Hedayati-Moghadam Mahdiyeh, Rezaee S A Rahim, Boskabady Mohammad Hossein, Mohamadian Roshan Nema, Saadat Saeideh, Bavarsad Kowsar, Niazmand Saeed
Student Research Committee, Mashhad University of Medical Sciences, Mashhad, Iran.
Department of Physiology, School of Medicine, Jiroft University of Medical Sciences, Jiroft, Iran.
Adv Biomed Res. 2021 Jan 30;10:6. doi: 10.4103/abr.abr_117_20. eCollection 2021.
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.
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 10 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.
In the HTLV-1-infected group, the peribronchitis score ( < 0.01), the number of total leukocytes, neutrophils, lymphocytes, and monocytes ( < 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 ( < 0.01), whereas the number of basophils of BALF was increased in the HTLV-1-infected group ( < 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 ( < 0.01).
The HTLV-1 infection seems to induce pulmonary inflammatory reactions by recruiting leukocytes as well as inducing oxidative stress in the lung tissue.
人类嗜T淋巴细胞病毒1型（HTLV-1）感染可能诱发非肿瘤性炎症性肺部疾病。因此，开展了一项实验研究，以评估HTLV-1感染的BALB/c小鼠肺组织和血液中白细胞数量变化及氧化应激情况，这可能有助于认识HTLV-1诱发肺部疾病的机制。
将20只雌性BALB/c小鼠分为对照组和HTLV-1感染组。HTLV-1感染组接种10个MT-2 HTLV-1感染细胞。两个月后，采用实时聚合酶链反应确认感染情况，然后评估肺部病理变化、血液及支气管肺泡灌洗液（BALF）中的总炎症细胞计数和分类计数，以及BALF和肺组织中的氧化应激生物标志物水平。
在HTLV-1感染组，支气管周围炎评分（<0.01）、血液和BALF中的总白细胞、中性粒细胞、淋巴细胞及单核细胞数量（<0.05）均增加。HTLV-1感染组血液中的嗜酸性粒细胞数量高于对照组（<0.01），而HTLV-1感染组BALF中的嗜碱性粒细胞数量增加（<0.001）。肺组织和BALF氧化应激结果显示，HTLV-1感染组的丙二醛（MDA）水平升高，而总巯基水平和超氧化物歧化酶活性降低（<0.01）。
HTLV-1感染似乎通过募集白细胞以及诱导肺组织氧化应激来诱发肺部炎症反应。
