Alterations in the serum levels of chemokines 20years after sulfur mustard exposure: Sardasht-Iran Cohort Study

Ghazanfari, Tooba; Yaraee, Roya; Kariminia, Amina; Ebtekar, Massoumeh; Faghihzadeh, Soghrat; Mahdavi, Mohammad Reza Vaez; Rezaei, Abbas; Vojgani, Mohammad; Soroush, Mohammad Reza; Kermani-Jalilvand, Arezou; Mohammadi, Pourya; Foroutan, Abbas; Hassan, Zuhair Mohammad

doi:10.1016/j.intimp.2009.08.022

Cited by 18 publications

(8 citation statements)

References 41 publications

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“…This was associated with a transient increase in neutrophils in BAL. Similar coordinate increases in BAL neutrophils and MCP-1 levels have been described in humans after sulfur mustard exposure (Emad and Emad, 2007; Ghazanfari et al, 2009), and in mice after CEES administration (Sunil et al, 2011a). Neutrophils are known to participate in both acute and chronic lung injury (Chapman et al, 2009; Chung, 2005).…”

Section: Discussionsupporting

confidence: 73%

Role of reactive nitrogen species generated via inducible nitric oxide synthase in vesicant-induced lung injury, inflammation and altered lung functioning

Sunil

Shen

Patel-Vayas

et al. 2012

Toxicology and Applied Pharmacology

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Pulmonary toxicity induced by vesicants is associated with oxidative stress. In the present studies we analyzed the role of reactive nitrogen species (RNS) generated via inducible nitric oxide synthase (iNOS) in lung injury and inflammation induced by vesicants using 2-chloroethyl ethyl sulfide (CEES) as a model. C57Bl/6 (WT) and iNOS−/− mice were sacrificed 3 d or 14 d following intratracheal administration of CEES (6 mg/kg) or control. CEES intoxication resulted in transient (3 d) increases in bronchoalveolar lavage (BAL) cell and protein content in WT, but not iNOS−/− mice. This correlated with expression of Ym1, a marker of oxidative stress in alveolar macrophages and epithelial cells. In contrast, in iNOS−/− mice, Ym1 was only observed 14 d post exposure in enlarged alveolar macrophages, suggesting that they are alternatively activated. This is supported by findings that lung tumor necrosis factor and lipocalin Lcn2 expression, mediators involved in tissue repair were also upregulated at this time in iNOS−/− mice. Conversely, CEES-induced increases in the proinflammatory genes, monocyte chemotactic protein-1 and cyclooxygenase-2, were abrogated in iNOS−/− mice. In WT mice, CEES treatment also resulted in increases in total lung resistance and decreases in compliance in response to methacholine, effects blunted by loss of iNOS. These data demonstrate that RNS, generated via iNOS play a role in the pathogenic responses to CEES, augmenting oxidative stress and inflammation and suppressing tissue repair. Elucidating inflammatory mechanisms mediating vesicant-induced lung injury is key to the development of therapeutics to treat mustard poisoning.

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Section: Discussionsupporting

confidence: 73%

Role of reactive nitrogen species generated via inducible nitric oxide synthase in vesicant-induced lung injury, inflammation and altered lung functioning

Sunil

Shen

Patel-Vayas

et al. 2012

Toxicology and Applied Pharmacology

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“…[ 8 ] and Ghazanfari et al . [ 9 ], respectively. Out of the pollen season, we found elevated serum levels of IL-8, which is consistent with the reported data taking in account that IL-8 inhibits release of histamine.…”

Section: Discussionmentioning

confidence: 99%

“…Ghazanfari et al . also reported significantly elevated levels of MCP-1 in the sera of sulfur mustard exposed individuals compared to control subjects, but in contrast to the other reports, they found significantly decreased levels of RANTES suggesting a different pathophysiology and diverse molecular mechanisms involved in this type of intoxication [ 9 ]. Greatly enhanced BALF levels of MCP-1, MIP-1α and RANTES were detected 4 h after the endobronchial allergen challenge of stable asthmatic patients compared to the saline-challenged control subjects.…”

