الفهرس 
Aim of the workOnly 14 pages are availabe for public view
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Abstract
Acne vulgaris (AV) is a chronic inflammatory dermatological disease affecting pilosebaceous follicles. Its clinical presentation ranges from white and blackheads, papules and pastules to severe inflammatory cystic acne. Acne occurs primarily in the oily areas of the skin, mostly on the face, back and chest. Acne affects approximately 80% of all individuals. It is a near-universal skin disease affecting mostly the adolescent population to varying degrees of severity, usually appears at the time of puberty, with slightly earlier onset in girls compared to boys.
Currently, it is believed that acne is a multifactorial disease as its clinical presentation depends on the interaction of several factors. It has complex etiology including sebum overproduction, abnormal follicular keratinization, P. acnes proliferation, inflammation, environmental and genetic factors. However, there are several areas in the pathogenesis of the disease that remain murky and although previous research has provided a better understanding of the pathogenic factors, there is still a great deal to be learned.
Acne vulgaris is mediated by polygenic inheritance or multifactorial inheritance attributed to the interplay between multiple genes and environmental factors. All candidate genes may influence each other and perpetuate disease process. The severity of the inflammatory reaction and the subsequent AV symptoms vary considerably in the affected subjects, in part because of individual genetic susceptibility factors.
Acne vulgaris is an inflammatory skin disease as inflammation plays an important role in its pathogenesis.
In the field of acne inflammation, research groups continue to provide insights into the immunological response to the presence of P. acnes.
The innate immune system recognizes pathogens via pattern recognition receptors, such as Toll-like receptors and Nod-like receptors (NLRs). NLR members, including NLRP3, can mediate responses to pathogen-associated molecular patterns and subsequently form multiprotein complexes, such as the inflammasome, with the adapter apoptotic speck-like protein containing caspase recruitment domain (CARD) (Apoptosis-associated Speck-like protein containing a CARD (ASC)) and pro-caspase-1. Caspase-1 is then activated, leading to processing and secretion of inflammatory cytokines IL-1β and IL-18, resulting in inflammation in vivo.
NLRP3 inflammosome can be activated by a group of bacterial toxins, the pathogen‐associated molecular pattern molecules (PAMPs) and the damage‐associated molecular pattern molecules (DAMPs), which are responsible for inducing diverse signal activations including Ca2+ signaling, generation of reactive oxygen species (ROS), and K+ efflux and lysosomal rupture.
The main objective of this study is to investigate the genetic association between NLRP3 gene and Acne Vulgaris patients.
The study was conducted at Biochemistry department; The patients had been selected from the outpatient Dermatology & Andrology clinic,
Faculty of Medicine, Menoufia University.
This case-control study was conducted on 40 acne patients and 10 age and sex matched healthy volunteers as a control group.