At Jena University Hospital, we rebuild the human gut, lung and liver on chip, as immunocompetent living tissue models that let us study how pathogens, microbiota and the immune system interact, without animal experiments.
We study infection and inflammation in human tissue, not in animals.
Most infection research still relies on animal models, which respond differently from the human immune system. We rebuild the relevant human context in microphysiological models, from organoids of induced pluripotent and adult stem cells to organ-on-chip and multi-organ systems, growing living tissues of the gut, lung and liver in which epithelium, immune cells and microorganisms interact.
Our focus is the organ-specific immune system and its interaction with commensal and pathogenic microorganisms in the tissue microenvironment. Because these models are human and immunocompetent, they let us study infection and inflammation in ways that reduce and increasingly replace animal experiments, following the 3R principle.
The gut is a constant negotiation between the microbiota, its metabolites and the immune system. Our immunocompetent intestine-on-chip rebuilds the mucosal barrier together with resident immune cells and a living microbiota, and reproduces the peristaltic motion of the tissue. It lets us follow how commensal colonisation, enteric infection and dysbiosis shift the balance between tolerance and inflammation, across questions that reach from cholera and Clostridioides difficile to inflammatory bowel disease, and test how microbial metabolites such as short-chain fatty acids and bile acids steer the tissue toward defence or disease.
From the nose through the bronchi to the alveolus, the airways defend a vast surface against inhaled pathogens. We rebuild the upper and lower respiratory tract on chip, modelling the nasal and bronchial mucosa alongside the immunocompetent alveolus, to follow influenza A infection, Staphylococcus aureus pneumonia and the bacterial superinfection and persistence that often follow a viral insult, together with antiviral and antibiotic drug responses. Together with our gut models, it also opens the gut-lung axis that links intestinal health to respiratory viral disease.
The liver orchestrates how the whole body reacts to infection. Our vascularised liver-on-chip models the hepatic acute-phase response, steatotic liver disease and drug metabolism along the gut-liver axis, revealing how the organ adapts, and sometimes fails, under inflammatory stress. As the filter organ of the circulation, it is also where pathogens spreading from distant sites are met and cleared. By connecting our lung and liver models into a multi-organ system, we open the lung-liver axis, following how infections such as Staphylococcus aureus disseminate through the body and how a compromised liver shifts the balance.
Across these organ models, our work centres on a single relationship, how the microbiota and the human immune system shape one another within the distinct microenvironment of each organ, in health and in disease. We are particularly interested in the plasticity of myeloid cells and in the tissue-resident immune niches that decide whether infection and inflammation resolve or progress to organ dysfunction. To study this we build immunocompetent organ-on-chip models on microfluidic biochips developed in our group, from primary human cells, induced pluripotent stem cells and adult stem cells, and read them out with spatial omics, advanced microscopy and quantitative image analysis, increasingly coupled with computational in silico models. Across viral and bacterial infection, mycoses, chronic inflammation and the immune toxicity of cellular cancer therapies, this lets us resolve disease mechanisms in human tissue and translate them into new approaches for prevention and treatment that reduce the need for animal experiments.
68 peer-reviewed original articles and 10 reviews, each listed with its full author line. See the complete publication list or the record on ORCID.
A selection of our ongoing, third-party funded work.
Alexander Mosig is a biochemist and cell biologist whose work is driven by the question, how the human immune system, and the innate immune system in particular, orchestrates its response to infection and inflammation. During his doctoral work he began using complex in vitro systems to study organ-specific immune responses, and his research has since centred on organ-on-chip models and the 3R principle of replacing, reducing and refining animal experiments.
He studied biochemistry and completed his doctorate on immune cells in vascular disease at Jena University Hospital, before turning to microphysiological models during his postdoctoral years. In 2017 he habilitated in biochemistry and cell biology at Friedrich Schiller University Jena with work on microphysiological systems of the liver and the blood-brain barrier. He heads the NAMIR research group at the Institute of Biochemistry II. In 2018 he co-founded Dynamic42, a spin-off that carries the organ-on-chip technology developed in Jena into industrial drug and safety testing.
His group studies the host-microbiota interface and the adaptive immune response to changes in the microbiota during infection and inflammation, with a particular focus on the plasticity of myeloid cells and the immunological niches shaped by microbes and their metabolites. Using primary human cells, adult stem cells and induced pluripotent stem cells, he models viral, bacterial, fungal and parasitic infection and inflammatory disease in the gut, lung and liver, work recognised among others by the 2017 research award of the German Federal Ministry of Food and Agriculture for 3R methods.
Full curriculum vitae →An interdisciplinary group of biochemists, cell biologists and microbiologists investigating infection, inflammation and the immune response in human tissue models.
We welcome partners, students and collaborators who share our commitment to human-relevant, animal-free research.