Section: Introductionmentioning

confidence: 96%

Ragweed-allergic subjects have decreased serum levels of chemokines CCL2, CCL3, CCL4 and CCL5 out of the pollen season

Kostova¹,

Batsalova²,

Moten³

et al. 2015

cejoi

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CC-chemokines are important mediators of the allergic responses and regulate the cell trafficking. The aim of this study was to examine the serum levels of CCL2/MCP-1, CCL3/MIP-1α, CCL4/MIP-1β and CCL5/RANTES, and to determine whether there are differences between ragweed-allergic subjects and healthy individuals out of the pollen season. Peripheral blood samples were collected from 24 subjects allergic to ragweed pollen and 12 healthy controls. Serum concentrations of chemokines/cytokines were measured by an enzyme-linked immunosorbent assay. We observed significantly decreased concentrations of CCL2/MCP-1, CCL3/MIP-1α, CCL4/MIP-1β and CCL5/RANTES in the sera of ragweed-allergic patients compared to the healthy individuals (32.2 vs. 106.4 pg/ml, 89.5 vs. 135.7 pg/ml, 63.4 vs. 119.2 pg/ml and 11.2 vs. 18.1 ng/ml, respectively, p < 0.01). In contrast to the CC-chemokines, the serum levels of IL-8/CXCL8 showed a significant increase (p < 0.05) in the allergic group compared to the non-allergic subjects. Interleukin 4 levels were similar in both groups. In the sera of allergic patients, we have also detected significantly elevated levels of ragweed-specific IgE and IgG. However, decreased serum concentrations of the four CC-chemokines and elevated levels of IL-8/CXCL8 can be used as biomarkers for more accurate evaluation of the allergic status of patients with pollen allergy out of the season, to study the mechanisms for activation/inhibition of the subclinical allergic responses and for development of therapeutic strategies.

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“…As it could be seen from Table 1, cytokines and chemokines have been well investigated in victims exposed to mustard by Emad, Ghanei and their colleagues from two different research groups in Iran (Aghanouri et al, 2004;Amiri et al, 2009;Attaran et al, 2010;Emad & Emad, 2007a,b,c,d,e;Ghazanfari et al, 2009;Pourfarzam et al, 2009;Yaraee et al, 2009;Zarin et al, 2010). However, results from Emad's group, and some of Ghanei's group (such as Aghanouri et al, 2004;Attaran et al 2010;Zarin et al, 2010) are more relevant to pulmonary diseases as they focused on localized tissue changes of cytokines and chemokines in bronchoalveolar lavage fluid or lung biopsies.…”

Section: Cytokines and Pulmonary Disordersmentioning

confidence: 99%

Sulfur mustard and respiratory diseases: Revisit with special reference to the “Comments on ‘Sulfur Mustard and Respiratory Diseases’, Tang and Loke () and a prepared Integrated Mechanism for Chronic Pulmonary Disease from Exposure to Sulfur Mustard” by Saburi and Ghanei ()

Tang

Loke

2013

Critical Reviews in Toxicology

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Alterations in the serum levels of chemokines 20years after sulfur mustard exposure: Sardasht-Iran Cohort Study

Cited by 18 publications

References 41 publications

Role of reactive nitrogen species generated via inducible nitric oxide synthase in vesicant-induced lung injury, inflammation and altered lung functioning

Role of reactive nitrogen species generated via inducible nitric oxide synthase in vesicant-induced lung injury, inflammation and altered lung functioning

Ragweed-allergic subjects have decreased serum levels of chemokines CCL2, CCL3, CCL4 and CCL5 out of the pollen season

Sulfur mustard and respiratory diseases: Revisit with special reference to the “Comments on ‘Sulfur Mustard and Respiratory Diseases’, Tang and Loke () and a prepared Integrated Mechanism for Chronic Pulmonary Disease from Exposure to Sulfur Mustard” by Saburi and Ghanei ()

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