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Subject basophils

Figure 2 Quantitation of basophil total IgE receptors by lactic acid elution and D. fari-nae (DF) and anti-IgE-induced basophil histamine release responses. (A) Mean RIST values for total IgE eluted from subjects basophils (n = 11) prior to infusion of E25 (pre), after 12 weeks of rhuMAb-E25 treatment (12 weeks of E25), one hour after last infusion of E25 (46 weeks of E25), and at termination from the postinfusion follow-up study (termination of post E25 study). Values are expressed as the mean SEM number of receptors per basophil. (B) Samples obtained at the same timepoints as in Figure 3 were examined for histamine release responses to optimal doses of D. farinae or anti-IgE. Results are expressed as mean percent of histamine release. (From Ref. 68.)... Figure 2 Quantitation of basophil total IgE receptors by lactic acid elution and D. fari-nae (DF) and anti-IgE-induced basophil histamine release responses. (A) Mean RIST values for total IgE eluted from subjects basophils (n = 11) prior to infusion of E25 (pre), after 12 weeks of rhuMAb-E25 treatment (12 weeks of E25), one hour after last infusion of E25 (46 weeks of E25), and at termination from the postinfusion follow-up study (termination of post E25 study). Values are expressed as the mean SEM number of receptors per basophil. (B) Samples obtained at the same timepoints as in Figure 3 were examined for histamine release responses to optimal doses of D. farinae or anti-IgE. Results are expressed as mean percent of histamine release. (From Ref. 68.)...
It is generally accepted (based on clinical and in vitro studies) that mast cells (and basophils), IgE and FceRI are involved in most cases of allergen-induced anaphylaxis in humans. However, it is difficult to define the exact roles and relative importance of mast cells, basophils, and other potential effector cells (e.g monocytes/macrophages, dendritic cells) in either IgE-dependent or IgE-independent human anaphylaxis. Unlike in mice, we neither have access to mast cell- or basophil-deficient humans nor can we genetically manipulate human subjects to produce such phenotypes. [Pg.47]

In mice and humans, it is possible that mast cells and basophils contribute to the pathophysiology of anaphylaxis both via direct effects on end organ targets and also by indirect effects, including the ability of mast cells and basophils to influence the responsiveness of such target cells to mediators generated in subjects with anaphylaxis. [Pg.47]

Inhaled and intravenous histamine causes bronchoconstriction as one of the first recognized properties of histamine, which is inhibited by Hi antihistamines. As a manifestation of airway hyperresponsiveness, asthmatic individuals are more sensitive to the bronchoconstrictor effect of histamine than normal individuals. In addition, in vitro studies have shown increased histamine release in basophils and mast cells obtained from asthmatic subjects compared with... [Pg.72]

Pramod, S. N., Venkatesh, Y. P, Mahesh, P. A. (2007). Potato lectin activates basophils and mast cells of atopic subjects by its interaction with core chitobiose of cell-bound non-specific immunoglobulin E. Clin. Exp. Immunol., 748,391 01. [Pg.123]

The Hi Receptor and its Ligands. The H receptor mediates effects, through an increase in cyclic adenosine monophosphate (cAMP). such as gastric acid secretion relaxation of airway smooth muscle and of pulmonary vessels increased lower airway mucus secretion esophageal contraclion inhibition of basophil, but not mas cell histamine release inhibition of neutrophil activation and induction or suppressor T cells. There is no evidence that the H- receptor causes significant modulation of lung function in the healthy human subject or in the asthmatic. [Pg.777]

