Focus of Research

The research at Herold Lab is dedicated to unraveling the mechanisms driving anti-viral host defense, to dissecting the cellular and molecular contributors to the tissue damage at the virus-host interface in the distal lung, and to defining pathways and mediators of organ regeneration in the context of viral infection. We focus on the interaction of macrophages with parenchymal cells of the distal lung and the epithelial stem cell niche.

Moreover, we study mechanisms that lead to increased susceptibility to bacterial infections during viral pneumonia or acid aspiration with a focus on alveolar macrophages. These aims will be achieved by using established models of in vivo virus infection, acid aspiration and bacterial superinfection of different levels of complexity (in vitro – ex vivo – in vivo) combined with analyses of patient samples.

In an attempt to define better tools for the modelling of human lung diseases we have established a complex human lung organoid system derived from human induced pluripotent stem cells (iPSC). Over time, these organoids mimic the branching morphogenesis of native human fetal lungs and can be used to study genetic mechanisms that affect lung development as well as for infection experiments.

We utilize state-of-the-art technologies such as FACS and cell sorting (LSR Fortezza, FACSAriaIII) as well as spectral cell sorting with our recently acquired FACSDiscover S8 cell sorter with CellView Imaging, NGS including single cell RNA-Seq and spatial transcriptomics techniques, and high-resolution microscopy/life imaging techniques. The ultimate goal is to find novel disease biomarkers defining susceptibility to and recovery from acute lung injury, and to identify distinct host targets to be harnessed for novel therapeutic strategies to combat severe respiratory viral and bacterial infections.

Prof. Dr. med. Susanne Herold, PhD
Prof. Dr. med. Susanne Herold, PhD

Lab Members

Clinician Scientists

Christina Malainou, MD PhD
Christina Malainou, MD PhD
Project description: Influenza virus-induced pneumonia initiates a variety of immune responses within the alveoli, which eventually compromise host defense, causing the depletion of the local, tissue-resident alveolar macrophage (TR-AM) pool, which paves the way for the establishment of secondary bacterial infections, with a potentially lethal outcome. In this project, we aim to elucidate the pathomechanisms behind influenza-associated TR-AM loss to attenuate disease progress and prevent the transition to post-influenza bacterial pneumonia.

PostDocs

Irina Kuznetsova, PhD
Irina Kuznetsova, PhD
Project description: In severe cases SARS-CoV2 disease-2019 (COVID-19), virus-induced pneumonia leads to development of disseminated intravascular coagulation, endothelial leakage, acute respiratory distress syndrome (ARDS) and multi-organ failure. The main goal of my project is to elucidate the molecular cross-talk between alveolar epithelial cells, tissue-resident alveolar macrophages and pulmonary microvascular endothelial cells in order to develop an approach for treatment of SARS-CoV2-induced lung injury.
Dr. biol. hom. Learta Pervizaj-Oruqaj
Dr. biol. hom. Learta Pervizaj-Oruqaj
Project description: This project is dedicated to elucidate the intricate mechanisms governing lung damage and recovery during severe Influenza A virus (IAV) infections, with a primary focus on alveolar macrophages and their expression of Placenta-expressed transcript 1 (Plet1). The project’s objectives encompass the advancement of our comprehension of the macrophage-epithelial cell crosstalk, ultimately preserving lung function and mitigating severe viral pneumonia consequences. Additionally, we are committed to delve into Plet1’s mode of action and signal transduction pathways it engages, to provide profound insights into lung repair, paving the way for innovative approaches to address respiratory infections and improve patient outcomes.
Maximiliano Ferrero, PhD
Maximiliano Ferrero, PhDGuest Scientist
Project description: The immune response to severe respiratory infections can contribute to lung damage, but it is also crucial to promote repair once the infection is resolved. By unraveling the immune-epithelial cell cross talk, we study how alveolar macrophages mediate epithelial regeneration to preserve the lung during severe viral pneumonia.
Simon Carlile, PhD
Simon Carlile, PhD EU Researcher, Marie Skłodowska-Curie Global Postdoctoral Fellowship
Project description: The aim of my work is to understand phenotypic changes in innate immune cells, such as macrophages, post infection. Understanding these changes will provide key insights into the development of excessive inflammatory responses observed in many respiratory pathologies, such as COPD and Bronchiectasis.

