Welcome to our sixth installment of our new regular monthly slot where we report on research from the world of immunology, highlighting work from BSI members that has hit the headlines over the past four weeks.
Protective compound in skin inspires eczema treatments
Atopic eczema is a common skin condition affecting 20% of children and 5% of adults in the UK. Sufferers experience red, itchy skin that can become dry and cracked. They are often at greater risk of infection by S. aureus, which can infect skin lesions and damage the skin barrier. Conventional steroid treatments are associated with unpleasant side-effects, and can lose effectiveness over time.
In a new study at the University of Edinburgh, researchers have identified therapeutic potential for a protective chemical, called human beta-defensin 2 (hBD2), which is typically missing in eczema patients. hBD2 possesses antibacterial properties and, when applied to skin cells grown in the lab, has been shown to both maintain and protect skin integrity. As such, it is a vital component against S. aureus infection.
It is hoped that this discovery could help develop alternative treatments for atopic influenza. Indeed, BSI member Dr Donald Davidson, who led the study published in the Journal of Investigative Dermatology, said: “This is a great chance to work with something that the body makes naturally to develop new therapies for atopic eczema, which affects so many people’s lives.”
Read the press release
Read the full article: Wang et al. 2016 Journal of Investigative Dermatology doi: 10.1016/j.jid.2016.08.025
New type 1 diabetes treatment tweaks the immune response
Type 1 diabetes is an increasingly common diagnosis affecting 400,000 people in the UK. It is an autoimmune disease caused by cells of the immune system mistakenly attacking and destroying the insulin-producing cells of the pancreas. Insulin is important for ensuring glucose in the blood is taken up by cells. As such, patients are required to take regular insulin injections.
Using the drug aldesleukin (recombinant interleukin-2), presently administered in high doses to combat kidney tumours and skin cancers, researchers at the University of Cambridge hope to tailor its dosage to modulate the immune response in type 1 diabetes. Aldesleukin raises T regulatory cell numbers, which regulate the immune response and prevent autoimmune disease. Lower doses of aldesleukin increase T regulatory cells by 10–20%, and this moderate rise appears to sufficiently pacify the attack on the pancreas, without suppressing the immune response enough to risk infection from bacteria and viruses.
Dr Frank Waldron-Lynch, the BSI member who led the trial now published in PLOS Medicine, said: “Our goal is to develop a treatment that could see the end to the need for these life-long, daily injections by curtailing the early damage caused by the patient’s own immune system.” Any treatment would initially target newly-diagnosed patients, as it would limit the damage inflicted at the pancreas, and allow the patients to continue to produce insulin for a longer time.
Read the press release
Read the full article: Todd et al. 2016 PLOS Medicine doi: 10.1371/joural.pmed.1002139
MRSA releases fatty decoys to avoid antibiotics
Methicillin-resistant Staphylococcus aureus (MRSA) is, as the name suggests, a highly resistant ‘superbug’ responsible for thousands of deaths every year. One of the very limited treatment options is the antibiotic daptomycin, yet 1 in 3 of all infections remains resistant to this treatment. The research at Imperial College London, and published in Nature Microbiology, has elucidated the mechanism behind this resistance.
MRSA releases decoy molecules that mimic the fatty surface layer of the cell. Daptomycin binds to the cell surface and drills a hole, killing the bacterium. However, when decoy molecules are released, lead author Dr Andrew Edwards, explains, “The antibiotic mistakenly targets the decoys, allowing the bacteria to evade destruction. This is the first time this decoy system has been seen in MRSA.” The fact that only some MRSA bacteria exhibit this decoy system may explain why 30% of all infections are not cured.
In the resistant infections, the communication system used by MRSA bacteria to ‘talk’ among each other is silenced, and with it the ability to release toxins that damage human cells. A similar decoy system was previously observed in E.coli, indicating that this mechanism conferring antibiotic-resistance may be severely underappreciated. Strikingly, targeting MRSA with the penicillin-like antibiotic, oxacillin, partially helps prevent the release of decoys. Furthermore, a next generation antibiotic in clinical trials stops production of the fatty decoys, providing another potential treatment option for MRSA.
Read the press release
Read the full article: Pader et al. 2016 Nature Microbiology doi:10.1038/nmicrobiol.2016.194