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We help scientists solve complex infection biology by modeling human tissues and immune responses in organ‑on‑chip systems, resulting in deeper, clinically relevant understanding of host-pathogen interaction and the microbiome.

Understanding host–pathogen interactions is essential for developing effective therapies. Conventional models lack the cellular and physiological complexity to capture immune dynamics and tissue-specific responses.
Immune responses often differ in humans and animals
In vitro models used to study host-pathogen interactions lack complexity
Some infections are human specific – animal models can’t predict human response in this case
Development timeframes for anti-infectious diseases treatments are too long

3D tissue architecture, perfusion, and physiologically relevant flow conditions create infection niches that better reflect in vivo host–pathogen encounters. Dynamic culture supports realistic immune-cell trafficking and helps distinguish true pathogen or immune-cell adhesion from static-culture artefacts.

Microfluidics allows tight regulation of chemical gradients, flow dynamics, tissue barriers, and biomechanical forces.

By combining epithelial, stromal, endothelial, and immune cells in defined compartments, organ-on-chip models recreate the cellular complexity and barrier organization of human tissues. This enables infection routes that are closer to in vivo biology, including pathogen entry through vascular channels, tissue invasion across barriers, and interactions with circulating immune cells.

Perfusion-driven 3D tissue architecture replicates essential aspects of human physiology. It maintains barrier integrity, facilitates the removal of metabolic waste and bacterial toxins, enables shear-dependent binding mechanisms, and sustains the physiological activity of host cells and pathogens over extended periods.

TEER and oxygen can be captured in real-time. Additionally, organ models enable sampling of supernatant and tissue allowing for all standard in vitro readouts.

Interconnected organ models enable the study of systemic infections, immune crosstalk, and pathogen dissemination across organ barriers.

Dynamic infection modeling supports the investigation of pathogenesis mechanisms and infection progression, enabling the reliable evaluation of treatment efficacy

Integrated tissue barriers, microbiome and immune components replicate physiological pathogen entry points and host defense and immune responses, improving translational relevance

Dynamic42 was founded as a spin‑off from University Hospital Jena and collaborates closely with the Leibniz Institute for Natural Product Research and Infection Biology, setting us exactly at the intersection of advanced human models and infection biology. Combined with multiple in‑house infection projects, this foundation enables us to support a wide range of physiologically relevant infection models for academic research.
/ Host-Microbiome Interaction
/ Integration of Pathogens (fungi, bacteria, viruses)
/ Immune cell perfusion & migration
/ Vasculature
/ Stable barrier function & marker expression
/ Near-physiological, human relevant 3D architecture of tissues
/ Sampling of supernatant & tissue for various analysis options
/ Real-time read-outs (TEER, O2)
/ Multi-organ models
/ Options for anaerobic bacteria
/ Perfusion & dynamic drug application
/ Infection ports on biochips
Microbiome dysbalance can weaken barrier functions, increasing the risk of infectious diseases. Understanding the complex interplay between host, microbiome and invading pathogens is essential to unravel pathogenesis mechanisms, host defense, and infection progression. Organ-on-chip technology provides a powerful platform to study these multifactorial host-pathogen interactions in a human-relevant, immunocompetent in vitro setting.
The microbiome plays a central role in immune regulation and homeostasis. Alterations in the microbial community lead to dysregulation of organ functions and increase the risk for chronic diseases and infections. Organ-on-chip technology makes it possible to model these complex microbiome-host interactions in a physiologically relevant environment.