Fig. 1. Pertussis toxin-mediated ADP ribosylation of membrane G proteins. Isolated cell membranes (50 ng of protein) from N1E 115 cells (mouse neuroblastoma cell line), N2A cells (mouse neuroblastoma cell line), S49-1 eye cells (S49(-) mutated mouse lymphoma cell line deficient in Ga ), 549 wt cells (wild-type mouse lymphoma cell line), RBL (RBL 2H3 rat basophilic leukemia cell line), GH3 cells (GH3 rat hypophyseal tumor cell line), PC-12 (rat pheochromocytoma cell line), HIT-T15 cells (hamster insulinoma cell line), Y-1 cells (mouse adrenal cortex tumor cell line), 108 cc 15 cells (mouse/rat neuroblastoma x glioma hybrid cell line), HL-60 cells (DMSO-differentiated human leukemia cell line), HL-60 (+PT) cells (HL-60 cells pretreated with 25 ng/ml of pertussis toxin for 24 h prior to preparation of membranes), RINm5F cells (rat insulinoma cell line), and C6-2 cells (rat glioma cell line) were subjected to P-ADP-ribosylation as described in section 4.3.3. Samples were precipitated as outlined in section 4.3.5 and subjected to SDS-PAGE with separating gels containing 8% acrylamide (w/v). An autoradiogram of the dried gel is shown. Molecular masses of marker proteins are indicated (kDa). Modified Ga proteins migrate at approximately 40 kDa. Radioactivity running in front of the 30 kDa marker protein comigrates with the dye front... Fig. 1. Pertussis toxin-mediated ADP ribosylation of membrane G proteins. Isolated cell membranes (50 ng of protein) from N1E 115 cells (mouse neuroblastoma cell line), N2A cells (mouse neuroblastoma cell line), S49-1 eye cells (S49(-) mutated mouse lymphoma cell line deficient in Ga ), 549 wt cells (wild-type mouse lymphoma cell line), RBL (RBL 2H3 rat basophilic leukemia cell line), GH3 cells (GH3 rat hypophyseal tumor cell line), PC-12 (rat pheochromocytoma cell line), HIT-T15 cells (hamster insulinoma cell line), Y-1 cells (mouse adrenal cortex tumor cell line), 108 cc 15 cells (mouse/rat neuroblastoma x glioma hybrid cell line), HL-60 cells (DMSO-differentiated human leukemia cell line), HL-60 (+PT) cells (HL-60 cells pretreated with 25 ng/ml of pertussis toxin for 24 h prior to preparation of membranes), RINm5F cells (rat insulinoma cell line), and C6-2 cells (rat glioma cell line) were subjected to P-ADP-ribosylation as described in section 4.3.3. Samples were precipitated as outlined in section 4.3.5 and subjected to SDS-PAGE with separating gels containing 8% acrylamide (w/v). An autoradiogram of the dried gel is shown. Molecular masses of marker proteins are indicated (kDa). Modified Ga proteins migrate at approximately 40 kDa. Radioactivity running in front of the 30 kDa marker protein comigrates with the dye front...
Li AR, Mackay GA, Hopkin JM Functional analysis of histamine release from basophils and mast cells in subjects with the Ile-181->Leu variant of Fc epsilon Rl-beta. Clin Sci 1997 93 279-286. (NC)... [Pg.30]

Coal Tar Products. In an industrial health survey of employees in four wood preservative plants in which coal tar creosote and coal tar were the main treatments used, hematological effects, including increased number of white blood cells (basophils), were noted in 6% (15 of 257) of the employees examined (TOMA 1979). Similarly, 8% of the employees in eight of nine coal tar plants surveyed had increased white blood cells (eosinophils) (TOMA 1981). Industrial hygiene surveys of coal tar pitch volatiles at the four wood preservative plants indicated that in 94% of the samples, airborne exposure to benzene-soluble components of the coal tar pitch volatiles was within the OSHA permissible limit of 0.2 mg/m3 (TOMA 1979). The other 6% of the samples ranged from 0.21 to 3.6 mg/m3 (TOMA 1979). No determination of exposure was made at the nine coal tar plants (TOMA 1981). Furthermore, no clear relationship could be established because exposure routes in addition to dermal were likely, such as inhalation and oral. Also, the ability to relate hematological effects to coal tar creosote and coal tar exposure was further confounded by the possibility that the subjects were also exposed to other chemicals and cigarette smoke (TOMA 1979, 1981). Additional limitations of the studies are noted above (see "Respiratory Effects"). [Pg.132]

In 10 healthy subjects ketoconazole 200 mg daily for 6 to 7 days caused a 50% rise in the levels of both total and unbound prednisolone, following a dose of either oral prednisone or intravenous prednisolone. In contrast, two other studies found that ketoconazole 200 mg daily for 6 days did not affect either the pharmacokinetics or the pharmacodynamics of prednisolone, as measured by the suppressive effects on serum cortisol, blood basophil and helper T-lymphocyte values of prednisolone. ... [Pg.1052]

Ying, S., Robinson, D.S., Meng, Q., Barata, L.T., McEuen, A.R. et al. (1999) C-C chemokines in allergen-induced late-phase cutaneous responses in atopic subjects association of eotaxin with early 6-hour eosinophils, and of eotaxin-2 and monocyte chemoattractant protein-4 with the later 24-hour tissue eosinophilia, and relationship to basophils and other C- C chemokines (Monocyte chemoattractant... [Pg.353]

In contrast to the above results, the basophil activation test was positive to the implicated quinolone in all five subjects with immediate reactions to a quinolone who were tested [19 ]. However, this assay quantified CD203C, which may be a more sensitive marker than CD63 for detecting IgE-mediated allergy. [Pg.401]

Immunologic-type agents are confirmed by specific positive radioallergosorbent tests (RASTs) and by negative tests on control subjects, rarely by passive transfer tests (Prausnitz-Kiistner tests) in animals. In vitro tests can also be used to assess the relationship with a possible IgE-mediated mechanism, namely, determination of histamine release from peripheral basophils or platelet cytotoxicity test, which explores the presence on platelets of specific IgE antibodies bound to the low-affinity receptor for IgE. [Pg.201]

In allergic subjects, IgE antibodies, as well as being free in serum, are fixed to the exfiacellular D1 distil and D2 proximal domains of the FceRl receptor on mast cells and basophils via the Ce2 and Ce3 domains of the antibody Fc region. [Pg.40]


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