A5080821025- Reproductive tract infections research
- Inflammasome and immune disorders
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Urinary Tract Infections Management
- Phagocytosis and Immune Regulation
- Reproductive System and Pregnancy
- Adolescent Sexual and Reproductive Health
- Syphilis Diagnosis and Treatment
- Immune Response and Inflammation
- Sexual function and dysfunction studies
- Cell death mechanisms and regulation
- SARS-CoV-2 and COVID-19 Research
- Calcium signaling and nucleotide metabolism
- Yersinia bacterium, plague, ectoparasites research
- Streptococcal Infections and Treatments
- Heme Oxygenase-1 and Carbon Monoxide
- Hereditary Neurological Disorders
- Extracellular vesicles in disease
- Clostridium difficile and Clostridium perfringens research
- Escherichia coli research studies
- Gut microbiota and health
- Autoimmune Bullous Skin Diseases
- Toxin Mechanisms and Immunotoxins
- Kawasaki Disease and Coronary Complications
University of North Carolina at Chapel Hill
2012-2022
Oslo University Hospital
2017
Duke Medical Center
2011-2012
Duke University
2008-2011
Duke University Hospital
2011
Inflammasomes activate caspase-1 in response to cytosolic contamination or perturbation. This inflammatory caspase triggers the opening of GSDMD pore plasma membrane, resulting lytic cell death called pyroptosis. We had previously assumed that pyroptosis releases intracellular bacteria extracellular space. Here, we find viable instead remain trapped within cellular debris pyroptotic macrophages. trapping appears be an inevitable consequence how osmotic lysis ruptures and may also apply...
Interferon (IFN)-inducible guanylate binding proteins (GBPs) mediate cell-autonomous host resistance to bacterial pathogens and promote inflammasome activation. The prevailing model postulates that these two GBP-controlled activities are directly linked through GBP-dependent vacuolar lysis. It was proposed the rupture of pathogen-containing vacuoles (PVs) by GBPs destroyed microbial refuge simultaneously contaminated cell cytosol with activators inflammasomes. Here, we demonstrate...
Inflammasomes activate caspase‐1, initiating a lytic form of programmed cell death termed pyroptosis, which is an important innate immune defense mechanism against intracellular infections. We recently demonstrated in mouse infection model pyroptosis that instead releasing bacteria into the extracellular space, remain trapped within pyroptotic corpse, pore‐induced trap (PIT). This trapping mediates efferocytosis PIT and associated by neutrophils; are subsequently killed via neutrophil ROS....
The obligate intracellular pathogen Chlamydia trachomatis secretes effector proteins across the membrane of pathogen-containing vacuole (inclusion) to modulate host cellular functions. In an immunological screen for secreted chlamydial proteins, we identified CT049 and CT050 as potential inclusion membrane-associated proteins. These acidic, nonglobular are paralogously related passenger domain polymorphic protein PmpC and, like other Pmp highly among C. ocular urogenital strains. We...
During infection of epithelial cells, the obligate intracellular pathogen Chlamydia trachomatis secretes serine protease protease-like activity factor (CPAF) into host cytosol to regulate a range cellular processes through targeted proteolysis. Here we report development an in vitro assay for enzyme and discovery cell-permeable CPAF zymogen-based peptide inhibitor with nanomolar inhibitory affinity. Treating C. trachomatis-infected HeLa cells this prevented cleavage intermediate filament...
Herpes simplex virus type 1 (HSV-1) infection can manifest locally as mucocutaneous lesions or keratitis and also spread to the central nervous system cause encephalitis. HSV-1 establishes a lifelong latent neither cure nor vaccine is currently available. The innate immune response first line of defense against infection. Caspases gasdermins are important components immunity. family cysteine proteases, most which mediate regulated cell death. Gasdermins pore-forming proteins that trigger...