SARS‑CoV‑2, the coronavirus responsible for the COVID‑19 pandemic, has caused more than 770 million reported cases worldwide, placing unprecedented pressure on global healthcare systems. The pandemic exposed the limitations of conventional preclinical models and underscored the need for more predictive, human‑relevant approaches to accelerate treatment development.
Our lung‑on‑chip model recreates key structural and functional features of the human lung, enabling physiologically relevant modeling of airborne infections and inflammatory lung diseases to study infection mechanisms and evaluate treatment efficacy in a controlled human context.
Pneumonia is a leading infectious disease worldwide, with influenza causing recurrent epidemics associated with high mortality. Clinical data shows that disease severity is often influenced by secondary bacterial co‑infections, including Staphylococcus aureus. Conventional 2D models fail to preserve essential alveolar functions and cannot capture the complex cellular and immune interactions driving viral-bacterial co-infections.
Our lung‑on‑a‑chip model provides a more predictive platform by recreating physiologically relevant alveolar functions, integrating functional vasculature and immune cells to maintain robust barrier integrity. This platform enables realistic investigation of viral–bacterial co‑infections, disease mechanisms, and therapeutic strategies in a human‑relevant context.
Human norovirus, a highly contagious virus that causes acute gastroenteritis, has long been difficult to cultivate in vitro due to the absence of physiologically relevant models. This is because the infected cells lack the 3D architecture and sufficient differentiation state found in the in vivo environment.
A stem-cell-derived, perfused gut-on-chip model with integrated immune cells overcomes this challenge by improving epithelial maturation and increased virus titers, resulting in a robust, reproducible norovirus infection model.
Clostridioides difficile infections (CDI) remain a major clinical challenge, as toxin‑mediated epithelial damage and excessive mucosal inflammation drive severe diarrhea and colitis.
However, insights into the pathogenesis of CDI remain limited, partly because conventional 2D in vitro models fail to capture the complexity of the pathogen-host interaction.
Our intestine‑on‑chip platform addresses this gap by recreating an immunocompetent, intestinal microenvironment. The system enables the investigation of C. difficile toxin biology, host barrier functions, and immune responses, supporting more predictive evaluation of preventive strategies against CDI.
Bacterial infections are a major clinical complication in patients with chronic liver disease. Pathogens such as Staphylococcus aureuscan invade tissue-resident macrophages as a strategy to evade host immune recognition.
Our liver-on-chip model recreates a multicellular, immunocompetent liver environment, enabling detailed investigation of pathogen immune response, barrier functions, and cellular targets under disease-relevant conditions.
This human‑relevant platform supports more predictive studies of bacterial infection mechanisms and therapeutic response.
Maintaining hypoxic conditions is crucial when investigating the pathogenesis of anaerobic pathogens. Traditional 2D cultures are less complex and often suffer from bacterial overgrowth, resulting in reduced long-term stability.
Our immunocompetent gut-on-a-chip model enables the culture of selective microbiota and allows for infection modelling to investigate pathogenicity mechanisms under hypoxic conditions.
Cholera, caused by the human‑specific pathogen Vibrio cholerae, is transmitted through contaminated water and food and can rapidly become life‑threatening if untreated. Intestinal pathogen colonization and infection depend on quorum‑sensing-regulated virulence mechanisms that are difficult to study in conventional models.
Our immunocompetent gut‑on‑chip infection model provides a human‑relevant platform to investigate quorum‑sensing‑driven pathogenicity, enabling deeper insight into V. cholerae infection dynamics.

Invasive pulmonary aspergillosis is a life-threatening disease with high mortality rates, particularly in immunocompromised patients. Using our lung-on-chip model infected with Aspergillus fumigatus, fungal growth and the invasive behavior of fungal hyphae can be investigated to understand fungal pathogenicity. This allows the characterization of cellular targets and testing of antifungal agents, such as caspofungin, in a controlled human in vitro environment.

Candida albicans is a common commensal of the human microbiota, typically residing in the gut without causing harm. In immunocompromised patients, Candida can shift to a pathogenic state, leading to invasive candidiasis with severe clinical consequences.
Traditional in vitro models lack the complex intestinal architecture and intravenous drug administration routes.
Our gut-on-chip model overcomes these limitations by mimicking the physiological intestinal environment and modelling intravenous drug administration, enabling more realistic studies of host-pathogen interactions and human drug response.
Our gut-on-chip model is designed to replicate human intestinal physiology for the study of drug absorption, barrier function, and immune interactions in the human intestinal system. It supports research in toxicology, host–microbiome interaction, infection and inflammatory disease modeling.
Changes to the microbial composition of the gut can lead to pathogenesis of opportunistic infections, chronic inflammation, and inflammatory bowel disease.
Here the authors created a gut-on-chip model with innate immune cells (mucosal macrophages and dendritic cells) and probiotic Lactobacillus rhamnosus and infected it with Candida albicans.
Pre-colonization of the intestine with L. rhamnosus reduced C. albicans-induced tissue damage, lowers its translocation, and limits fungal burden.
Maintaining hypoxic conditions is crucial for gut microbiome research. The majority of the intestinal microbial community is anaerobic, and traditional aerobic in vitro cultures often fail to capture the microbial diversity.
Our immunocompetent gut-on-a-chip model enables the development of physiologically relevant microbiome and infection models to investigate host-microbiome interactions or pathogen infection mechanisms under hypoxic conditions.
In this case study, the author applies purified toxins from Clostridioides difficile to a gut-on-chip model in our 2-channel chip BC002. The objective is to test this with live bacteria under hypoxic conditions in subsequent studies.
In addition to the kit, you will require a peristaltic pump. If you don’t have one you can order a DynamicOrgan® System and will receive a peristaltic pump in addition to your kit of choice.
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