De la Mora Alfonso, Trigo Francisco, Jaramillo Laura, Garfias Yonathan, Solórzano Carlos, Agundis Concepción, Pereyra Ali, Lascurain Ricardo, Zenteno Edgar, Suárez-Güemes Francisco
Laboratorio de Patología, Instituto de Investigaciones en Ciencias Veterinarias, Universidad Autónoma de Baja California, Mexicali, BC, Mexico.
Vet Immunol Immunopathol. 2006 Sep 15;113(1-2):148-56. doi: 10.1016/j.vetimm.2006.04.011. Epub 2006 Jun 15.
In this work we identified specific bovine leukocytes that were bound by the Mannheimia haemolytica adhesin molecule (MhA) and the biological effect on the leukocytes. Histochemical staining and flow cytometry showed that MhA bind neutrophils (90%) and monocytes (5%). MhA induced an oxidative response in purified neutrophils; this effect was 1.5-fold higher than the effect observed with control cells activated with Zymosan. Cellular binding by MhA was inhibited with GlcNAc and its oligomers, as well as by glycoproteins containing tri- and tetra-antennary N-glycosydically linked glycans. MhA-induced oxidative burst was significantly inhibited by GlcNAc, iodoacetamide, superoxide dismutase, and piroxicam (p<0.05). Our findings suggest that among bovine leukocytes, neutrophils are the main target for MhA, inducing production of oxidative radicals by non-opsonic mechanism that seem to play an important role in tissue damage during mannheimiosis.
在本研究中，我们鉴定了被溶血曼氏杆菌粘附分子（MhA）结合的特定牛白细胞及其对白细胞的生物学效应。组织化学染色和流式细胞术显示，MhA可结合嗜中性粒细胞（90%）和单核细胞（5%）。MhA可诱导纯化嗜中性粒细胞产生氧化反应；该效应比用酵母聚糖激活的对照细胞所观察到的效应高1.5倍。MhA与细胞的结合可被N-乙酰葡糖胺及其寡聚物以及含有三触角和四触角N-糖基连接聚糖的糖蛋白所抑制。N-乙酰葡糖胺、碘乙酰胺、超氧化物歧化酶和吡罗昔康可显著抑制MhA诱导的氧化爆发（p<0.05）。我们的研究结果表明，在牛白细胞中，嗜中性粒细胞是MhA的主要靶标，其通过非调理机制诱导氧化自由基的产生，这似乎在曼氏杆菌病期间的组织损伤中起重要作用。
