Interaction between the the immune system and the gut’s microbiome in the development of psoriasis and its accompanying lesions was the focus of the study, “Intestinal Microbiota Promotes Psoriasis-Like Skin Inflammation by Enhancing Th17 Response,” published recently in the journal PLOS One. The findings suggest the microbiome’s composition may be a therapeutic target for disease management.

The gut microbiome has been previously seen as a therapeutic target for the immune system. As one microbiome expert, Dr. Herbert Dupont, previously said in an interview with BioNews Services, “ the intestinal bacteria look like a Persian carpet with tens of thousands of species of bacteria that form little interlocking walls to keep microbes that may cause mischief in the gut from producing — kind of walling them off. Well, when people get courses of antibiotics the diversity of these bacteria is depleted, and instead of a Persian carpet, it is a carpet with one or two colors in it, and now disease can occur.”

Researchers focused on the distinct interactions of the gut microbiome and specific immune system cells known as Th17, which have been previously linked to the formation of psoriatic lesions, and the role this interaction plays on the development of psoriasis.

They utilized three different experimental animal models:

Mice that have been bred to have zero mico-organisms (bacteria, fungi, viruses, etc.) on their skin, known as germ-free (GF) mice Mice treated with broad spectrum antibiotics, known a conventional (CV) mice Inbred strains of mice commonly used in experimental laboratory studies, known as C57BL/6 mice

Each distinct mouse model was treated with imiquimod (IMQ), a potent immune activator developed to induce psoriatic lesions in the animals. The interactions between the gut microbiome and the immune system were then measured, as was the degree of lesion formation.

After analysis, the findings showed that:

GF and CV mice were more resistant to IMQ-induced skin inflammation than C57BL/6 mice

The antibiotic treatment in CV mice resulted in major changes in measures of diversity of gut bacteria, and this change was sustained when IMQ was applied

The antiobiotic treatment resulted in an increase in certain gut bacteria, such as Lactobacillales, and a significant decrease in other bacteria, such as in Coriobacteriales and Clostridiales

When compared to C57BL/6 mice, IMQ-induced a lower degree of local and systemic Th17 activation in both GF and CV mice.

Taken together, such results mean that the distinct interactions between the gut microbiome and the immune system could be a potential clinical target for therapeutic management and prevention of lesion forming activity in patients.

“Our results suggest that host interactions with live microbes, [a]re involved in the pathogenesis of IMQ-induced skin inflammation by influencing the Th17 cell reactivity. The positive effect of gut microbiota modulation by antibiotics on the severity of skin inflammation suggests the involvement of gut-skin axis and may represent the groundwork for novel approaches in psoriatic patient’s management,” the researchers concluded.