Rosacea: the Cytokine and Chemokine Network

Gerber, Peter Arne; Buhren, Bettina Alexandra; Steinhoff, Martin; Homey, Bernhard

doi:10.1038/jidsymp.2011.9

Cited by 129 publications

(142 citation statements)

References 92 publications

(114 reference statements)

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“…Therefore, therapeutic procedures may be established throughout using either antagonists of CXCL12 or blocking of their receptors. Additionally, it has been documented that chemokines play their roles in immune responses in a network format [64]; hence, it appears that a supportive therapy should be carried out with attention to the chemokines with redundancy effects. This therapeutic method in combination with other regulatory intervention strategies could contribute as a curative treatment for T2D and its complications.…”

Section: Discussionmentioning

confidence: 99%

Significance of CXCL12 in Type 2 Diabetes Mellitus and Its Associated Complications

Karimabad

Hassanshahi

2014

Inflammation

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Immune responses are extensively accepted as primitive etiological leading causes involved in immune system diseases. It is now well established that chemokines as the main arms of the immune system play critical roles in the regulation of immune responses in the pathogenesis of different diseases. Several environmental and genetic elements of the immune system are also believed to potentially affect both the onsets of immunological diseases. The stromal cell-derived factor-1 alpha (SDF-1α) which in new nomenclature is nominated as C-X-C motif ligand 12 (CXCL12) is involved in the development and progression of immune responses. The CXCL12 is an extensively active chemokine that serves as a recruiter for migration and trafficking of leukocytes and hematopoietic progenitor cells. Patients suffering type 2 diabetes (T2D) that ascribe heterozygous SDF-1 3'A genotype (801G/A in the 3' untranslated region) have increased insulin-dependent mobilization of adult progenitor cells, which are known to participate in angiogenesis and vascular repair. Conversely, homing of progenitor cells contributes to the diabetes vascular complications. Because carriers of the SDF-1 3'A genotype show increased levels of the CXCL12 messenger RNA (mRNA) in their peripheral blood mononuclear cells. Genetic variations of CXCL12 gene might affect trafficking of inflammatory cells or defected precursors and hence induced tendency to diabetic complications. The SDF-1 3'A genetic variation of CXCL12 influences the development of late vascular diabetic complications, and previous studies reported that this genetic variation regulates the expression of CXCL12. Therefore, the main goal of the present study was to collect the most recent reports regarding the relation between serum concentrations and SDF-1 3'A genetic variation of CXCL12 in T2D.

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Section: Discussionmentioning

confidence: 99%

Significance of CXCL12 in Type 2 Diabetes Mellitus and Its Associated Complications

Karimabad

Hassanshahi

2014

Inflammation

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“…Our molecular characterization of the different subtypes of rosacea as compared with healthy human skin by gene array analysis and real-time PCR indicates that a variety of cytokines, chemokines, metalloproteinases, proteases, and reactive oxygen species molecules, as well as lipid mediators, contribute to dysregulation of the inflammatory responses in rosacea (Figure 2a; Gerber et al . 2011).…”

Section: Classification and Epidemiology Of Rosaceamentioning

confidence: 95%

Clinical, Cellular, and Molecular Aspects in the Pathophysiology of Rosacea

Steinhoff

Buddenkotte

Aubert

et al. 2011

Journal of Investigative Dermatology Symposium Proceedings

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235

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Rosacea is a chronic inflammatory skin disease of unknown etiology. Although described centuries ago, the pathophysiology of this disease is still poorly understood. Epidemiological studies indicate a genetic component, but a rosacea gene has not been identified yet. Four subtypes and several variants of rosacea have been described. It is still unclear whether these subtypes represent a “developmental march” of different stages or are merely part of a syndrome that develops independently but overlaps clinically. Clinical and histopathological characteristics of rosacea make it a fascinating “human disease model” for learning about the connection between the cutaneous vascular, nervous, and immune systems. Innate immune mechanisms and dysregulation of the neurovascular system are involved in rosacea initiation and perpetuation, although the complex network of primary induction and secondary reaction of neuroimmune communication is still unclear. Later, rosacea may result in fibrotic facial changes, suggesting a strong connection between chronic inflammatory processes and skin fibrosis development. This review highlights recent molecular (gene array) and cellular findings and aims to integrate the different body defense mechanisms into a modern concept of rosacea pathophysiology.

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“…В настоящее время об-суждают роль таких триггерных факторов, как уль-трафиолетовое облучение, стресс, тепло, острая пи-ща [1][2][3][4]7]. Употребление алкоголя было связано с минимальным риском повышения заболеваемости.…”

Section: Discussionunclassified