A temporary bacterial infection of the skin can change the immune system long -lasting and increase all -angry inflammation. This is shown by a study published in the top journal “Science Immunology” under the direction of the Medical University of Vienna and the Cemm Research Center for Molecular Medicine. Research reveals a previously unknown connection between the skin, bone marrow and lungs and promises the development of new treatment strategies for allergic diseases such as asthma.
The research team examined in a mouse model how a local infection with Staphylococcus Aureus (S. Aureus) influences the immune system. S. Aureus is a worldwide bacterium that can appear both as a harmless skin settler and as a pathogen. The researchers found that as a result of a S. Aureus skin infection, not only typical immune cells (neutrophil granulocytes), which are known for the defense against bacteria, immigrated to the inflamed area. Eosinophils could also be demonstrated, a special unit of white blood cells that play an important role in allergic diseases. Particularly noteworthy: the skin infection changed the bone marrow in the long term, in which eosinophilic is formed. “Our extensive analyzes showed that the Eosinophiles from infected mice had a long -lasting, inflammatory signature. This embossing remained long after the healing of the skin infection,” reports first author Mariem Radhouani (University Clinic for Internal Medicine I of the MedUni and Cemm).
Increased reaction to house dust mite allergens
In order to investigate the effects of this immunological reprogramming, the researchers suspended the previously infected mice in-house dust mite allergens, the most common triggers of allergic asthma “The results were clear: animals with an earlier skin infection were increased by contact with the allergens. They showed an increased number of eosinophils in the lungs. An increased production of allergy -promoting antibodies and a restricted lung function, ”explains Student Director Philipp Starkl (University Clinic for Internal Medicine I of the MedUni Vienna) the newly gained knowledge. The researchers were also able to demonstrate that this increased immune reaction was conveyed by the eosinophiles from the changed bone marrow. A transplantation of eosinophils from previously infected mice on healthy animals was sufficient to cause increased allergic inflammation in the recipient mice.
According to a further observation of the research team, two messenger substances of the body are crucial for this immune change: interleukin-33 (IL-33) and C5A. IL-33 promotes the multiplication of the Eosinophils in the bone marrow, while C5A directs the changed immune cells into the lungs. “A targeted blockade of these signal paths could represent a new treatment strategy in allergic diseases such as asthma or avoid their origin prophylactically,” said the study author: Inside further research, which should deepen and confirm the results.
Publikation: Science Immunology
Eosinophil innate immune memory after bacterial infection promotes allergic lung inflammation.
Mariem Radhouani, ASMA FARHAT, Anna Hakobyan, Sophie Happing, Lisabeth Pimenov, Alina Fokina, Anastasiya Hladik, Karin Lakovits, Jessica Brösamlen, Vojtech Dvorak, Natalia Nunes, Andreas Zech, Marco Idzko, Thomas Krausgruber Uluckan, Jiri Kovarik, Kai Hoehlig, Axel Vater, Margret Eckhard, Andy Sombke, Nikolaus Fortelny, Jörg Menche, Sylvia Knapp, Philipp Starkl.
https://www.science.org/doi/10.1126/sciimmunol.adp6231