Sport als Risikofaktor und therapeutisches Prinzip in der Dermatologie

Karamfilov, Theodor; Elsner, Peter

doi:10.1007/s001050100204

Cited by 16 publications

(8 citation statements)

References 31 publications

(31 reference statements)

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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: 56%

“…In fact, several findings indicate a balancing role for nerve-immune cell interaction under defined conditions (2-4, 6, 12). For example, stress during allergen sensitization can block contact hypersensitivity (12), and the following observations suggest that stress-induced suppression of inflammation may involve the NNA: SP is released by the repeated application of either capsaicin (13), UV light (14-16), physical exercise (17)(18)(19), or calcineurin inhibitors (20), all of which can be considered as repeated mild stress exposures and generally result in improved allergic inflammation in atopics.…”

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confidence: 99%

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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: 56%

mentioning

confidence: 99%

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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“…24 Intake of performance-enhancing substances might also cause striae. 25 Mechanical stretch has been shown to modify transforming growth factor (TGF)-b expression at the messenger RNA and protein levels in various in vivo and in vitro models. [26][27][28] Involvement of this signaling pathway in response to mechanical stress is noteworthy, because MS symptoms are now known to be, at least partially, mediated by abnormal TGF-b signaling.…”

Section: Discussionmentioning

confidence: 99%

A case-control study of cutaneous signs in adult patients with Marfan disease: Diagnostic value of striae

Ledoux¹,

Beauchet²,

Fermanian³

et al. 2011

Journal of the American Academy of Dermatology

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“…Considering the pathophysiological aspects, the main striae causal agents are related to genetic predisposition, mechanical stretching, and hormonal factors …”

Section: Introductionmentioning

confidence: 99%

Unraveling the molecular and cellular mechanisms of stretch marks

Schuck

Carvalho

Fávero

et al. 2019

J of Cosmetic Dermatology

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Background: Striae distensae, commonly known as stretch marks, are cutaneous lesions that accompany the hormonal upheavals of the major stages of life: puberty and pregnancy. Stretch marks occur in 90% of women, and they appear as red or purple lines that slowly fade to pale lines on the skin. There have been few studies regarding stretch mark origins, and new preventive and corrective treatments are needed. Aims: The aim of this work was to understand the primary genes and proteins involved in the regulation of striae compared to normal skin and to identify the differentially expressed genes and biochemical aspects of SA and SR Importantly, this is the first published study to use a molecular high-throughput approach combined with in vivo evaluation. Methods: In this study, we analyzed the molecular differences between skin with and without stretch marks (rubra [SR] and alba [SA]) of female volunteers using DNA microarray (Whole Human Genome Microarray Kit, 4×44 K, Agilent Technologies) analyses of cutaneous biopsies (2 mm) and in vivo confocal Raman spectroscopy of selected buttock regions, a technique recently introduced as a noninvasive skin evaluation method. Results: We identified gene expression alterations related to ECM, cellular homeostasis, and hormones such as secretoglobulins. Spectral analyses of collagen, fibrillin, and glycosaminoglycans were conducted by Raman spectroscopy at different skin depths. The main differences observed when comparing skin with and without stretch marks were at depths between 75 and 95 μm, corresponding to the dermalepidermal junction and dermis regions and showing differences between normal skin and stretched skin regarding collagen, collagen hydration, and elastin fibers. Conclusion: The results obtained by RNA and protein analyses are complementary and show that significant changes occur in the skin affected by stretch marks. These results suggest new strategies and opportunities to treat this skin disorder and for the development of new and eficiente cosmetic products. K E Y W O R D S molecular biology, Raman, striae distensae | 191 SCHUCK et al. 1 | INTRODUC TI ON Striae distensae (SD), or stretch marks, are linear, atrophic, well-defined cutaneous lesions that occur secondary to changes in connective tissue, which can be associated with obesity, growth spurts, or excess steroids. Many researchers believe that the pathogenesis of SD involves abnormalities of elastic fibers, collagen fibrils, or other ECM components 1 ; however, the specific mechanisms involved are still unclear. Different categories can be used to classify striae, such as striated atrophy, striae distensae, traumatic striae, and striae gravidarum (related to pregnancy), among others. They are normally parallel to each other and perpendicular to the cleft of the skin, suggesting a localized elastic imbalance. 2,3 Striae can be considered a type of dermal scarring, where there is a collagen rupture and separation, and this gap is filled by newly synthesized and realigned collagen. 5,6 In the early stag...

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Sport als Risikofaktor und therapeutisches Prinzip in der Dermatologie

Cited by 16 publications

References 31 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

A case-control study of cutaneous signs in adult patients with Marfan disease: Diagnostic value of striae

Unraveling the molecular and cellular mechanisms of stretch marks

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