Spotting the problem

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  • Published: Aug 25, 2008
  • Author: Steve Down
  • Channels: Proteomics & Genomics
thumbnail image: Spotting the problem

It's every teenager's nightmare. The slow, relentless spread of spots and blackheads that transforms an acceptable visage into a social stigma. Those youngsters who suffer from serious attacks of acne often have to cope with the teasing and bullying of their more fortunate peers, as well as the affliction itself. The psychological effects often outweigh any physical discomfort.

It has been estimated that this disease affects more than 50 million people in the USA alone but it is not limited to adolescents. Acne vulgaris, to give it its formal name, can also infect adults and can leave permanent scarring on the face and upper body.

So what causes acne? Contrary to popular belief, acne is not a disease of poor hygiene. In fact, too vigorous washing of the face can aggravate the condition. It is also not affected by diet, dispelling the myth that sweet or greasy foods make it worse.

It is a chronic inflammatory disease that results from blocked hair follicles that prevent the naturally produced sebum from flowing to the skin through pores. Under these conditions, the bacterium Propionibacterium acnes, which exists on the skin, grows in the plugged follicles to cause inflammation. The plugged follicle can remain under the skin to produce a whitehead, or the plug can travel to the surface of the skin where the sebum is oxidised to form a blackhead.

The good news is that acne is treatable. However, topical applications work by soothing the symptoms and preventing the formation of new lesions, not by shrinking existing ones, so treatment must be an ongoing process. There are some recommended antibiotic therapies but they also target other skin bacteria and can induce antibiotic-resistant strains of P. acnes. For serious cases, a retinoid drug can be prescribed but it has dangerous side effects such as a high risk of depression and an increased rate of birth defects.

The search for new anti-acne drugs and vaccines has been hampered by the fact that animals do not produce sufficient lipids to host P. acnes. Various animal models such as rabbit ears and mouse ears have been used in the past but their biochemistry is different to that of human hair follicles. Genetically modified mice with acne-like skins have also been created for screening anti-acne drugs but their immune system cannot generate antibodies for developing acne vaccines.

A new solution developed by a multi-organisational group of scientists approaches the problem from a different viewpoint. Chun-Ming Huang and colleagues from the University of California at San Diego, the VA San Diego Healthcare Center, the Burnham Institute for Medical Research in La Jolla and the Dessau Medical Center in Germany have designed a special tissue chamber to implant into small mammals to mimic bacterial infections. The team reviewed their technique in the journal Proteomics.

The design is based on a cylindrical PTFE tissue chamber that is 1 cm long and has internal and external diameters of 1.5 and 3.0 mm, respectively. It has 12 small holes to allow host cells to infiltrate the chamber and react with injected bacteria and is an accurate mimic of bacterial infections in vivo.

In practice, a piece of dead dermis from a mouse was seeded with human sebocytes (sebaceous adipose cells) which grew and formed a layer on the surface and migrated inside. This dermis was inserted into the tissue chamber and implanted into the abdominal skin of a mouse. A few days after implantation, the P. acnes bacterium or phosphate-buffered saline (as control) was injected into the chamber to induce an immune response. A few days later, tissue chamber fluids were withdrawn for testing.

In the control chamber, no bacteria were detected but in the P. acnes-injected chamber, the number of bacteria increased markedly, indicating that the environment is a good growth medium. Lipid testing showed that the tissue chamber allowed the human sebocytes to survive without rejection.

Having established the success of the model system, the researchers decided to see what changes in the proteome were induced by the interaction of the bacterium, sebocytes and the murine immune system. The tissue fluids from the chamber were labelled with isotopically light and heavy forms of an isotope-coded derivative to quantify the differences in protein levels between the control and infected systems.

The labelled proteins were reduced and alkylated and digested with trypsin in the conventional manner for analysis by liquid chromatography/mass spectrometry followed by database searching to identify the proteins.

A total of 13 proteins were identified in the tissue chamber fluid, originating from secreted proteins, mouse cell matrix proteins, human cells and P. acnes. Of those, 4 showed altered concentrations. S100A9, also known as myeloid-related protein 14, was increased, possibly due to a host antimicrobial response. Conversely, serine protease inhibitor A3K was significantly decreased after infection. These altered proteins provide potential new targets for treatment.

This new humanised acne microenvironment allows the in vivo study of acne infections by P. acnes that should lead to a better understanding of the way the bacterium interacts with the host and, eventually, to targeted therapies.

The views represented in this article are solely those of the author and do not necessarily represent those of John Wiley and Sons, Ltd.


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