Abstract

MIF is an innate immune mediator plays a complex role in the host response to bacterial infections, also associated with lung pathology, especially acute lung injury. The aim of the research was to study the peculiarities of alteration of structural elements of lung tissue at MIF mediated acute lung injury. The study was conducted on 24 adult male Wistar Albino rats subdivided into two groups: “Control” (N12) and “MIF” (N12). The obtained lung tissue from both animal groups prepared into paraffin and Araldite-Epon blocks. The gained thin sections from blocks analyzed on light, also ultrathin sections studied on transmission electron (JEM-1400, Japan) microscopes. Acute lung injury is characterized by complex specified multicellular activation, also inflammatory cells influx into the lung tissue. Cytokine MIF influenced to immune and nonimmune cells of the lungs, as well as to alveolar-capillary membrane for cellular communication during acute lung injury. These interactions are important to the initiation and procreation of the inflammatory response leading to pulmonary injury. Investigation on main groups animals detected some patological injury, including alveolar and interstitial inflammation. Sharply detected alveolar septal thickening due to infiltration of cells and edema. Increased vascular permeability leads to congestion of capillaries, also accumulated odematous fluid around vessels and within interstisium. In addition, detected recruitment of neutrophils, macrophages, lymphocytes, eosinophils into the lung tissue. These findings suggest that MIF plays a crucial pathological role leading to acute lung injury and anti-MIF therapy may represent a novel therapeutic approach for reducing lung patology.