Enhanced nerve growth factor expression by mast cells does not differ significantly between idiopathic and allergic rhinitis.

BACKGROUND: The role of neurotrophins in allergic rhinitis (AR) has been well studied, but it has not been evaluated in idiopathic rhinitis (IR). OBJECTIVE: We aimed to evaluate the nasal ß-nerve growth factor (ß-NGF) expressions of mast cells in patients with AR and IR. METHODS: Seventeen patients with house dust mites-induced persistent moderate/severe allergic rhinitis (mean age: 29.7 ± 11.96), 14 patients with idiopathic rhinitis (mean age, 29.3 ± 10.62), and 16 healthy controls (29.9 ± 11.57) were included in the study. Nasal biopsy specimens were taken from the posterior part of the inferior turbinate from all of the study subjects. Nasal ß-nerve growth factor and its receptors, pan-neurotrophin receptor p75, and tyrosine kinase A (trkA) were assessed with an immunofluorescence assay. Mast cells were determined by both an immunofluorescence assay and immunohistochemistry as tryptase-positive cells. RESULTS: The ß-NGF, trkA, and p75 receptor counts were significantly higher in AR and IR patients than in the control group (P < .001, for each), but they were not different between AR and IR patients. Similarly, the ratio of ß-NGF+ mast cells/total mast cells and the ratio of ß-NGF+ mast cells/total ß-NGF+ cells in AR and IR patients was found to be elevated when compared with the control group (P < .001, P < .001, P < .001, and P = .046, respectively); furthermore, the 2 ratios were not statistically different between the 2 patient groups. CONCLUSION: The increase in ß-NGF-expressing mast cells does not differ between idiopathic and allergic rhinitis. Therefore, we propose that mast cells do play a role in the pathogenesis of IR as important as in that of AR.

On diphtheria toxin fragment A release into the cytosol--cytochalasin D effect and involvement of actin filaments and eukaryotic elongation factor 2.

Diphtheria toxin has been well characterized in terms of its receptor binding and receptor mediated endocytosis. However, the precise mechanism of the cytosolic release of diphtheria toxin fragment A from early endosomes is still unclear. Various reports differ regarding the requirement for cytosolic factors in this process. Here, we present data indicating that the distribution of actin filaments due to cytochalasin D action enhances the retention of diphtheria toxin in early endosomes. Treating cells with cytochalasin D reduces the cytosolic fragment A activity and leads to changes in the intracellular distribution and size of early endosomes with toxin cargo. F-actin and eukaryotic elongation factor 2 can promote fragment A release from toxin-loaded early endosomes in an in vitro translocation system. Moreover, these proteins bind to toxin-loaded early endosomes in vitro and promote each other's binding. They are thus thought to be involved in the cytosolic release of fragment A. Finally, ADP-ribosylation of eukaryotic elongation factor 2 is shown to inhibit fragment A release and, via a feed-back mechanism, to account for the minute amounts of fragment A normally found in the cytosol.

Ischemia/reperfusion in rat: antioxidative effects of enoant on EEG, oxidative stress and inflammation.

PRIMARY OBJECTIVE: The present study was undertaken to evaluate whether enoant, which is rich in polyphenols, has any effect on electroencephalogram (EEG), oxidative stress and inflammation in ischemia/reperfusion (I/R) injury. METHODS: Ischemia was induced by 2-hour occlusion of bilateral common carotid artery. Animals orally received enoant. Group 1 was the ischemic control group. Group 2 was treated with enoant of 1.25 g kg⁻¹ per day for 15 days after I/R. Group 3 received the same concentration of enoant as in group 2 for 15 days before and after I/R. Group 4 was the sham operation group. EEG activities were recorded and the levels of TNF-α, IL-1ß and IL-6, TBARS and GSH were measured in the whole brain homogenate. RESULTS: There were significant changes in EEG activity in groups treated with enoant either before or after ischemia when compared with their basal EEG values. TNF-α, IL-6 and IL-1ß levels were significantly increased after I/R. GSH levels in group 3 treated with enoant in both pre- and post-ischemic periods were significantly increased and TBARS concentration was decreased compared with the ischemic group. CONCLUSION: The findings support that both pre-ischemic and post-ischemic administrations of enoant might produce neuroprotective action against cerebral ischemia.

The role of solid food intake in antimuscarinic-induced convulsions in fasted mice.

Animals treated with scopolamine after fasting develop convulsions after they are allowed to eat ad libitum. This study was aimed at investigating the effect on these convulsions of liquid food intake, feeding by gavage, and placebo. Fasted mice treated with saline or scopolamine were allowed to eat solid food, slurry food or liquid food ad libitum, given placebo, or given liquid food by gavage. After 30 min, all animals were allowed to eat food pellets and observed for 30 min for the incidence and onset of convulsions. Scopolamine treatment caused convulsions only in the animals given solid food in the first 30 min; no convulsions were observed in the animals given slurry food, liquid food ad libitum, gavage, or placebo. When the animals that did not develop convulsions during the experiment were allowed to eat solid food, convulsions occurred. These findings indicate that complex mechanisms trigger scopolamine-induced convulsions in fasted animals eating solid food.