BACKGROUND:Several studies have demonstrated that mesenchymal stem cel s exhibit strong immunomodulation on al ergic asthma. However, there are no reports to compare therapeutic effects under different administration ways.
OBJECTIVE:To examine the immunomodulatory effects of MSCs via different administration routes on asthmatic mice.
METHODS:Seventy-two Balb/c mice experienced three independent tests, and 24 mice were selected for each test. Twenty-four mice were randomly divided into four groups (n=6):control group, model group, intravenous treatment group and intratracheal treatment group. The mouse model of asthma was induced via intraperitoneal injection of ovalbumin at 1, 7, 14 days and 30-minute aerosol inhalation of ovalbumin at 22-26 days. In the latter two groups, mesenchymal stem cel s were injected intravenously (200μL, 5×109/L) or intratracheal y (50μL, 2×109/L) into the mice at 1 day before aerosol inhalation.
RESULTS AND CONCLUSION:Compared with the control group, the airway inflammatory response was significantly increased in the model group. Intravenous administration of mesenchymal stem cel s significantly al eviated the symptoms of al ergic airway inflammation, including the airway hyperreactivity, the inflammatory cel counting in the bronchoalveolar lavage fluid, inflammatory cel infiltration in the lung tissue. Meanwhile, the levels of Th2 type cytokines in the bronchoalveolar lavage fluid and IgE in serum also decreased after intravenous administration of mesenchymal stem cel s. However, the intratracheal application of mesenchymal stem cel s did not exhibit the similar effects. Intravenous, not intratracheal, application of mesenchymal stem cel s can exert immunomodulatory effects through the blood circulation.

OBJECTIVE: To study the clinical diagnosis, course and combined therapy of aggressive rhinocerebral mucormycosis. METHOD: The clinical feature, diagnosis and therapy were analyzed in 5 cases with rhinocerebral mucormycosis throughout disease progress. Good treatments were found by analyzing curative effect of different treatment. RESULT: One patient died within three weeks in hospital three patients survived from 2 months to 2 years; and one patient was alive over 3 years. The mortality rate was 80% in this study. CONCLUSION Rhinocerebral mucormycosis is always secondary to patients with severe diseases and bad immunologic function. The lesion can invade the orbit and brain quickly, and the mortality rate is high. The cause of the disease can be retarded by clearing up the focus early and removing the environment of fungi thriving with combined therapy. It is effective of remodelling the necrotic tissues by nasal endoscopy.
Adult ; Brain Diseases ; diagnosis ; microbiology ; therapy ; Female ; Humans ; Male ; Middle Aged ; Mucormycosis ; diagnosis ; therapy ; Nose Diseases ; diagnosis ; microbiology ; therapy

OBJECTIVETo evaluate the possible role of tight junction protein Occludin in nasal polyps.

METHODSThe expression of Claudin-1, Occludin and ZO-1 in nasal polyps (n = 20) and healthy uncinate mucosa (n = 15) were examined using immunohistochemical staining, real-time quantitative polymerase chain reaction (PCR) and Western blot analysis. The regulatory effects of proinflammatory cytokines (IFN-γ, IL-13, IL-17, TGF-β, TGF-α) on the expression of Occludin in cultured human nasal epithelial cells were investigated.

RESULTSThe immunohistochemical results showed that Claudin-1, Occludin and ZO-1 were detected both in the nasal polyp group and the control group. The expression sites were the cell membrane and cytoplasm of nasal mucosa epithelial cells. The mean optical density of Claudin-1, Occludin and ZO-1 were 0.187 ± 0.076,0.172 ± 0.109 and 0.098 ± 0.035 respectively in the nasal polyp group and were significantly lower than those in the control group (0.312 ± 0.101, 0.220 ± 0.069 and 0.233 ± 0.093 respectively), the differences were significant (t = 9.345, t = 3.301, t = 13.323, all P < 0.01).RT-PCR results showed that the relative expression of Occludin mRNA was 0.000 117 ± 0.000 035 in the nasal polyp group and was significantly lower than that in the control group(0.000 464 ± 0.000 134), and the difference was significant (Z = -5.0, P < 0.01) . There was no statistically significant difference in the relative expression of Claudin-1 and ZO-1 mRNA between the nasal polyp group and the control group (P > 0.05) . After the cultured human nasal epithelial cells were stimulated by IL-13, IL-17, IFN-γ and other proinflammatory cytokines, the relative expression of Occludin mRNA was 0.631 ± 0.039, 0.581 ± 0.029 and 0.648 ± 0.040, respectively. Compared with the unstimulated control group, the differences were statistically significant (t = 16.299, 24.669 and 14.995 respectively, all P < 0.05).Western blot analyse showed that the relative grayscale in the above proinflammatory cytokines stimulation groups was 0.650 ± 0.061,0.482 ± 0.106 and 0.536 ± 0.109, respectively. Compared with the unstimulated control group, the differences were statistically significant (t = 9.880, 8.442 and 7.310 respectively, all P < 0.05).

CONCLUSIONSThe reduced expression of Occludin might be involved in the pathogenesis of nasal polyps.

Claudin-1 ; Cytokines ; Epithelial Cells ; Humans ; Interleukin-13 ; Interleukin-17 ; Nasal Mucosa ; Nasal Polyps ; metabolism ; Occludin ; genetics ; metabolism ; RNA, Messenger ; Tight Junctions ; metabolism ; Transforming Growth Factor alpha ; Zonula Occludens-1 Protein