Barley leaf stripe disease.

Leaf stripe is one of the most important diseases of barley in Iran especially in Gorgan, Mazandran and near Tehran (Varamin). Most obvious symptoms of the disease are described. Long pale or yellow stripes become darker as the fungus sporulates on the leaf surface. Infected plants usually are stunted and produce sterile spikes, rarely a few seeds are produced. Infected spikes and late-forming tillers may produce fertile spikes. The fungus is seed brone and survives in the outer layers of infected seed. To study the seed-borne disease, we have used the different methods (ISTA). Coleoptiles of seedlings are infected by the fungus under cool, moist conditions, a soil temperature below 15 degrees C is necessary for seed infection. The fungus penetrates through coleoptiles and grows systemically within the plant, produces toxin and kills cells and discolors leaf tissue between veins, thus causing striped lesions. When conditions are wet or humid, spores are produced on the surface of leaves at above the time spikes of healthy plant. Morphological characteristics of the vegetative and reproductive structures of the fungus show that it is Drechslera graminea (Rabenh) Shoemaker.

Human eotaxin induces eosinophil extravasation through rat mesenteric venules: role of alpha4 integrins and vascular cell adhesion molecule-1.

Eotaxin is a potent eosinophil-specific CC-chemokine, which has been shown to play a role in the selective induction of eosinophil accumulation in a number of allergic models of inflammation. Many aspects of the mechanism by which eotaxin induces eosinophil accumulation in vivo remain unresolved. In the present study, we investigated the direct effect of synthetic human eotaxin on leucocyte/endothelial cell interactions within rat mesenteric venules, as quantified by intravital microscopy. Topical eotaxin (30 pmol) induced rapid firm adhesion and extravasation of leucocytes within the rat mesentery, the extravasated leucocytes all being eosinophils, as determined by histological analysis. Whilst eotaxin was unable to stimulate the interaction of rat eosinophils with vascular cell adhesion molecule-1 (VCAM-1) under static conditions in vitro, eotaxin-induced responses in vivo were significantly suppressed by anti-alpha4 integrin and anti-VCAM-1 monoclonal antibodies (mAbs). The anti-alpha4 integrin mAb, HP2/1 (3.5 mg/kg), inhibited the eotaxin-induced firm adhesion and extravasation, 60 min postapplication of the chemokine, by 89% and 84%, respectively. In the same set of experiments, the anti-VCAM-1 mAb, 5F10 (3.5 mg/kg), inhibited leucocyte adhesion and extravasation by 61% and 63%, respectively. These results demonstrate that eotaxin-induced migration of eosinophils through rat mesenteric venules in vivo is dependent on an alpha4 integrin/VCAM-1 adhesion pathway, the significance of which may only be evident under flow conditions and/or following the ligation of other adhesion molecules expressed on eosinophils.