Allergens in Japanese patients with allergic conjunctivitis in autumn.

PURPOSE: The purpose of the current study is to evaluate the relation between various specific class E immunoglobulins (IgE) in the serum and allergic conjunctivitis in autumn. METHODS: Total IgE and specific IgE to 12 inhalant allergens were measured using the CAP system in 32 patients with allergic conjunctivitis in spring (spring group), 27 patients with allergic conjunctivitis in autumn (autumn group), and 40 healthy volunteers (control group). RESULTS: Specific IgE levels caused by house dust, Dermatophagoides pteronyssinus, and orchard grass were higher in the autumn group than in the spring group. The highest positivity rate for a specific allergen was 51.9% for house dust, followed by D. pteronyssinus(48.1%) in the autumn group, while the highest rate was 68.8 % for cedar pollen, followed by cypress pollen (59.4%) in the spring group. Correlation analysis showed that house dust was significantly correlated with animal epithelia, D. pteronyssinus, acarus, and Alternaria tenuis in the autumn group (P<0.001). CONCLUSIONS: These results suggest that house dust is the main cause of allergic conjunctivitis during autumn. In spring, cypress pollen is the largest cause of allergic conjunctivitis, while indoor allergens such as house dust, animal epithelia, D. pteronyssinus, and acarus are not causative allergens in Japan.

Depression of long term potentiation in gerbil hippocampus following postischemic hypothermia.

To investigate the mechanism of chronic cell death following postischemic hypothermia, the change of N-methyl-D-aspartate receptor (NMDAR) were examined by immunohistochemistry of NMDAR1 and long-term potentiation (LTP) in the CA1 subfield of the gerbil hippocampus. At 1 week following postischemic hypothermia (32 degrees Cx4 h), all CA1 neurons survived; however, immunoreactivity of NMDAR1 increased in neuronal perikarya whereas decreased in dendrites in the CA1 neurons. The abnormality was still observed in remaining CA1 neurons at 1 month after hypothermia. LTP was also significantly depressed at 1 week after hypothermia. These results suggest that some abnormalities in the glutamate receptor may be caused by ischemia; such abnormality would persist in spite of hypothermia treatment, resulting in the depression of LTP.

Analysis of immunomodulatory activities of aqueous humor from eyes of mice with experimental autoimmune uveitis.

Aqueous humor (AqH) contains immunosuppressive factors, especially TGF-beta2, that contribute to the immune privileged status of the anterior chamber. However, this may not be true when the blood-ocular barrier is compromised by ocular inflammation. To determine the immunosuppressive status of AqH from murine eyes afflicted with experimental autoimmune uveitis, B10.A mice were immunized with interphotoreceptor retinoid-binding protein. AqH was collected from eyes of affected mice periodically after immunization and then evaluated for content of TGF-beta, proinflammatory cytokines, and the capacity to suppress anti-CD3-driven T cell proliferation. mRNA expression of selected cytokines in iris and ciliary body from inflamed eyes was analyzed by ribonuclease protection assay. We found that TGF-beta levels were significantly increased in AqH from EAU eyes on days 11, 17, and 28. AqH collected on day 11 (onset of disease) failed to suppress T cell proliferation and contained large amounts of locally produced IL-6 that antagonized TGF-beta. In contrast, AqH collected at 17 days (when ocular inflammation was progressively severe) re-expressed the ability to suppress T cell proliferation, in this case due to high levels of blood-derived TGF-beta1 and eye-derived TGF-beta2 in the absence of IL-6. Thus, during the onset of experimental autoimmune uveitis, the ocular microenvironment loses its immunosuppressive properties due to local production of IL-6. But as inflammation mounts, AqH IL-6 content falls, and the fluid reacquires sufficient TGF-beta eventually to suppress immunogenic inflammation. The paradoxical roles of IL-6 in antagonizing TGF-beta, while promoting TGF-beta accumulation during ocular inflammation, is discussed.

cDNA cloning and functional expression of a human monocyte chemoattractant protein 1 receptor.

A novel human G-protein-coupled seven-transmembrane-type receptor gene, 24-1, has been cloned from THP-1 cells. The 24-1 was 56% and 34% identical to the macrophage inflammatory protein-1 alpha (MIP-1 alpha) receptor and the interleukin-8 (IL-8) receptors at the amino acid level, respectively. To examine the ligand specificity of the receptor, we have established a stable transfectant of this gene with human kidney 293 cells. Monocyte chemoattractant protein-1 (MCP-1) induced a rapid increase of Ca++ influx in the 24-1-transfectant, while other C-C chemokines tested did not. This indicates that the 24-1 encodes the human MCP-1 receptor.