Interleukin-6 and airflow limitation in chemical warfare patients with chronic obstructive pulmonary disease

Attaran, Davood; Lari, Shahrzad M.; Towhidi, Mohammad; Ghobadi, Hassan; Ayatollahi, Hossein; Khajehdaluee, Mohammad; Ghanei, Mostafa; Basiri, Reza

doi:10.2147/copd.s12545

Cited by 23 publications

(20 citation statements)

References 36 publications

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“…Specific alterations in circulating T-lymphocyte subpopulations and immunoglobulin subclasses have also been reported (Ghazanfari et al, 2013a, b). Serum levels of matrix metalloproteinase (MMP)s, elastase and IL-6 are also elevated, with levels directly correlating with the severity of pulmonary disease (Attaran et al, 2010; Kiani et al, 2013; Pourfarzam et al, 2013). Expression of inflammatory mediators including tumor necrosis factor (TNF)-α and IL-1β, as well as specific isoforms of TGF-β, are also chronically elevated in the lungs of SM exposed victims and related to the severity of symptoms (Yaraee et al, 2013; Zarin et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Mustard vesicant-induced lung injury: Advances in therapy

Weinberger

Malaviya

Sunil

et al. 2016

Toxicology and Applied Pharmacology

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Most mortality and morbidity following exposure to vesicants such as sulfur mustard is due to pulmonary toxicity. Acute injury is characterized by epithelial detachment and necrosis in the pharynx, trachea and bronchioles, while long-term consequences include fibrosis and in some instances, cancer. Current therapies to treat mustard poisoning are primarily palliative and do not target underlying pathophysiologic mechanisms. New knowledge about vesicant-induced pulmonary disease pathogenesis has led to the identification of potentially efficacious strategies to reduce injury by targeting inflammatory cells and mediators including reactive oxygen and nitrogen species, proteases and proinflammatory/cytotoxic cytokines. Therapeutics under investigation include corticosteroids, N-acetyl cysteine, which has both mucolytic and antioxidant properties, inducible nitric oxide synthase inhibitors, liposomes containing superoxide dismutase, catalase, and/or tocopherols, protease inhibitors, and cytokine antagonists such as anti-tumor necrosis factor (TNF)-α antibody and pentoxifylline. Antifibrotic and fibrinolytic treatments may also prove beneficial in ameliorating airway obstruction and lung remodeling. More speculative approaches include inhibitors of transient receptor potential channels, which regulate pulmonary epithelial cell membrane permeability, non-coding RNAs and mesenchymal stem cells. As mustards represent high priority chemical threat agents, identification of effective therapeutics for mitigating toxicity is highly significant.

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Section: Introductionmentioning

confidence: 99%

Mustard vesicant-induced lung injury: Advances in therapy

Weinberger

Malaviya

Sunil

et al. 2016

Toxicology and Applied Pharmacology

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“…As mentioned earlier, 48 , 49 COPD is not confined to the lungs and is a systemic inflammatory condition. 5 Fabri and Rabe suggested the term “chronic systemic inflammatory syndrome” to reflect the complexity of the condition.…”

Section: Assessment Of Symptomsmentioning

confidence: 86%

Improving communication between the physician and the COPD patient: an evaluation of the utility of the COPD Assessment Test in primary care

Lari¹,

Attaran²,

Tohidi³

2014

PROM

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Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide. It is now considered a systemic inflammatory syndrome and is associated with important comorbidities. In addition to spirometry for evaluating the severity of airflow obstruction, an instrument is required for comprehensive assessment of the disease. The COPD Assessment Test (CAT) is a simple and valid tool for evaluating patient symptoms. The CAT can improve patient–physician communication during routine clinical visits and is useful for assessing functional status and response to treatment. The CAT has a strong correlation with other health status questionnaires, such as the St George’s Respiratory Questionnaire. The main advantages of the CAT are its thorough coverage of the important clinical aspects of disease burden and the shorter time involved in completing it. The aim of this paper is to review the role of the CAT, to compare it with other health-related quality of life questionnaires in the assessment and management of COPD patients, and to emphasize the importance of patient–physician communication in the management of patients with the disease.

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“…Interestingly, when the IL-6 level was highest at 4 h, the splenocyte apoptosis percentage of the SM group was not significantly different compared to the PG group; meanwhile, the necrosis percentage was also at the highest level. In vivo studies found that the serum IL-6 was increased in patients with sulfur mustard poisoning and COPD [ 48 ]. In vitro , treatment with 100 μmol/L of SM for 24 hours resulted in a significantly increased level of IL-6 secretion by human epidermal keratinocytes (HEKs) and human skin fibroblasts (HSFs) [ 49 ].…”

Section: Discussionmentioning

confidence: 99%

“…These results were consistent with our finding that the IL-6 level increased after SM exposure. The main sources of IL-6 are monocytes, macrophages, T and B cells, fibroblasts, epithelial cells, and smooth muscle cells [ 48 ]. Therefore, we speculated that the gradual decrease in IL-6 was mainly due to the significant necrosis and apoptosis of T and B lymphocytes in the intoxicated spleen.…”

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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Interleukin-6 and airflow limitation in chemical warfare patients with chronic obstructive pulmonary disease

Cited by 23 publications

References 36 publications

Mustard vesicant-induced lung injury: Advances in therapy

Mustard vesicant-induced lung injury: Advances in therapy

Improving communication between the physician and the COPD patient: an evaluation of the utility of the COPD Assessment Test in primary care

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

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