Abstract: The present study aimed to evaluate mice as a candidate of the experimental model of Mycoplasma ovipneumoniae (Mo) infection, and screen the optimal method of Mo infection mice model. Sixty healthy BALB/c mice were randomly divided into control group, Mo infection group 1, infection group 2, infection group 3 and infection group 4 (n=12). Mice in Mo infection group 1 were challenged once with 30 μL and 25 μL 10⁸ CCU ·mL^-1 NJ01 strain cells by nasal and intraperitoneal drip, respectively. Mice in Mo infection group 2 and 3 were intranasally inoculated twice and three times 30 μL 10⁸ CCU ·mL^-1, respectively. Mice in Mo infection group 4 were inoculated twice 50 μL 10⁸ CCU ·mL^-1 by throat spry. The control group were inoculated with the normal liquid culture. The body weight was respectively determined on the 0, 7th and 14th day post-infection (DPI). Mice in five groups were killed on the 14th DPI, blood and lung tissue samples were collected. To determine whether the infection model was established successfully and evaluate the optimal establishment method of M. ovipneumoniae infection model, the histopathological examination of lung tissue were observed by HE staining and histopathologic score, the payload of Mo in lung tissue was detected by quantitative PCR, and Mo IgG level in serum was determined by ELISA. On the 14th DPI, compared with control group, the body weight of mice in infection group 2 and group 4 significantly reduced 17.2% (P < 0.05) and 21.6% (P < 0.05). A mice died on the 13th DPI in infection group 2 and group, 4 respectively. On the 14th DPI, mice had inflammation in lung and lung histopathologic score was 3.5 and 3.3 in infection group 2 and group 4, respectively, which were significantly higher than both infection group 1 (P < 0.05) and 3 group (P < 0.05). No lung lesion was found in control mice. Histopathological examination showed that different degrees of interstitial pneumonia were observed in the lungs of the Mo infection groups. Inflammatory cell infiltration was seen in alveolar cavity. In the control group, the lung tissue structure was normal and intact, and there was no obvious inflammatory cell in alveolar cavity. The DNA copy numbers of Mo in infection group 1 and group 3 were 10^2.56 and 10^3.21 copies ·g^-1, respectively. The infection group 2 and group 4 were 10^3.84 and 10^3.77 copies ·g^-1 respectively. They were significantly higher than both group 1 (P < 0.05) and group 3 (P < 0.05). Control group was negative. The serum antibody OD_{450 nm} of Mo infection mice were 0.63, 1.05, 0.81 and 0.99 in infection group 1 group 2, group 3 and group 4, respectively, which were all significantly higher than control group (P < 0.05). Mo antibody level in infection group 2 and group 4 were significantly higher than infection group 1 (P < 0.05). Mice model infected M. ovipneumoniae were successfully developed in this experiment by nasal drip and throat spray 1×10⁸ CCU ·mL^-1 for continued two times Mo which can provide important basis for investigating the pathogenesis and therapy of mycoplasma pneumonia of sheep.

Key words: Mycoplasma ovipneumoniae, mice, infection model