ABSTRACT
Objective:To investigate the effect of type ⅡNKT cells activated by sulfatide on airway inflammation in a murine model of asthma.Methods:Thirty-two BALB/c mice were randomly divided into four groups:normal control group ( n=8 ) , asthma group (n=8),sulfatide treatment group (n=8) and adoptive transfer group (n=8).The murine model of asthma was established by sensitization with intraperitoneal injection of ovalbumin ( OVA) and intranasal challenge in all animals except for the normal control group where PBS was used instead.Intraperitoneal injection of sulfatide in a sulfatide treatment group, adoptive transfer of sulfatide-activated typeⅡNKT cells in adoptive transfer group and PBS in asthma group were carried out 1 hour before the first challenge.PBS was used for intraperitoneal administration in the normal control group.Lung histology and goblet cell hyperplasia were analyzed by HE or PAS staining.Differential cell count in bronchial alveolar lavage ( BALF) was measured by May-Gruenwald Giemsa;levels of OVA-specific IgE in serum and L-4,IL-5 in BALF were measured by ELISA.The percentages of lung type Ⅱ NKT cells,IL-4+and IFN-γ+typeⅡNKT cells were detected by flow cytometry.Results:Inflammatory cell infiltration in lung tissue and goblet cell hyperplasia in the airway were decreased in sulfatide treatment group and adoptive transfer group.Percentages of eosinophil in BALF,level of OVA-specific IgE in serum,and levels of IL-4,IL-5 in BALF in sulfatide treatment group and adoptive transfer group were significantly lower than those in asthma group (all P<0.05).The percentages of lung IL-4+and IFN-γ+typeⅡNKT cells in sulfatide treatment group was significantly higher than those in asthma group ( P<0.01 ).Conclusion: Type Ⅱ NKT cells activated by sulfatide may inhibit airway inflammation in a murine model of asthma.
ABSTRACT
Peripheral nerve damage in leprosy would be related to the local cell-mediated immune response to mycobacterial antigens and, presumedly, metabolic and biochemical changes of Schwann cell or circulating demyelinating factors and otherwise, autoimmune process would be involved. The neuralipid composing of cholesterol, ethanolamine glycerophosphatide, sphingomyelin, galactocerebroside(GalC), ethanolamine plasmalogen, serine and choline glycerophophatide, sulfatide are abundant in the myelin and have immunogenicity. Especially, GalC and sulfatide are known to play an important role in myelin function and its stability. The study was undertaken to detect the titers of anti-GalC and anti-sulfatide antibodies for the neural destruction mechanism of leprosy. Subjects tested were 53 leprosy patients with polar type consisting of 25 in tuberculoid leprosy(TT) and 28 in lepromatous leprosy(LL). The titeration of the antibody was done in the sera of patients and controls by enzyme-linked immunosorbent assay(ELISA). The results obtained were as follows ; 1. The detection rate of anti-GalC antibody was in 13(24.5%) of the 53 leprosy patients compared with 3(13.0%) of the 23 normal controls. Among the leprosy patients, there was 8(32.0%) in TT and 5(17.9%) in LL. 2. The detection rate of anti-sulfatide antibody was in 24(45.3%) of leprosy patients compared with 7(26.1%) of normal controls. Both types showed almost same rate of 46.4% and 44.0%, respectively. 3. Mean titer of anti-GalC antibody was 18.9+/-17.0EU/ml in leprosy patients and 12.8+/-8.8EU/ml in normal controls, with statistically insignificant level(p>0.05, one-way ANOVA). Among the leprosy patients, mean titer was 24.7+/-20.9EU/ml in TT and 13.8+/-10.5EU/ml in LL, with significance in TT(p0.05). Among the leprosy patients, mean titer was 26.0+/-15.4EU/ml in TT and 24.7+/-14.0EU/ml in LL, which was nearly same quantities in both types. 5. Examinations using Pearson correlation analysis revealed that the association between anti-GalC and anti-sulfatide antibodies was non-specific in LL(r=0.09) and TT(r=0.04). The analysis between duration of illness and anti-GalC antibody was decreasing correlation(r=-0.89, p0.05). In comparison with anti-sulfatide antibody and duration, LL was higher in 41-50 years, while being higher in 31-40 years in TT, but correlation in both types could not be found(r=0.08, -0.06) In conclusion, the anti-GalC and anti-sulfatide antibodies seemed to be related with nerve damage. Hereafter we think that more study for other neural lipid should be investigated