Team:Montgomery Cougars NJUSA/Project/PathogenesisofAcne

From 2014hs.igem.org

(Difference between revisions)
(Pathogenesis of Acne)
(Pathogenesis of Acne)
Line 6: Line 6:
1. Blockage of sebaceous follicles.
1. Blockage of sebaceous follicles.
-
<p>2. The epithelial cells in sebaceous follicles under go abnormal desquamation (shedding of the skin).  Comedogenesis is the obstruction of sebaceous follicles due to greater cohesiveness of the follicular epithelial cells and sebum. As keratinous material gathers in the sebum filled follicle, the wall thins and swells. </p>
+
<p>2. The epithelial cells in sebaceous follicles undergo abnormal desquamation (shedding of the skin).  Comedogenesis is the obstruction of sebaceous follicles due to greater cohesiveness of the follicular epithelial cells and sebum. As keratinous material gathers in the sebum filled follicle, the wall thins and swells. </p>
<p>3. The anaerobic, commensual bacterium ''Propionibacterium acnes'' proliferates in a lipid rich environment, such as when there is an overproduction of sebum. Excessive sebum production is caused by androgenic stimulation of sebaceous glands.</p>  
<p>3. The anaerobic, commensual bacterium ''Propionibacterium acnes'' proliferates in a lipid rich environment, such as when there is an overproduction of sebum. Excessive sebum production is caused by androgenic stimulation of sebaceous glands.</p>  

Revision as of 17:12, 16 June 2014

Pathogenesis of Acne

Acne Vulgaris is caused by four main factors:

1. Blockage of sebaceous follicles.

2. The epithelial cells in sebaceous follicles undergo abnormal desquamation (shedding of the skin). Comedogenesis is the obstruction of sebaceous follicles due to greater cohesiveness of the follicular epithelial cells and sebum. As keratinous material gathers in the sebum filled follicle, the wall thins and swells.

3. The anaerobic, commensual bacterium Propionibacterium acnes proliferates in a lipid rich environment, such as when there is an overproduction of sebum. Excessive sebum production is caused by androgenic stimulation of sebaceous glands.

4. P. acnes produces proinflammatory mediators that cause microcomedones to inflame and become papules, pustules, and nodulocystic lesions. A microcomedone is the precursor to acne, an accumulation inside a pore, causing the pore to be plugged by dead skin cells and sebum. Lipases, proteases, and hyaluronidases, produced by the bacteria, act as proinflammatory products.

Acne can manifest itself on the skin in a variety of manners, from mild comedonal form to severe inflammatory cystic on the face, back, and chest. When androgen is released throughout the body, it precipitates activity in the sebaceous glands, promoting comedone and seborrhoea formation, propagating the inflammatory P. acnes. P. acnes is actually present in the pilosebaceous ducts as an anaerobe.

"Acne Path" width="50" height="50"