, J. Cell. [Pg.71]

AJthough IgE rheumatoid factors have been identified in both the serum of patients with rheumatoid arthritis (Zuraw et al., 1981) and rheumatoid synovial fluid (De Clerck et al., 1991 Burastero et al., 1993), it is quite likely that IgE-independent modes of mast cell activation operate in non-allergic inflammatory processes. These might include C3a and C5a generated by activation of the complement cascade (Moxley and Ruddy, 1985 Brodeur et al., 1991) by immune complexes containing rheumatoid factors, substance P, and as yet unidentified mediators of mast cell secretion. From the above descriptions of the different mast cell mediators and cytokines it is easy to imagine how these may participate in the development of joint patholt. ... [Pg.72]

Franzen, L. and Norrby, K. (1994). Local mitogenic effect of tissue mast cell secretion. Cell Tissue Kinet. 13, 635-642. [Pg.77]

Vliagoftis, H., Boucher, W. S., Mak, L. L., and Theodarides, T. C. (1992). Inhibition of mast cell secretion by oxidation products of natural polyamines. Biochem. Pharmacol. 43, 2237-2245. [Pg.152]

R.M. Williams, J.B. Shear, WR. Zipfel, S. Maiti, W.W. Webb, Mucosal mast cell secretion processes imaged using three-photon microscopy of 5-hydroxytryptamine autofluorescence. Biophys. J. 76, 1835-1846 (1999)... [Pg.143]

EP2 Butaprost None smooth muscle, leukocytes,mast cells, sensory neurons, lung, kidney smooth muscle relaxation, Inhib. mast cell secretion, stim. Intestinal secretion cAMP... [Pg.150]


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See also in sourсe #XX -- [ Pg.1006 ]




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