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Human T-cell leukemia virus type 1 changes leukocyte number and oxidative stress in the lung and blood of female BALB/c mice
Mahdiyeh Hedayati-Moghadam1, S A Rahim Rezaee2, Mohammad Hossein Boskabady3, Nema Mohamadian Roshan4, Saeideh Saadat5, Kowsar Bavarsad6, Saeed Niazmand3
1 Student Research Committee, Mashhad University of Medical Sciences, Mashhad; Department of Physiology, School of Medicine, Jiroft University of Medical Sciences, Jiroft; Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
2 Immunology Research Center, Division of Inflammation and Inflammatory Diseases, Mashhad University of Medical Sciences, Mashhad, Iran
3 Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
4 Department of Pathology, Ghaem Hospital, Mashhad University of Medical Sciences, Mashhad, Iran
5 Department of Physiology, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran
6 Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Correspondence Address:
Dr. Saeed Niazmand
Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad
Iran
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/abr.abr_117_20
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Background: Human T-cell leukemia virus type 1(HTLV-1) infection is likely to induce nonneoplastic inflammatory pulmonary diseases. Therefore, an experimental study was conducted to evaluate the leukocytes' number alteration and oxidative stress in the lung and blood of HTLV-1-infected BALB/c mice, which could be of benefit for the recognition of HTLV-1 mechanism in the induction of pulmonary disorders. Materials and Methods: Twenty female BALB/c mice were divided into two groups of control and HTLV-1-infected animals. The HTLV-1-infected group was inoculated with 106 MT-2 HTLV-1-infected cells. Two months later, the infection was confirmed using real-time polymerase chain reaction, and then lung pathological changes, total and differential inflammatory cell counts in the blood and bronchoalveolar lavage fluid (BALF), along with oxidative stress biomarker levels in the BALF and lung tissue were evaluated. Results: In the HTLV-1-infected group, the peribronchitis score (P < 0.01), the number of total leukocytes, neutrophils, lymphocytes, and monocytes (P < 0.05) in the blood and BALF were increased. The number of eosinophils in the blood of the HTLV-1-infected group was higher than in the control group (P < 0.01), whereas the number of basophils of BALF was increased in the HTLV-1-infected group (P < 0.001).The lung and BALF oxidative stress results showed that the MDA level was increased, while the total thiol level and superoxide dismutase activity were decreased in the HTLV-1-infected group (P < 0.01). Conclusion: The HTLV-1 infection seems to induce pulmonary inflammatory reactions by recruiting leukocytes as well as inducing oxidative stress in the lung tissue.
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