ArticleMilitary Medical Research2014
The injury progression of T lymphocytes in a mouse model with subcutaneous injection of a high dose of sulfur mustard.
Article in Military Medical Research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Divinyl sulfone, an oxidative metabolite of sulfur mustard, induces caspase-independent pyroptosis in hepatocytes.Archives of toxicology · 2024Article
- Cutaneous Exposure to Arsenicals Is Associated with Development of Constrictive Bronchiolitis in Mice.American journal of respiratory cell and molecular biology · 2023Article
- Sulfur Mustard-induced Changes in Blood Urea Nitrogen, Uric Acid and Creatinine Levels of Civilian Victims, and Their Correlation with Spirometric Values.Iranian journal of public health · 2018Article
- Emerging targets for treating sulfur mustard-induced injuries.Annals of the New York Academy of Sciences · 2016Review
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8 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundIn clinical studies, the findings on sulfur mustard (SM) toxicity for CD3(+)CD4(+) and CD3(+)CD8(+) T lymphocyte subsets are contradictory. In animal experiments, the effect of SM on the T cell number and proliferation is incompatible and is even the opposite of the results in human studies. In this study, we observed the dynamic changes of T lymphocytes in the first week in a high-dose SM-induced model.
methodsMice were exposed to SM by subcutaneous injection (20 mg/kg) and were sacrificed 4 h, 24 h, 72 h and 168 h later. Spleen T lymphocyte proliferation was evaluated by (3)H-TdR. Flow cytometric analysis was used to observe the percentage of CD3(+)CD4(+) and CD3(+)CD8(+) T lymphocyte subsets. The IL-1β, IL-6, IL-10 and TNF-α levels in plasma were assayed using the Luminex method. DNA damage in bone marrow cells was observed with the single cell gel electrophoresis technique (SCGE).
resultsSM continuously inhibited the proliferation of lymphocytes for 7 days, and there was a significant rebound of Con A-induced T lymphocyte proliferation only at 24 h. The percentage of CD3(+)CD4(+) and CD3(+)CD8(+) lymphocytes was upregulated, which was accompanied by increased IL-1β and TNF-α and decreased IL-10. The IL-6 level was gradually decreased in the PG group at 4 h. The peak of lymphocytic apoptosis and DNA damage occurred at 24 h and 72 h, respectively.
conclusionOur results show that SM significantly inhibited T lymphocyte proliferation as well as induced CD3(+)CD4(+) and CD3(+)CD8(+) upregulation. SM intoxication also significantly increased the levels of pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) and inhibited the level of anti-inflammatory cytokine IL-10. Our results may partly be due to the significant SM induced significant apoptosis and necrosis of lymphocytes as well as DNA damage of bone marrow cells. The results provided a favorable evaluation of SM immune toxicity in an animal model.
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