No abstract

Background: Atopic dermatitis (AD) can be exacerbated or induced in genetically predisposed individuals by psychological stress, which causes the release of substance P (SP). Therefore, SP may play an etiological role in the mechanisms underlying AD. Methods: Changes in the number of mast cells and SP-containing mast cells in lesional skin, and the serum concentrations of SP and IgE during the development of AD-like disease up to 8 weeks after the start of picryl chloride (PiCl) induction in NC/Nga mice were examined. Results: Clinical signs and symptoms seen in PiCl-treated NC/Nga mice as a model of AD-like disease began with erythema and haemorrhage, followed by oedema, superficial erosion, deep excoriation, scaling and dryness of the skin, as well as retarded growth, and the changes were exacerbated with an increase in the number of PiCl applications. An increase in the number of mast cells and eosinophil infiltration was observed in the lesional skin. The increase in SP-positive mast cells in the dermis in this model was significant from 1 week after the start of induction treatment, compared with intact mice, and SP-positive nerve fibres were observed in the dermis. Conclusion: SP is a crucial mediator of both dermatitis and scratching behaviour in this model.

Lipopolysaccharide endotoxin (LPS) was extracted from Haemophilus influenzae type b by using Westphal's phenol water method. The ears of 40 adult male guinea pigs were subsequently inoculated with 10 micrograms/ml solutions of LPS by transmeatal injections. Groups of animals were then sacrificed from day 2 to day 24 after the injections to observe the pathological changes produced. Massive serous effusions filled the tympanic bullae on days 2 and 4, after which the amount of fluid present gradually decreased so that it could hardly be seen on day 11. Pathological changes found in the mucosa included marked interstitial edema, dilated capillaries, as well as elevated and thickened epithelium with intracellular edema. These findings gradually subsided by day 24. We believe that the major pathogenetic factors present were due to the transudation and injury of the middle ear epithelium disturbing mucociliary transport activity, with increased secretions participating somewhat in inducing the effusion. We further suggest that H. influenzae endotoxin may play an active role in the clinical development of otitis media with effusion.

Peritoneal carbonyl stress derived from uremia as well as peritoneal dialysis procedure might contribute to the vascular proliferation through induction of bioactive molecules and to an increased functional area, eventually leading to ultrafiltration failure. Pyridoxamine may be beneficial in protection of uremic peritoneal membrane on peritoneal dialysis.