The composition of the microbiome—the countless bacteria, fungi, and viruses that colonize our body surface, skin, intestines, or lungs—makes a decisive contribution to human health or disease. However, biological mechanisms that cause inflammation in the microbiome are still largely unknown.

Together with a group of researchers from the University of Kiel and the University Hospital of Schleswig-Holstein, professor Dr. Oliver Cornely (head of the Center of Excellence for Invasive Fungal Diseases at Cologne University Hospital) has deciphered a mechanism by which specific intestinal microbiota amplify inflammatory reactions in the lungs. The results of the study, published in Cell, could accelerate the development of new therapies for common diseases.

"The fungus Candida albicans, which colonizes the intestines, skin, and mucous membranes, is actually harmless," Cornely said. "However, our study has shown that C. albicans affects the balance of our immune system."

C. albicans stimulates the immune system to produce specific defense cells, so-called Th17 cells. However, some of these Th17 cells then attack other fungi, such as Aspergillus fumigatus. This phenomenon is called cross-reactivity. The research showed that immune-compromised individuals have an increased level of cross-reactive Th17 cells in their lung tissue. This concentration is associated with a deterioration of these patients' health. The protective Th17 reaction in the intestine seems to amplify pathogenic immune processes in the lungs.

"With this observation, we were able to show for the first time how a single member of the microbiome, C. albicans, influences the specific immune response to a large group of other microbes. Immune cross-reactivity is probably a common mechanism by which the microbiome manipulates the immune system—with both protective and harmful effects," Cornely remarked.

Deciphering such specific effects of individual microbes will, in future, contribute to the development of targeted therapies.