Modification of Cɛ mRNA Expression by EBV-Encoded Latent Membrane Protein 1

To evaluate the effect of expression of latent membrane protein (LMP) 1 encoded by Epstein-Barr virus (EBV) on Cɛ mRNA expression, mRNA levels were examined by RT-PCR or Northern blot analysis upon transient transfection of LMP1 in the splenocytes derived from Brown-Norway rats with or without immunization with 2,4-dinitrophenyl-conjugated Ascaris suum antigen. Splenocytes were transfected with LMP1 expression vector, pSG5-LMP1, using lipofection method. Cɛ mRNA levels were considerably increased by transfection with pSG5-LMP1 in the splenocytes derived from the nonimmunized rats; however, Cɛ mRNA levels were decreased in the splenocytes derived from the immunized rats. Cɛ mRNA expression in IgE-producing cells are modulated by LMP1, which might depend on the differentiation status of B cells upon exposure to allergen

Azelastine and suplatast shorten the distribution half-life of IgE in rats.

We aim to clarify whether suplatast and azelastine (anti-allergic drugs) can shorten the half-life of imnunoglobulin E (IgE) in the circulating blood. Thirty Wistar rats were divided into six groups. Distilled water or anti-allergic drugs were given orally for 6 days after the first sensitization. Two milligrams of monoclonal dinitrophenyl (DNP)-specific rat IgE was administered to the rats, which had been given suplatast or azelastine orally. The level of DNP-specific rat IgE in the serum was estimated by IgE-capture enzyme-linked immunosorbent assay, and the turnover of IgE was analyzed from its pharmacokinetic parameters. The elimination half-life of rat IgE was about 12 h irrespective of the sensitized state. The intercompartmental rate constants (Kct and Ktc) in the suplatast-administered or azelastine-administered group were larger than those of the distilled water-administered group under non-sensitized conditions. These findings suggested that the anti-allergic drugs used in the present study facilitated the excretion of IgE from the circulation in rats

Permeability of rat IgE across rat aortic endothelial cell is enhanced by histamine

Background: It is a well-known fact that IgE is a key substance that induces an allergic reaction in extravascular tissue. However, it remains to be elucidated how IgE in the circulating blood transfers to the site of the allergic reaction in the extravascular tissue. In the present paper, rat IgE passage through cultured rat aortic endothelial cells (RAEC) was first examined using a dual-chamber system. Second, we examined the effects of histamine, which is thought to affect endothelial permeability, on IgE passage through the RAEC in comparison with the effects of albumin and IgG2a. Methods: The permeability constant (PC) was used to evaluate the degree of IgE passage through the RAEC. Results: The value of the PC for rat IgE (0.58 ±0.11 x 10−5cm/s) was lower than that for IgG2a and albumin (0.88 ± 0.28 x 10−5 and 0.93 ± 0.26 x 10−5 cm/s, respectively) under conditions of non-exposure to histamine. In contrast, the PC of rat IgE was significantly increased by exposure to histamine (10−10 mol/L) at 12 h after exposure. However, the PC for IgG2a and albumin were not significantly increased following exposure to histamine. The enhancement by histamine of IgE passage through the RAEC was not inhibited by diphenhydramine, a histamine H receptor antagonist, but were inhibited by cimetidine, a histamine H2 receptor antagonist. Conclusions: On the basis of results from the present study, histamine, acting via H2 receptors, enhances the permeability of rat IgE across the RAEC monolayer. The increased permeability of endothelial cells induced by histamine may contribute greatly to the transfer of IgE from circulating blood to extravascular tissue