الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Acne is a chronic inflammatory disease of the pilosebaceous units. Acne vulgaris is a self limited disease , seen primarily in adolescents, involving the sebaceous follicle . Most cases of acne are pleomorphic , presenting with a variety of lesions consisting of comedones , papules , pustules , nodules ,and , as sequelae to active lesions , pitted or hypertrophic scars. Although classically classified as a sebaceous gland disease , it is actually a process that involves the pilosebaceous unit.
Four ultimate factors are responsible for acne:
1) increased sebum production
2) hypercornification of pilosebaceous duct
3) abnormal bacterial function
4) production of inflammation.
The sebaceous gland is a holocrine gland, and its secretion is formed by the complete disintegration of the glandular cells. Excreting sebum is the major function of sebaceous glands, and increased sebum excretion is a major concurrent event that parallels the development of acne lesions. The pilosebaceous unit is an immunocompetent organ. Keratinocytes and sebocytes may act as immune cells capable of pathogen recognition and abnormal lipid presentation. Seborrhoea is, indeed, not a sufficient condition for the development of the pathology,Several variations in lipid metabolism have been described in acne patients, including a decreased amount of linoleic acid ,desaturation of sebaceous fatty acids may contribute to acne development.
Propionibacterium acnes (P. acnes), a gram-positive anaerobic bacterium part of the normal skin flora, plays a critical role in the development of inflammatory lesions in acne. Various mechanisms can explain the role of P. acnes in skin inflammation. First, it is widely accepted that inflammation may be induced by the immune response of the host to P. acnes.
Beside the immune response of the host, a direct effect of P. acnes on keratinocytes has also been suspected in the initiation of the inflammatory process. Indeed, P. acnes interacts with toll-like receptors TLR-2 and TLR-4 on keratinocytes.
Interleukin-18 is a proinflammatory cytokine that stimulates natural killer cells (NK) and T cells and enhances innate immunity as well as specific Th1 immune responses. Human keratinocytes produce IL-18, like monocytes and macrophages do, being two major sources of this molecule. IL-18 acts directly on NK cells to stimulate INF-γ synthesis and upregulate their killing capacity. It is believed that IL-18 derived from keratinocytes might be involved in the cutaneous Th1- type immune response.
Interleukin (IL-)18, initially described as an interferon γ (IFN-γ) inducing factor, is a recently characterized cytokine that shares structural features with the IL-1 family of proteins. IL-18 was first purified and subsequently cloned from the livers of mice treated with heat-inactivated Propionbacterium acnes followed by lipopolysaccharide (LPS).
The IL-18 receptor (IL-18R) complex is a heterodimer containing an α chain responsible for extracellular binding of IL-18 and a nonbinding, signal-transducing β chain.
IL-18R shares downstream effector pathways with critical immune regulatory molecules such as toll-like receptors to give (IFN-γ). The ability of IL-18 to induce CC and CXC chemokines places IL-18 in a strategic role in inflammation. By using freshly obtained human PBMCs, mature recombinant IL-18 induced IL-8 gene expression and synthesis.
Study was a trial to detect difference in level of IL-18 between acne patient and control and to determine it is relation to severity using (GAGA ) system .
This study was carried out on two groups( 30 patient, including 9 females and 21 males, ranging in age from 16 to 26 years with a mean age of 21.5 years, suffering from different grades of acne vulgaris) and( 15 acne free control subject 7 males and 8 females of matched age and sex, ranging in age from 16 to 26 years with a mean age of 21.5 years .
Group (I) acne vulgaris patients:
The diagnosis of acne vulgaris was done in 30 patients by clinical examination and classified according to (GAGS) in to four groups
A) Score of 1-18 is considered mild;
B) Score of 19-30, moderate
C) Score of 31-38, severe
D) Score >39, very severe.
Group (II) control subjects:
15 subjects with no acne and matching age and sex were included as control and subjected to the tissue biopsy.
Exclusion criteria:
• Patients receiving topical or systemic therapy for at least 2 weeks prior to tissue sample collection.
• Patients receiving reteniods for at least 6 weeks prior to tissue sample collection
• Patients with history of androgen secreting tumor, hypertension, cardiovascular disease, renal disease ( as they are known to increase IL-18 level ) .
All patients were subjected to the following:
• Full history taking and thorough clinical examination.
• Dermatological examination.
• Tissue biobsy from the acne lesion in back and shoulder of patients and detection of IL-18 level by real time PCR.
The present study showed a statistical difference in the level of IL-18 between the patients and the controls as its level was significantly higher in the patients group than acne free group, and also related to severity as follow:
■ In acne free patient the level of IL-18 was ranging from (0.01 – 0.90) ) with a mean ± SD (0.33 ± 0.37).
■ In cases with mild acne the level of IL-18 was ranging from ( 0.0 – 7.30 ) with a mean ± SD =(3.27 ± 2.93) .
■ In cases with moderate acne the level of IL-18 was ranging from ( 9.71 – 14.60 ) with a mean ± SD =(12.28 ± 1.61) .
■ while in cases with severe and very severe acne the level of IL-18 was ranging from (18.10 – 28.90) with a mean ± SD =(23.40 ± 4.56) .
Also, positive family history was detected in nearly more than half of cases 56% mainly in moderate and severs cases.