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Soluble tropoelastin is a precursor of elastin. It is transported by elastin binding protein (EBP) into intercellular space. The EBP-tropoelastin complex undergoes disintegration in the intercellular space. EBP returns to the cell and tropoelastin joins with microfibril proteins. Lysine residues of tropoelastin undergo oxidative deamination. Desmosine, isodesmosine and cross bonds arise. Thus tropoelastin loses solubility and transforms to elastin. The elastic fiber created consists of microfibrils on the periphery and an elastin core inside. Elastin provides blood vessels, lungs, cartilage and skin with the ability to reverse deformations. A decrease of elastin content or changes in this protein structure results in pathological conditions such as aneurysms and pulmonary emphysema.
To define the role of activated neutrophils in lung injury during bovine respiratory tract infections (BRTI) their in vitro function was investigated. As a means to achieve this goal the comparison of secretory action between neutrophils from the BRTI group and control was made on the basis of elastase, myeloperoxidase (MPO), alkaline phosphatase (ALK-P) release, and nitric oxide production. We noted that there is an interdependence between secretory response of neutrophils and clinical severity of BRTI. The release of elastase was greater in the BRTI group than in the control group (49.17 ±4.41 versus 46.43 ±4.95% of the total content). Neutrophils from infected heifers exhibited a significantly (p<0.05) higher value of MPO release than from healthy heifers and reached 39.23 ± 10.18 versus 25.54 ± 8.41% of the total content. ALK-P containing granules released significantly (p<0.001) more enzyme in the group with BRTI than in the control group (22.42 ± 6.27 versus 13.74 ± 2.01% of the total enzyme content). The level of nitrite accumulation rose in the culture of cells isolated from heifers with BRTI from 4 ± 0.53 μM after 0.5h to 6.9 ± 0.52 μM after 72 h. Our data suggest that during BRTI the increase of neutrophil secretory action results in augmentation of enzyme release including elastase, MPO and ALK-P, and the nitrite production. During an excessive secretory response of neutrophils all these factors contribute to lung injury and worsen the course of a disease and might be recognised as markers of lung injury. Moreover, such a destructive action of neutrophils must be taken into account during the introduction of new methods of BRTI treatment.
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