Repeated subinflammatory ultraviolet B irradiation increases substance P and calcitonin gene-related peptide content and augments mustard oil-induced neurogenic inflammation in the skin of rats

Legat, Franz J.; Griesbacher, Thomas; Schicho, Rudolf; Althuber, Petra; Schuligoi, Rufina; Kerl, Helmut; Wolf, Peter

doi:10.1016/s0304-3940(02)00428-7

Cited by 28 publications

(18 citation statements)

References 15 publications

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“…Thus, SP appears to directly block the production of Th2 cytokines in AlD (18,19), whereas it is directly responsible for the rise in Th1 cytokines both in AlD and stressed AlD (14)(15)(16)(17). Strikingly, we also measured a significant increase in the level of a cytokine relevant for CD25 + Treg survival and proliferation, IL-2 (49), in cocultures of CD11c + DC and allogeneic T cells from stress plus AlD mice.…”

Section: Stress Induces An Elevated Release Of Th1 Cytokines and Il-2mentioning

confidence: 79%

Substance P Is a Key Mediator of Stress-Induced Protection from Allergic Sensitization via Modified Antigen Presentation

Pavlović

Liezmann

Blois

et al. 2011

The Journal of Immunology

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Interaction between the nervous and immune systems greatly contributes to inflammatory disease. In organs at the interface between our body and the environment, the sensory neuropeptide substance P (SP) is one key mediator of an acute local stress response through neurogenic inflammation but may also alter cytokine balance and dendritic cell (DC) function. Using a combined murine allergic inflammation/noise stress model with C57BL/6 mice, we show in this paper that SP—released during repeated stress exposure—has the capacity to markedly attenuate inflammation. In particular, repeated stress exposure prior to allergen sensitization increases DC-nerve fiber contacts, enhances DC migration and maturation, alters cytokine balance, and increases levels of IL-2 and T regulatory cell numbers in local lymph nodes and inflamed tissue in a neurokinin 1-SP-receptor (neurokinin-1 receptor)-dependent manner. Concordantly, allergic inflammation is significantly reduced after repeated stress exposure. We conclude that SP/repeated stress prior to immune activation acts protolerogenically and thereby beneficially in inflammation.

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Section: Stress Induces An Elevated Release Of Th1 Cytokines and Il-2mentioning

confidence: 79%

Substance P Is a Key Mediator of Stress-Induced Protection from Allergic Sensitization via Modified Antigen Presentation

Pavlović

Liezmann

Blois

et al. 2011

The Journal of Immunology

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“…Neuropeptides in the skin including calcitonin gene‐related peptide and substance P are significantly upregulated in UVB‐exposed skin and play a significant role in UV‐induced immune suppression (34,35). Neuropeptides such as these are also likely to mediate other UV effects including skin ageing and photocarcinogenesis (36).…”

Section: Immune Mechanisms In Polymorphic Light Eruptionmentioning

confidence: 99%

New insights into the mechanisms of polymorphic light eruption: resistance to ultraviolet radiation‐induced immune suppression as an aetiological factor

Wolf

Byrne

Gruber‐Wackernagel

2009

Experimental Dermatology

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An abnormal immune response has long been thought responsible for the patho-aetiology of polymorphic light eruption, the most common photodermatosis. Recent evidence indicates that polymorphic light eruption patients are resistant to the immune suppressive effects of sunlight, a phenomenon that leads to the formation of skin lesions upon seasonal sun exposure. This immunological abnormality in polymorphic light eruption supports the concept of the biological significance and evolutionary logic of sunlight-induced immune suppression, i.e. the prevention of immune responses to photo-induced neoantigens in the skin, thereby preventing autoimmunity and skin rashes. This article focuses on the immunological alterations in polymorphic light eruption and the pathogenic significance to the disease state and skin carcinogenesis.

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“…14,15 In addition, the focusing effect of the cornea, which concentrates UV light onto the limbus, 1 can injure corneal nerves as they leave the limbal plexus to enter the cornea proper. As sensory nerves are reported to participate in wound healing, inflammation, and cutaneous photo-ageing, 16,17 they could play similar roles in the UV-injured cornea and be responsible for directing cell migration in pterygia.…”

mentioning

confidence: 99%

The Role of Substance P in the Pathogenesis of Pterygia

Chui

Girolamo

Coroneo

et al. 2007

Invest. Ophthalmol. Vis. Sci.

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Repeated subinflammatory ultraviolet B irradiation increases substance P and calcitonin gene-related peptide content and augments mustard oil-induced neurogenic inflammation in the skin of rats

Cited by 28 publications

References 15 publications

Substance P Is a Key Mediator of Stress-Induced Protection from Allergic Sensitization via Modified Antigen Presentation

Substance P Is a Key Mediator of Stress-Induced Protection from Allergic Sensitization via Modified Antigen Presentation

New insights into the mechanisms of polymorphic light eruption: resistance to ultraviolet radiation‐induced immune suppression as an aetiological factor

The Role of Substance P in the Pathogenesis of Pterygia

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