Low-dose sulfur mustard primes oxidative function and induces apoptosis in human polymorphonuclear leukocytes

Levitt, Jonathan M.; Lodhi, Irfan J.; Nguyen, Phu Kim; Ngo, Vinh; Clift, Russell E.; Hinshaw, Daniel B.; Sweeney, John F.

doi:10.1016/s1567-5769(03)00075-4

Cited by 12 publications

(8 citation statements)

References 25 publications

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“…This raises the possibility that early infiltrating PMN are directly exposed to low doses of SM. We have previously shown that exposure to low doses of SM primes PMN production of ROS [20]. In this study, we have extended our previous findings to show that SM also primes PMN phagocytic function and degranulation but that SM does not directly act as a chemoattractant.…”

Section: Discussionsupporting

confidence: 80%

“…Previously, we have shown that exposure to lowdose sulfur mustard primes oxidative function in PMN [20], suggesting that the resulting enhanced response might contribute to tissue injury and delayed wound healing in sulfur mustard lesions. While ROS produced by PMN have been shown to augment tissue damage as part of the inflammatory response, the products released from preformed granules could also contribute to autoimmune injury.…”

Section: Introductionmentioning

confidence: 95%

“…Using a t 1/2 of 24 min, exposure to neat SM ( c 8 M) would yield an estimated residual concentration of approximately 300 AM at 6 h postexposure [20]. Because PMN are known to infiltrate SM lesions as early as 30 min [1] and peak at 6 -12 h postexposure [11], they could be exposed to low doses of SM provided that exposed skin is a reservoir for unreacted SM.…”

Section: Introductionmentioning

confidence: 99%

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Sulfur mustard primes phagocytosis and degranulation in human polymorphonuclear leukocytes

Vavra

Laurent

Ngo

et al. 2004

International Immunopharmacology

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Section: Discussionsupporting

confidence: 80%

Section: Introductionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

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Sulfur mustard primes phagocytosis and degranulation in human polymorphonuclear leukocytes

Vavra

Laurent

Ngo

et al. 2004

International Immunopharmacology

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“…These previous studies indicated that neutrophil-derived MPO could play a vital role in vesicant-induced skin lesions (Jain et al, 2011a; Pal et al, 2009; Tewari-Singh et al, 2010). Though some studies have examined the role of neutrophils in injury with SM (Ham et al, 2012; Levitt et al, 2003; Shakarjian et al, 2010; Vavra et al, 2004), little is known about the mechanism and role of neutrophil-derived MPO-mediated inflammation and injury in vesicant-exposed skin tissue. Accordingly, the current study was designed to evaluate the role of neutrophil derived MPO in NM-induced skin injury by utilizing C57BL/6J wild type and MPO knockout (B6.129X1-Mpo tm1Lus /J) mice.…”

Section: Introductionmentioning

confidence: 99%

Myeloperoxidase deficiency attenuates nitrogen mustard-induced skin injuries

et al. 2014

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The pathologic mechanisms of skin injuries, following the acute inflammatory response induced by vesicating agents sulfur mustard (SM) and nitrogen mustard (NM) exposure, are poorly understood. Neutrophils which accumulate at the site of injury, abundantly express myeloperoxidase (MPO), a heme protein that is implicated in oxidant-related antimicrobial and cytotoxic responses. Our previous studies have shown that exposure to SM analog 2-chloroethyl ethyl sulfide (CEES) or NM results in an inflammatory response including increased neutrophilic infiltration and MPO activity. To further define the role of neutrophil-derived MPO in NMinduced skin injury, here we used a genetic approach and examined the effect of NM exposure (12 h and 24 h) on previously established injury endpoints in C57BL/6J wild type (WT) and B6.129X1-MPOtm1Lus/J mice (MPO KO), homozygous null for MPO gene. NM exposure caused a significant increase in skin bi-fold thickness, epidermal thickness, microvesication, DNA damage and apoptosis in WT mice compared to MPO KO mice. MPO KO mice showed relatively insignificant effect. Similarly, NM-induced increases in the expression of inflammatory and proteolytic mediators, including COX-2, iNOS and MMP-9 in WT mice, while having a significantly lower effect in MPO KO mice. Collectively, these results show that MPO, which generates microbicidal oxidants, plays an important role in NM-induced skin injuries. This suggests the development of mechanism-based treatments against NM-and SM-induced skin injuries that inhibit MPO activity and attenuate MPO-derived oxidants.

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“…However, HD is well known to induce ROS generation in endothelial and immune cells [23,24]. Thus, oxidative stress may occur in v a result of immune cell attack in response to keratinocyte-derived pro-inflammatory cytokines, such as TNF-α [9].…”

mentioning

confidence: 99%

Topical Application of Liposomal Antioxidants for Protection Against CEES Induced Skin Damage

Stone¹,

Paromov²

2007

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show abstract

Low-dose sulfur mustard primes oxidative function and induces apoptosis in human polymorphonuclear leukocytes

Cited by 12 publications

References 25 publications

Sulfur mustard primes phagocytosis and degranulation in human polymorphonuclear leukocytes

Sulfur mustard primes phagocytosis and degranulation in human polymorphonuclear leukocytes

Myeloperoxidase deficiency attenuates nitrogen mustard-induced skin injuries

Topical Application of Liposomal Antioxidants for Protection Against CEES Induced Skin Damage

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