- Immune Cell Function and Interaction
- Tuberculosis Research and Epidemiology
- Asthma and respiratory diseases
- Pneumocystis jirovecii pneumonia detection and treatment
- Escherichia coli research studies
- Immune responses and vaccinations
- Mycobacterium research and diagnosis
- Macrophage Migration Inhibitory Factor
- Adenosine and Purinergic Signaling
- Immune Response and Inflammation
- Immunodeficiency and Autoimmune Disorders
- Bacteriophages and microbial interactions
- Antimicrobial Peptides and Activities
National Institute of Allergy and Infectious Diseases
2018-2022
National Institutes of Health
2018-2022
Research Center Borstel - Leibniz Lung Center
2020
German Center for Infection Research
2020
Host resistance to Mycobacterium tuberculosis (Mtb) infection requires the activities of multiple leukocyte subsets, yet roles different innate effector cells during are incompletely understood. Here we uncover an unexpected association between eosinophils and Mtb infection. In humans, decreased in blood but enriched resected human lung lesions autopsy granulomas. An influx is also evident infected zebrafish, mice, nonhuman primate granulomas, where they functionally activated degranulate....
Influx of eosinophils into the lungs is typically associated with type II responses during allergy and fungal parasitic infections. However, we previously reported that accumulate in lung lesions I inflammatory to Mycobacterium tuberculosis (Mtb) humans, macaques, mice, which they support host resistance. Here show migrate macaques mice as early one week after Mtb exposure. In this influx CCR3 independent instead requires cell-intrinsic expression oxysterol receptor GPR183, highly expressed...
Abstract IL-1R1 deficiency in mice causes severe susceptibility to Mycobacterium tuberculosis. Mice and macrophage cultures lacking display increased bacterial growth, suggesting that phagocytes may require IL-1R1–dependent antimicrobial signals limit intracellular M. tuberculosis replication directly. However, the myeloid-cell–intrinsic versus –extrinsic requirements for control infection have not been directly addressed. Using single-cell analysis of infected cells, competitive mixed bone...
Mycobacterium tuberculosis resides in the lungs various lesion types with unique microenvironmental conditions. This diversity is line heterogeneous disease progression and divergent drug efficiency. Fluorescent reporter strains can be used to decipher micromilieu guide future treatment regimens. Current reporters using replicating plasmids, however, are not suitable for long-term mouse infections or studies non-human primates. Using a combination of recombinant DNA protein optimization...
Abstract Signal peptide peptidase–like 2a (SPPL2a) is an aspartyl intramembrane protease essential for degradation of the invariant chain CD74. In humans, absence SPPL2a leads to Mendelian susceptibility mycobacterial disease, which attributed a loss dendritic cell (DC) subset conventional DC2. this study, we confirm depletion DC2 in lymphatic tissues SPPL2a−/− mice and demonstrate dependence on CD74 using CD74−/− mice. Upon contact with mycobacteria, bone marrow–derived DCs show enhanced...
ABSTRACT Host resistance to Mycobacterium tuberculos is infection requires the activities of multiple leukocyte subsets, yet roles different innate effector cells during tuberculosis are incompletely understood. Here we uncover an unexpected association between eosinophils and Mtb infection. In humans, decreased in blood but enriched resected human lung lesions autopsy granulomas. Influx also evident infected zebrafish, mice, nonhuman primate granulomas, where they functionally activated...
SUMMARY Influx of eosinophils into the lungs is typically associated with type-II responses during allergy, fungal and parasitic infections. However, we previously reported that accumulate in lung lesions type-I inflammatory to Mycobacterium tuberculosis (Mtb) humans, macaques, mice where they contribute host resistance. Here show migrate macaques as early one week after Mtb-exposure. In this influx was CCR3 independent instead required cell-intrinsic expression oxysterol-receptor GPR183,...