Projects

Here, we  investigate how arachidonic acid metabolites formed via the cyclooxygenase (COX-2) pathway ("prostanoids") regulate tissue repair, host defense and macrophage functions in different type 2 immune responses (allergic asthma and helminth infection).

Worm parasites (helminths) have unique capacities

to suppress type 2 immune responses. Here, we aim to identify the key molecules that are responsible for these immune regulatory effects. This may result in new biotherapeutics against type 2 inflammatory diseases (e.g. severe asthma and nasal polyposis) and foster vaccine design against parasitic worms.

Ferroptosis is a special form of iron-mediated oxidative cell death. Ferroptosis has been associated with type 2 inflammation (e.g. in severe asthma). However, the underlying mechanisms and functional consequences are incompletely understood. Here, we aim to define mechanisms that drive or regulate ferroptosis in type 2 immune responses. We also aim to understand what is the role of ferroptosis in different type 2 immune responses.

Our previous work has uncovered an inflammatory memory in macrophages from human asthmatics. In this project, we study the mechanisms and functional consequences of this "training" in different asthma and infection models.

Leukotrienes (LTs) are key lipid (arachidonic acid) metabolites involved in type 2 inflammation (ashma, nasal polyposis, aspirin/ NSAID intolerance). Here, we aim to understand how different myeloid cell types (macrophages, neutrophils, eosinophils) contribute to LT production in severe asthma and how this impacts cellular reprogramming and functionality in infection and inflammation.

Together with our colleagues from the Technical University of Munich (Prof. Clarissa Prazeres da Costa) and collaboration partners within the DFG TRR355 we aim to define the mechanisms that drive Treg function and stability in inflammatory diseases. In our subproject, we are focusing on prostanoids as key regulators of Treg cell differentiation in asthma.