PhD Students

Afaq Mushtaq
Afaq Mushtaq
Project description: Stem cells niches in the lung are known for promoting tissue regeneration and helping in the resolution of infection. However, the implication of aged stem cell niches is not yet fully understood in the context of influenza-infections. The aim of this project is to establish in vitro models to determine how the age-related reprogramming of the lung stem cell population affects the outcome of infection and how to modulate therapies to improve cellular function.
Muhammad Faizan Tariq
Muhammad Faizan Tariq
Project description: The iPSC derived human organoids mimic several structural and functional aspects of lung tissue, but the extent of their cellular fidelity and spatial organization remains insufficiently understood. To address this, the key aim of my project is to generate a comprehensive cellular and spatial atlas of human iPSC-derived lung organoids. This will facilitate their informed application in modeling respiratory infections, age-associated tissue remodeling, patient-specific pulmonary diseases and novel mechanistic insights into human lung development, homeostasis, and pathology.
Johanna Kohlhaas, MD
Johanna Kohlhaas, MD
Project description: Tuberculosis even nowadays remains one of the most relevant infectious diseases worldwide. About ¼ of the world population carries the latent infection, but only 5-10% of those transition into the active pulmonary disease, which is transmittable. The immune regulatory mechanisms of this transition are still not fully understood. The aim of this project is to determine the role of macrophages in the microenvironment of tuberculosis infection and their effect on disease progression or control. For this we will analyse the immune cell profiles of tuberculosis patients and implement the findings in a novel cell culture granuloma model.

Master Students

Ayesha Akter
Ayesha Akter
Project description: The study investigates whether recombinant Plet1 (rPlet1) can promote lung tissue repair and restore alveolar integrity following injury in an elastase-induced emphysema model. Using precision-cut lung slices (PCLS) as a physiologically relevant ex vivo system, we analyze how rPlet1 treatment influences structural preservation, inflammatory signaling, and epithelial regeneration after elastase-induced damage. The PCLS model allows us to monitor lung tissue responses in real time, maintaining the native architecture and cell–cell interactions of the lung environment. Through this study we aim to evaluate the therapeutic potential of rPlet1 as a regenerative molecule capable of counteracting emphysematous injury and supporting lung repair mechanisms.
Farhana Bithy
Farhana Bithy
Project description: The focus is on understanding how the absence of Placenta-expressed transcript 1 (Plet1) influences the susceptibility of the lung to emphysema development. Using an elastase-induced emphysema model, we employ precision-cut lung slices (PCLS) derived from Plet1 flox/tom and Plet1 knockout mice. By comparing the extent of tissue destruction, inflammatory responses, and repair signaling between genotypes, the project aims to define the contribution of Plet1 to maintaining alveolar stability and resilience against injury. These findings will help elucidate mechanisms underlying emphysema susceptibility and identify potential pathways for therapeutic intervention in chronic lung disease.

MD students

Klara Sophie Knippenberg, DZIF MD Program
Klara Sophie Knippenberg, DZIF MD Program
Project description: Tissue-resident alveolar macrophages (TR-AM) are crucial in defending against lung pathogens and influence the outcome of pulmonary infections. While severe viral infections can deplete TR-AM, their fate after bacterial pneumonia is less understood. This project aims to investigate the kinetics, phenotypic, and metabolic changes of TR-AM in various bacterial pneumonia models to better understand host defense mechanisms and identify new therapeutic targets.
Katharina Franz, JLU TRAINEE Program
Katharina Franz, JLU TRAINEE Program
Project description: Tissue-resident alveolar macrophages (TR-AM) are crucial in defending against lung pathogens and influence the outcome of pulmonary infections. While severe viral infections can deplete TR-AM, their fate after bacterial pneumonia is less understood. This project aims to investigate the kinetics, phenotypic, and metabolic changes of TR-AM in various bacterial pneumonia models to better understand host defense mechanisms and identify new therapeutic targets.
Maximilian Löwe
Maximilian Löwe
Project description: Passive transfer of broadly neutralizing anti-HIV-1 antibodies (bNAbs) protects against infection, making the elicitation of bNAbs like IOMA through vaccination a major goal of HIV-1 vaccine efforts. This highly collaborative project aimed to investigate the antibody response after sequential immunization in a mouse model with the goal of evaluating newly designed Env immunogens intended to elicit IOMA-like antibodies. Furthermore, it discusses mechanisms that may interfere with the development of antibody breadth and potency.

