There is no evidence probiotics can relieve the symptoms of eczema, but there is some evidence that they may occasionally cause infections and gut problems.  These findings from The Cochrane Library come at a time when use of probiotics to treat eczema is increasing.

Eczema is an itchy skin condition that affects more than 1 in 20 people at some time in their lives and is especially common in children.  Its cause is complex and not well understood, but sufferers do have different bacteria in their guts compared to unaffected people.  Consequently, some nutritionists have suggested that eating live gut-dwelling bacteria, such as those found in probiotic yoghurts and some infant formulas, could be beneficial.

“Some doctors are recommending probiotics as a cheap treatment for eczema, but having carried out a systematic review we have found no evidence that they work for treating eczema,” says lead researcher Robert Boyle of Imperial College, London, UK.

The Cochrane Researchers looked at 12 studies that together involved 781 children diagnosed with eczema.  These studies compared severity of the disease in children given live bacteria to severity in those given a placebo.  The researchers found that probiotics provided no significant health improvement.  Similar bacteria were given across all studies, so the researchers could not rule out the possibility that other strains might be beneficial.  Moreover they found that in separate studies 46 patients had been reported to suffer side effects from using probiotics, including infection and bowel damage.

“There is no evidence that probiotics are a worthwhile treatment for eczema, and they may be harmful for certain groups of people,” says Boyle.  “However, further studies of new probiotics are needed, because it is possible that different types of probiotics which haven’t yet been studied in eczema treatment could be more effective.”

Some animal species have developed conspicuous traits produced by melanin pigments (for instance, dark manes in lions, black stripes in some birds and fishes).  These traits are used as signals during contests for resources and/or contribute to increase the mating opportunities.  However, the efficiency of these traits as signals depends on the fact that they transmit honest information about the quality of the bearer.  This would be only assured by the fact that producing or maintaining the signal inevitability implies a cost.  Thus, only those individuals able to afford the cost would also be able to conveniently express the signal.

Signals produced by melanin pigments have challenged our understanding because they are apparently cost-free and strongly controlled by the genotype.  Melanin pigments are not as limited in production as carotenoids, yellow-red pigments common in vertebrates and only obtained from certain food items.  In fact, melanin is constructed from amino acids present in proteins of the organism.  However, recent experimental studies have become to disentangle the cost at the basis of melanin-based signals.

A recent article by Ismael Galván at the Museo Nacional de Ciencias Naturales (CSIC) in Madrid and Carlos Alonso-Alvarez at IREC-CSIC, Spain, published in the online, open-access journal PloS ONE proposes a novel hypothesis suggesting that these traits could indicate the ability of the bearer in fighting free radicals and oxidative damage.  On the basis of medical bibliography, the researchers realized that tissue melanization is constrained in the presence of high enough levels of a key intracellular antioxidant named glutathione, which is considered one of the most powerful antioxidants present in virtually all animal cells.

The scientists hypothesized that low levels of this substance are also required to express melanin-based signals present in many animals.  This implies that individuals able to express these signals should be also able to fight off an oxidative challenge, as a consequence of the low levels of the cited antioxidant.  Only those animals with alternative antioxidant resources would be able to afford the cost of signaling.  By chemically inhibiting the production of glutathione at the red blood cells, authors were able to significantly increase the size of a black stripe present in the feathers of the breast of great tits (a common garden bird).  This stripe is a conspicuous trait playing a significant role during combats for territory, food or mates.

Furthermore, the reduction of glutathione levels also induced a mobilization of other antioxidant molecules to the blood plasma, supporting the cost, such as hypothesized by Alonso-Alvarez and colleagues.

Xiao-Jing Wang and colleagues, at Oregon Health & Science University, Portland, have provided new insight into the role of the signaling molecule Smad2 in skin cancer by analyzing human skin cancer tissue and a mouse model of skin cancer.

In the study, human squamous cell skin cancer samples were found to frequently lose expression of Smad2.  In particular, Smad2 expression was lost in all samples characterized as “poorly differentiated” (which means they had progressed to become aggressive tumors).  Consistent with this, mice lacking Smad2 in cells of the skin known as keratinocytes developed chemically induced skin cancer more rapidly than normal mice, and the cancers were all characterized as “poorly differentiated”.  The mouse cancers also underwent a process known as epithelial-mesenchymal transition (EMT) and this was found to contribute to the accelerated progression of the skin cancer to an aggressive form.  These data identify Smad2 as a suppressor of skin cancer development and progression to an aggressive form, and future studies will investigate in more detail the mechanisms underlying the role of Smad2 loss in human skin cancer progression.

Psoriasis is a chronic skin disease that affects approximately 2–3% of individuals in the Western world.  New data, generated by Karin Scharffetter-Kochanek and colleagues, at the University of Ulm, Germany, have indicated that a subset of immune cells known as Tregs (which act to prevent other immune cells from responding inappropriately) are dysfunctional in a mouse model of psoriasis and that this dysfunction contributes substantially to the development of disease.

Mice that express a reduced amount of the protein CD18 (Cd18hypo mice) develop a skin disease that resembles the symptoms of individuals with psoriasis.  In the study, Tregs isolated from Cd18hypo mice failed to suppress the proliferation of disease-causing immune cells because they secreted lower levels of the soluble factor TGF-beta than normal Tregs.  This was also important for their inability to control disease in vivo, as transplantation of normal Tregs into Cd18hypo mice resulted in a substantial improvement in the psoriasis-like disease, whereas if these cells were transplanted in the presence of antibodies that neutralized TGF-beta there was no improvement in disease.  The authors therefore conclude that psoriasis-like disease in Cd18hypo mice is caused mainly by a defect in Treg function and suggest that maintaining CD18 levels is important for ensuring that Tregs function optimally.