Protein contact dermatitis associated with food allergy to fish

Sánchez, Cristina Díaz; Martínez, J. Lacuna; Cadarso, A. Iglesias; Pan, Cun-Mei

doi:10.1111/j.1600-0536.1994.tb01913.x

Cited by 12 publications

(3 citation statements)

References 6 publications

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“…DE alone or in the context of antigen exposure also increases expression of the Th2 cytokines IL-4 and IL-13, while decreasing expression of the Th1 cytokine IFN-γ [30-32]. Exposure to DE causes oxidative stress in target cells [28,33] through development of reactive oxygen species (ROS) that induce the transcription of phase II enzymes including heme-oxygenase 1 (HO-1) and catalase [33,34].…”

Section: Introductionmentioning

confidence: 99%

Role of oxidative stress on diesel-enhanced influenza infection in mice

et al. 2010

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Numerous studies have shown that air pollutants, including diesel exhaust (DE), reduce host defenses, resulting in decreased resistance to respiratory infections. This study sought to determine if DE exposure could affect the severity of an ongoing influenza infection in mice, and examine if this could be modulated with antioxidants. BALB/c mice were treated by oropharyngeal aspiration with 50 plaque forming units of influenza A/HongKong/8/68 and immediately exposed to air or 0.5 mg/m3 DE (4 hrs/day, 14 days). Mice were necropsied on days 1, 4, 8 and 14 post-infection and lungs were assessed for virus titers, lung inflammation, immune cytokine expression and pulmonary responsiveness (PR) to inhaled methacholine. Exposure to DE during the course of infection caused an increase in viral titers at days 4 and 8 post-infection, which was associated with increased neutrophils and protein in the BAL, and an early increase in PR. Increased virus load was not caused by decreased interferon levels, since IFN-β levels were enhanced in these mice. Expression and production of IL-4 was significantly increased on day 1 and 4 p.i. while expression of the Th1 cytokines, IFN-γ and IL-12p40 was decreased. Treatment with the antioxidant N-acetylcysteine did not affect diesel-enhanced virus titers but blocked the DE-induced changes in cytokine profiles and lung inflammation. We conclude that exposure to DE during an influenza infection polarizes the local immune responses to an IL-4 dominated profile in association with increased viral disease, and some aspects of this effect can be reversed with antioxidants.

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Section: Introductionmentioning

confidence: 99%

Role of oxidative stress on diesel-enhanced influenza infection in mice

et al. 2010

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“…The development of immediate contact reactions usually requires repeated skin contact although earlier sensitization through ingestion can also result in protein contact dermatitis (2, 3). Previous cases of contact urticaria after handling seafood have been already reported (4).…”

Section: Discussionmentioning

confidence: 99%

Occupational contact urticaria caused by seafood handling*

et al. 2005

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“…They concluded that 4 main groups of ''proteins'' cause PCD: (i) fruits, vegetables, spices and plants; (ii) animal proteins; (iii) grains; (iv) enzymes. Since then, additional cases of PCD caused by the above agents have been reported (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21). PCD is mostly occupational and develops on the hands and forearms (4).…”

Section: Discussionmentioning

confidence: 99%

Occupational fingertip protein contact dermatitis from grain flours and natural rubber latex

Kanerva

1998

Contact Dermatitis

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Protein contact dermatitis associated with food allergy to fish

Cited by 12 publications

References 6 publications

Role of oxidative stress on diesel-enhanced influenza infection in mice

Role of oxidative stress on diesel-enhanced influenza infection in mice

Occupational contact urticaria caused by seafood handling*

Occupational fingertip protein contact dermatitis from grain flours and natural rubber latex

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