Reduced expression of CXCL16/CXCR6 is involved in the pathogenesis of hidradenitis suppurativa

Abstract

Hidradenitis suppurativa (HS), also known as acne inversa, is a chronic inflammatory skin disease that mainly affects apocrine-bearing areas, with a prevalence rate of 0.03%-1.2% worldwide. 1,2 It severely affects the patient's social, working and psychological quality of life in a manner that significantly exceeds that of psoriasis and other skin diseases. 3 Cumulating data have shown that the pathogenesis of HS is multifactorial and involves immunology, bacterial colonization, hormones, genetics, etc. However, the aetiology of HS remains unclear.Mutations in the γ-secretase complex have been found in familial HS kindreds, following autosomal dominant inheritance with incomplete penetrance. 4,5 Remarkably, no specific gene mutation has been identified in sporadic HS cases, which comprise two-thirds of all HS

Enfermedad anal en pacientes candidatos a cirugía bariátrica: estudio descriptivo

“…En nuestra muestra existe una prevalencia de hidrosadenitis supurativa el 11,4%. Estudios recientes 25 demuestran que la obesidad altera la metilación del ADN, lo que genera una desregulación del Ligando CXC16 de la quimiocina (CXCL16) y su receptor a nivel tisular en los pacientes con hidrosadenitis 25 . Por otro lado, en el paciente obeso existe una hiperproducción de adipocinas (leptina, resistina, visfatina) implicadas en la patogénesis de la hidrosadenitis supurativa poque conducen a un estado proinflamatorio que exacerba brotes de la enfermedad 26 .…”

Unraveling the Epigenetic Tapestry: Decoding the Impact of Epigenetic Modifications in Hidradenitis Suppurativa Pathogenesis

“…In another study conducted by Wang et al [43], whole-genome DNA methylation sequencing on lesional and unaffected skin derived from HS patients was performed. The authors found an hypermethylation of CXC chemokine ligand 16 (CXCL16), which acts as a mediator of the innate immunity of epidermal keratinocytes by attracting CXC chemokine receptor (CXCR) 6-expressing cells, such as activated T cells and Natural Killer (NK) T cells [44].…”

“…Hypermethylation of CXCL16 induced decreased expression of this chemokine, which could affect chemotaxis of CXCR6-bearing cells thus impairing both innate and adaptive immune responses in HS patients. In addition, considering the antimicrobial properties of CXCL16, its downregulation could also promote bacterial colonization by perpetuating the inflammatory loop [43].…”