Stress-Induced Mast Cell Activation in Glabrous and Hairy Skin

Căruntu, Constantin; Boda, Daniel; Musat, Sorin; Căruntu, Ana; Mandache, E

doi:10.1155/2014/105950

Cited by 36 publications

(33 citation statements)

References 73 publications

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“…The genetic background and the environmental factors have a major impact on disease susceptibilities in different populations. This leads to increased medical and socioeconomic costs and influences the patient's quality of life (65).…”

Section: Discussionmentioning

confidence: 99%

Psoriasis: Association of interleukin-17 gene polymorphisms with severity and response to treatment (Review)

et al. 2019

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Psoriasis is a chronic, inflammatory disease with a complex pathogenesis that is not yet fully understood. Although it is a multifactorial disease, the genetic factor has a major role in the pathogenesis of psoriasis. Genome wide association studies have identified over 50 genetic loci associated with psoriasis risk. Beside TNF-α or IL-23, the IL-17 family is a newer group that has proven implications in the pathogenesis of psoriasis. The most important members of the family, with pro-inflammatory qualities, are IL-17A and IL-17F. These interleukins are produced by a varied number of cells, but by far the most important are Th17 cells. Of the patients 20-30% present moderate-to-severe psoriasis, therefore, systemic medication (phototherapy, methotrexate, cyclosporine, acitretin or biologic agents) is mandatory. The necessity of an individualized treatment plan, for each patient, is imperative in order to establish the best strategy for non-responders to classical treatment or to other biologic treatments. The discovery of Th17 pathway improved the treatment and prognosis of psoriasis. Anti-psoriatic agents against IL-17 or its receptors are a novel group of biologic agents; these include ixekizumab, secukinumab and brodalumab. Polymorphisms of IL-17 family have been correlated with the severity and response to treatment in psoriasis, and also with the risk of inflammatory, infectious, autoimmune or neoplastic pathologies. The significant difference in the presence or absence of susceptibility loci in different population is due to genetic background and environmental factors that have a major impact on disease predisposition. In this study, we reviewed the importance and influence of the IL-17 polymorphisms as predictors of response to treatment and severity of the disease.

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Section: Discussionmentioning

confidence: 99%

Psoriasis: Association of interleukin-17 gene polymorphisms with severity and response to treatment (Review)

et al. 2019

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“…Mast cells however, appear to be the key players in modulating stress-induced cutaneous inflammatory reactions (38). …”

Section: Cellular Neuro-immune Interactionsmentioning

confidence: 99%

Neuroendocrine factors: The missing link in non-melanoma skin cancer

Lupu

Căruntu²,

Căruntu

et al. 2017

Oncology Reports

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Non-melanoma skin cancer (NMSC) is the most common form of cancer worldwide, comprising 95% of all cutaneous malignancies and approximately 40% of all cancers. In spite of intensive efforts aimed towards awareness campaigns and sun-protective measures, epidemiological data indicate an increase in the incidence of NMSC. This category of skin cancers has many common environmental triggers. Arising primarily on sun-exposed skin, it has been shown that ultraviolet radiation is, in the majority of cases, the main trigger involved in the pathogenesis of NMSC. Aside from the well-known etiopathogenic factors, studies have indicated that several neuroactive factors are involved in the carcinogenesis of two of the most common types of NMSC, namely basal cell carcinoma (BCC) and squamous cell carcinoma (SCC), with the exception of penile SCC, for which a paucity of specific data on their pathogenic role exists. The complex interaction between the peripheral nervous system and target cells in the skin appears to be mediated by locally released neuroendocrine factors, such as catecholamines, substance P, calcitonin gene-related peptide and somatostatin, as well as neurohormones, such as proopiomelanocortin and its derived peptides, α-melanocyte-stimulating hormone and adrenocorticotropin. All these factors have been, at least at some point, a subject of debate regarding their precise role in the pathogenesis of NMSC. There is also a significant body of evidence indicating that psychological stress is a crucial impact factor influencing the course of skin cancers, including SCC and BCC. Numerous studies have suggested that neuroendocrine factor dysregulation, as observed in stress reactions, may be involved in tumorigenesis, accelerating the development and progression, and suppressing the regression of NMSC. Further studies are required in order to elucidate the exact mechanisms through which neuroactive molecules promote or inhibit cutaneous carcinogenesis, as this could lead to the development of more sophisticated and tailored treatment protocols, as well as open new perspectives in skin cancer research.

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“…It mainly affects the skin and joints (1). Some environmental factors, such as stress, are considered to lead to an immune dysregulation, but only in patients with genetic predisposition, resulting in an abnormal proliferation and maturation of keratinocytes, proliferation of dermal blood vessels, mast cell activation and skin infiltration by inflammatory cells (2)(3)(4). The inflammatory nature of psoriasis was illustrated by a systemic and dermal secretion of cytokines such as interleukins (IL): IL-2, IL-6, IL-8, IL-17, IL-18, IL-22, IL-23, IL-24, interferon-γ (INF-γ) and tumor necrosis factor-α (TNF-α) (5).…”

Section: Introductionmentioning

confidence: 99%

Inflammatory marker alteration in response to systemic therapies in psoriasis

et al. 2020

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Substantial research has focused on the presence of biomarkers involved in both the pathogenesis of psoriasis and its comorbidities. The identification of these biomarkers has a crucial role in establishing the diagnosis and prognosis, in understanding the physiopathological mechanism and in determining the therapeutic response. The aim of this study was to emphasize the alteration in inflammatory markers in response to systemic therapies in psoriasis. Evolution of inflammatory marker alteration was studied in 194 patients with psoriasis, aged between 7 and 87 years. Two groups were set up: the first comprised of patients treated with methotrexate (n=51), while the second comprised patients treated with biological therapy (n=143). Each group was evaluated for blood values of C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and fibrinogen before and after treatment, the fluctuation of these values according to the treatment, the interrelation between inflammatory markers and inflammatory activity of the disease and the evolution of the disease after treatment. In group I, 46 out of 51 patients had elevated levels of acute phase reactants before treatment. After treatment with methotrexate 7.5 mg/week, 12 out of 46 patients had elevated blood levels of ESR and 18 out of 46 patients of CRP and fibrinogen. Before treatment with biological therapy, 138 patients out of 143 presented abnormal high range for acute phase reactants. After treatment with biological therapy, 18 patients out of 138 had elevated blood levels of ESR and 37 patients out of 138 had elevated CRP and fibrinogen. A favorable evolution was noted in 98 patients out of 138. It was concluded that the systemic treatment with both methotrexate and biological therapy showed a marked decline in the patients with abnormal values of CRP, ESR and fibrinogen, indirectly showing a decline in the inflammatory activity of psoriasis.

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Stress-Induced Mast Cell Activation in Glabrous and Hairy Skin

Cited by 36 publications

References 73 publications

Psoriasis: Association of interleukin-17 gene polymorphisms with severity and response to treatment (Review)

Psoriasis: Association of interleukin-17 gene polymorphisms with severity and response to treatment (Review)

Neuroendocrine factors: The missing link in non-melanoma skin cancer

Inflammatory marker alteration in response to systemic therapies in psoriasis

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