Technical staff

Larissa Hamann
Larissa Hamann
Florian Lück
Florian Lück
Julia Stark
Julia Stark
Josefine Guth
Josefine Guth

Laboratory Veterinarian

Sandra Rinnert
Sandra Rinnert

FACS Operator

Dr. Nelli Baal
Dr. Nelli Baal

FACS & Data Analyst

Olga Dakischew
Olga Dakischew

Study Nurses

Nicole Tewes
Nicole Tewes
Magda Zanella
Magda Zanella
Yuliia Vasylkevych
Yuliia Vasylkevych
Sonja Friese

Alumni

Margarida Barroso, PhD
Theresa Schäfer, PhD
Dr. med. Martin Langelage
Jun-Prof. Dr. Ana Ivonne Vazquez-Armendariz
Christin Peteranderl, PhD
Dr. rer. nat. Lucie Sauerhering
Jennifer Quantius, PhD
Dr. Carole Schmoldt
Dr. Julia Bespalowa
Balachandar Selvakumar, PhD
Lina Jankauskaite, MD PhD
Anna-Lena Ament, M.Sc.

Featured Publications

  • TNF superfamily member 14 drives post-influenza depletion of alveolar macrophages, enabling secondary pneumococcal pneumonia.

    18. March 2026

    J Clin Invest. Malainou C, Peteranderl C, Ferrero MR, Vazquez-Armendariz AI, Alexopoulos I, Franz K, […]

  • Cell type–specific efferocytosis determines functional plasticity of alveolar macrophages

    5. May 2025

    Sci Immunol. Better J, Estiri M, Wetstein M, Pervizaj-Oruqaj L, Malainou C, Ogungbemi-Alt V, […]

  • Alveolar macrophage-expressed Plet1 is a driver of lung epithelial repair after viral pneumonia

    2. January 2024

    Nat Commun. Pervizaj-Oruqaj L, Selvakumar B, Ferrero MR, Heiner M, Malainou C, Glaser RD, Wilhelm […]

  • Alveolar macrophages in tissue homeostasis, inflammation, and infection: evolving concepts of therapeutic targeting

    2. October 2023

    J Clin Invest. Malainou C, Abdin SM, Lachmann N, Matt U, Herold S. Alveolar […]
  • Cyclosporin A Reveals Potent Antiviral Effects in Preclinical Models of SARS-CoV-2 Infection

    15. April 2022

    Am J Respir Crit Care Med. Sauerhering L, Kuznetsova I, Kupke A, Meier L, Halwe […]

  • Multilineage murine stem cells generate complex organoids to model distal lung development and disease

    2. November 2020

    EMBO J. Vazquez-Armendariz AI, Heiner M, El Agha E, Salwig I, Hoek A, Hessler […]
  • Toward a universal flu vaccine

    21. February 2020

    Science. Herold S, Sander LE. Toward a universal flu vaccine. 2020 Feb 21;367(6480):852-853. doi: […]

Funding & Cooperation Partners

Herold Lab is always open for collaborations with partners from academia, industry, and the public sector. We are interested in translating our research findings into practice and jointly developing innovative solutions. Funding is a crucial part of our work, enabling us to conduct our research at the highest level. Therefore, we appreciate any contribution that supports us in achieving our goals. Please feel free to contact us for more information.