Effect of Skin Sensitizers on Inducible Nitric Oxide Synthase Expression and Nitric Oxide Production in Skin Dendritic Cells: Role of Different Immunosuppressive Drugs

Cruz, Maria Teresa; Neves, Bruno Miguel; Gonçalo, Margarida; Figueiredo, Américo; Duarte, Carlos B.; Lopes, María Celeste

doi:10.1080/08923970701512304

Cited by 8 publications

(5 citation statements)

References 60 publications

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“…57 Cruz and colleagues demonstrated that dendritic cell-derived NO directly triggers skin inflammation after applications of contact sensitizers and irritants. 58 These reports, along with our findings, support that NO from iNOS-positive LCs mediates skin immunoreactions during the development of pain behavior in db/db mice.…”

supporting

confidence: 87%

Interleukin-10 Reduces Neurogenic Inflammation and Pain Behavior in a Mouse Model of Type 2 Diabetes

Yanik¹,

Dauch²,

Cheng³

2020

JPR

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supporting

confidence: 87%

Interleukin-10 Reduces Neurogenic Inflammation and Pain Behavior in a Mouse Model of Type 2 Diabetes

Yanik¹,

Dauch²,

Cheng³

2020

JPR

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“…On the other hand, the PI3K inhibitor LY294002 induced an increase in the Trx-1 protein levels by 98.1% (*P < 0.05), when compared with LPS alone. Neither dexamethasone nor cyclosporin A, immunosuppressors that inhibit the transcription factor NF-B in FSDC, as previously demonstrated by us [17,63], had an eVect on Trx-1 protein levels in LPS-stimulated cells.…”

Section: Intracellular Signalling Pathways Involved In the Increase Omentioning

confidence: 54%

“…In addition, the eVect of the immunomodulators such as dexamethasone (5 M) and cyclosporin A (1 M) was also evaluated on Trx-1 protein expression induced by LPS. Dexamethasone and cyclosporin A are immunosuppressors that inhibit the transcription factor NF-B in FSDC, as previously demonstrated by us [17,63].…”

Section: Chemical Treatmentmentioning

confidence: 70%

Effect of lipopolysaccharide, skin sensitizers and irritants on thioredoxin-1 expression in dendritic cells: relevance of different signalling pathways

et al. 2009

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Thioredoxin-1 is a ubiquitous protein involved in phenotypical and functional changes in dendritic cells (DC). We investigated the eVect of lipopolysaccharide (LPS), skin sensitizers, and irritants on thioredoxin-1 by Western blot and immunoXuorescence and on mRNA by real-time PCR. As DC models, we used a skin DC line and DC derived from human blood monocytes. We observed that all tested chemicals increased thioredoxin-1 expression, which is only transient for irritants, being the strongest eVect observed for LPS (63 § 15%). To address the involvement of thioredoxin-1 in DC maturation, we analysed the eVect of an activator of thioredoxin-1 expression, hydrogen peroxide, on CD86 expression, a marker of DC maturation. We found that hydrogen peroxide increases thioredoxin-1 and CD86 expression reinforcing thioredoxin-1 involvement in DC maturation. Because mitogen-activated protein kinases and PI3K are activated upon DC maturation, we also analysed their involvement in thioredoxin-1 modulation. We veriWed that LPS-induced upregulation of thioredoxin-1 expression was dependent on PI3K pathway.

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“…It has generally been believed that iNOS is involved in CHS as a producer of NO and a trigger of inflammatory responses (Cals-Grierson and Ormerod, 2004) reported that iNOS and NO were produced in human skin subjected to positive patch tests to contact allergens (Cruz et al, 2007;Ormerod et al, 1997) and to the irritant sodium lauryl sulfate; nevertheless, it remains controversial whether iNOS is inhibitory or augmentative in CHS (Ross and ReskeKunz, 2001). It has also been reported that an iNOS inhibitor exerted a suppressive effect on the CHS response to 2,4,6-trinitrochlorobenzene (TNCB) (Musoh et al, 1998), although this effect was limited to the first few hours of the response, and neither NO production, NO-expressing cells, nor NOS isoenzymes were identified.…”

Section: Discussionmentioning

confidence: 97%

Inducible Nitric Oxide Synthase Downmodulates Contact Hypersensitivity by Suppressing Dendritic Cell Migration and Survival

Sugita

Kabashima

Yoshiki

et al. 2010

Journal of Investigative Dermatology

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Nitric oxide (NO) has several important roles in various physiological settings; one of the NO synthases, inducible NO synthase (iNOS), is induced by external stimulation of the skin. A prototypic example of external stimulation is hapten exposure, which induces the T-cell-mediated immune response known as contact hypersensitivity (CHS). We herein report on cutaneous dendritic cell (DC) function in the presence of an iNOS-specific inhibitor during the sensitization phase of CHS. First, we examined epidermal cell (EC) suspensions using flow cytometry with an iNOS antibody and confirmed that iNOS was expressed in the cytoplasm of Langerhans cells (LCs). We then studied the role of iNOS in CHS, and found that responses to DNFB were enhanced by the addition of an iNOS inhibitor during sensitization. Similarly, the iNOS inhibitor augmented FITC-induced migration of cutaneous DCs, including Langerin(+) LCs and Langerin(-) dermal DCs, to draining lymph nodes. Finally, we showed that iNOS inhibitor enhanced LC survival in vitro. We concluded that NO suppresses migration and survival of cutaneous DCs, resulting in a downmodulation of CHS.

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Effect of Skin Sensitizers on Inducible Nitric Oxide Synthase Expression and Nitric Oxide Production in Skin Dendritic Cells: Role of Different Immunosuppressive Drugs

Cited by 8 publications

References 60 publications

Interleukin-10 Reduces Neurogenic Inflammation and Pain Behavior in a Mouse Model of Type 2 Diabetes

Interleukin-10 Reduces Neurogenic Inflammation and Pain Behavior in a Mouse Model of Type 2 Diabetes

Effect of lipopolysaccharide, skin sensitizers and irritants on thioredoxin-1 expression in dendritic cells: relevance of different signalling pathways

Inducible Nitric Oxide Synthase Downmodulates Contact Hypersensitivity by Suppressing Dendritic Cell Migration and Survival

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