Eczema patients not protected by intradermal flu vaccine

When I talked to Donald Leung earlier this week (he's head of pediatric allergy & immunology at National Jewish Health, and leads the Atopic Dermatitis Research Network) he mentioned one interesting result that has already emerged from a small-scale ADRN trial. Leung and others showed that patients with atopic dermatitis were not adequately protected, by FDA standards, by the new influenza vaccine Fluzone.

Fluzone is administered using a super-short needle--the technique is called "intradermal" injection in which the vaccine gets squirted into the upper skin layers rather than muscle tissue.

Presumably the super-short needle is less scary than a regular needle, and more people will get their flu vaccinations this way; it could be a public health issue in the event of a flu pandemic.

Scientists know that the immune system functions differently in the skin of patients with eczema. Leung and colleagues looked at how 20 eczema patients fared with Fluzone, compared to 20 non-atopic patients. Twenty-eight days after vaccination, they measured the levels of flu antibodies in the patients' blood. The non-atopic patients met the FDA standard; the eczema patients did not.

The scientists published their results in a preliminary form as an abstract at the meeting earlier this year of the American Academy of Allergy, Asthma and Immunology.

Benign bacteria help T cells signal skin infection

Benign bacteria on our skin partner with T cells to alert the immune system to the presence of dangerous pathogens, according to research recently published online in the journal Science.

The NIH press release explains the science very well, probably better than I could, so I have copied their text below.

The most relevant point that I can see is that this work shows that microbes living on healthy skin have an important role in our immune system. It's a philosophical question whether the microbes are separate from us--or are part of us, even though they don't share our DNA. If you overuse antibiotic ointments (that is, apply them for periods longer than required to treat an infection), you are killing off helpful microbes and weakening your immune response.

NIH team describes protective role of skin microbiota
Commensal bacteria and immune cells work together to fight harmful microbes

WHAT: A research team at the National Institutes of Health has found that bacteria that normally live in the skin may help protect the body from infection. As the largest organ of the body, the skin represents a major site of interaction with microbes in the environment.

Although immune cells in the skin protect against harmful organisms, until now, it has not been known if the millions of naturally occurring commensal bacteria in the skin—collectively known as the skin microbiota—also have a beneficial role. Using mouse models, the NIH team observed that commensals contribute to protective immunity by interacting with the immune cells in the skin. Their findings appear online on July 26th in Science.

The investigators colonized germ-free mice (mice bred with no naturally occurring microbes in the gut or skin) with the human skin commensal Staphylococcus epidermidis. The team observed that colonizing the mice with this one species of good bacteria enabled an immune cell in the mouse skin to produce a cell-signaling molecule needed to protect against harmful microbes. The researchers subsequently infected both colonized and non-colonized germ-free mice with a parasite. Mice that were not colonized with the bacteria did not mount an effective immune response to the parasite; mice that were colonized did.

In separate experiments, the team sought to determine if the presence or absence of commensals in the gut played a role in skin immunity. They observed that adding or eliminating beneficial bacteria in the gut did not affect the immune response at the skin. These findings indicate that microbiota found in different tissues—skin, gut, lung—have unique roles at each site and that maintaining good health requires the presence of several different sets of commensal communities.

This study provides new insights into the protective role of skin commensals, and demonstrates that skin health relies on the interaction of commensals and immune cells. Further research is needed, say the authors, to determine whether skin disorders such as eczema and psoriasis may be caused or exacerbated by an imbalance of skin commensals and potentially harmful microbes that influence the skin and its immune cells.

Hormone works in tandem with vitamin D to fight skin infections

A certain hormone works in tandem with vitamin D to control how skin cells produce a natural microbe-fighting agent, and can compensate for a lack of vitamin D, scientists have found.

The new results help explain something that has confused researchers for a long time: although it is known that vitamin D plays a role in the immune defense, there are very few clinical trials that show that taking supplemental vitamin D helps prevent infection.

The work was led by Richard Gallo, a professor of medicine and pediatrics and chief of the Division of Dermatology at the University of California, San Diego. It was published this week in the journal Science Translational Medicine.

The skin makes natural antimicrobial compounds (protein fragments called peptides) to kill unwanted bacteria, fungi, and viruses. Eczema patients produce these compounds at lower levels than normal; psoriasis patients, at higher levels. Vitamin D initiates production of cathelicidin, a broad-spectrum antimicrobial.

Gallo and colleagues showed that human skin cells produce parathyroid hormone (PTH) when treated with a bacterial compound known to trigger the immune system. The same cells, stimulated with vitamin D, manufactured copies of the receptor for PTH. And the skin cells produce far more cathelicidin when they are treated with parathyroid hormone and vitamin D than with either compound alone.

The results suggest a model in which, in humans, vitamin D can stimulate cathelicidin production by itself—but PTH is doing so by a parallel pathway, which vitamin D can amplify.

The scientists also showed that PTH helps reduce the severity and extent of Streptococcus skin infections in mice—but it does so much more strongly in normal mice, compared to mice genetically engineered to be unable to convert vitamin D to its active form. (Apparently it is very difficult to make a mouse deficient in vitamin D.)

What this means for eczema patients is not clear yet. The research gets us further toward understanding how vitamin D and other factors participate in the skin’s immune response. If I were a doctor, it would make me hesitant to recommend that patients with normal vitamin D levels should take supplements.