Inhibition of function of T cell subpopulations and decrease in cytokine production during subacute poisoning with various toxicants

Забродский, П. Ф.; Germanchuk, V. G.; Mandych, V. G.

doi:10.1007/s10517-008-0256-6

Cited by 4 publications

(2 citation statements)

References 6 publications

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“…For instance, dimethoate was shown to have the lowest cytotoxic and genotoxic potential in cultured cells, compared to other three organophosphates and the organochlorine endosulfan;80 however, its administration in experimental female mice caused a decrease in total immunoglobulins and IgM and in the number of plaque forming cells;81 the same effects were observed over three generations following repeated administration of low doses dimethoate in outbred Wistar rats 82. Functional activity of Th1 lymphocytes, immune reactions associated with these cells, and interferon- γ production were impaired after subacute malathion intoxication in albino rats,83 while thymic atrophy and reduction in splenic germinal centres followed methylparathion administration in rabbits 84. Such immunosuppressive effects do not seem related to acetylcholinesterase inhibition, the typical toxicological mechanism of organophosphate poisoning, and cover a large number of pesticides, including organochlorines, organophosphates, carbamates and pyrethroids 85 86.…”

Section: Discussionmentioning

confidence: 95%

Lymphoma risk and occupational exposure to pesticides: results of the Epilymph study

et al. 2012

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Objectives Several agricultural pesticides have shown a carcinogenic potential in experimental animals. Methods In 1998-2003, 2337 incident lymphoma cases and 2434 controls participated in the EPILYMPH case-control study in six European countries. A detailed occupational history was collected in cases and controls. Specifi c questions for farm workers included type of crop, farm size, pests being treated, type and schedule of pesticide use. We conducted a preliminary analysis of risk of lymphoma and its major subtypes associated with occupational exposure to groups of pesticides. The OR and its 95% CI was calculated with unconditional logistic regression for all lymphomas, and its major subtypes, adjusting by age, gender, and education. Results Lymphoma risk did not increase among those exposed to inorganic (OR = 1.3, 95% CI 0.9 to 1.7) or organic pesticides (OR = 1.1, 95% CI 0.9 to 1.4). Risk of CLL was signifi cantly increased among those exposed to pesticides (OR = 1.5 95% CI 1.0 to 2.2), and particularly to organophosphates (OR = 2.2, 95% CI 1.1 to 4.4). No other signifi cant associations were observed. Conclusions Our results confi rm previous reports of an increase in risk of specifi c lymphoma subtypes associated with exposure to specifi c agrochemicals.

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Section: Discussionmentioning

confidence: 95%

Lymphoma risk and occupational exposure to pesticides: results of the Epilymph study

et al. 2012

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“…For example, IL-17 likely plays an important role in the pathogenesis of SM-induced lung injury [ 39 ]. The numbers and proliferation activity of T cells could affect the levels of many cytokine types [ 39 , 41 , 42 ]. A variety of cytokines secreted by T cells, including IL-1β, IL-6, IL-10 and TNF-α, are reported to be associated with respiratory damage.…”

Section: Discussionmentioning

confidence: 99%

The injury progression of T lymphocytes in a mouse model with subcutaneous injection of a high dose of sulfur mustard

Mei¹,

Zhang²,

Jiang³

et al. 2014

Military Med Res

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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 3H-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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Methanol Induces a Discrete Transcriptional Dysregulation that Leads to Cytokine Overproduction in Activated Lymphocytes

Désy

Carignan

Caruso

et al. 2010

Toxicological Sciences

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Methanol is an important cause of acute alcohol intoxication; it is ubiquitously present at home and in the workplace. Although the existing literature provides a reasonable insight into the immunological impact of ethanol and to a much lesser extent of isopropanol, much less data are available on methanol. We hypothesized on structural grounds that methanol would share the immunosuppressive properties of the two other short-chain alcohols. We report here that methanol increases the proliferative capacity of human T lymphocytes and synergizes with the activating stimuli to augment cytokine production. The cytokine upregulation was observed in vitro at methanol concentrations as low as 0.08% (25mM) as measured by interleukin-2, interferon-γ, and tumor necrosis factor-α release in T cells. Methanol did not affect the antigen receptor-mediated early signaling but promoted a selective and differential activation of the nuclear factor of activated T cells family of transcription factors. These results were further substantiated in a mouse model of acute methanol intoxication in which there was an augmented release of proinflammatory cytokines in the serum in response to the staphylococcal enterotoxin B. Our results suggest that methanol has a discrete immunological footprint of broad significance given the exposure of the general population to this multipurpose solvent.

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Inhibition of function of T cell subpopulations and decrease in cytokine production during subacute poisoning with various toxicants

Cited by 4 publications

References 6 publications

Lymphoma risk and occupational exposure to pesticides: results of the Epilymph study

Lymphoma risk and occupational exposure to pesticides: results of the Epilymph study

The injury progression of T lymphocytes in a mouse model with subcutaneous injection of a high dose of sulfur mustard

Methanol Induces a Discrete Transcriptional Dysregulation that Leads to Cytokine Overproduction in Activated Lymphocytes

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