infection causes skin ulcers, typically found in localized cutaneous leishmaniasis (LCL). This tissue pathology associates with different modalities of cell necrosis, which are subverted by the parasite as a survival strategy. Herein we examined the participation of necroptosis, a specific form of programmed necrosis, in LCL lesions and found reduced RIPK3 and PGAM5 gene expression compared to normal skin. Assays using infected macrophages demonstrated that the parasite deactivates both RIPK3 and MLKL expression and that these molecules are important to control the intracellular replication. Thus, LCL-related necroptosis may be targeted to control infection and disease immunopathology.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6172319 | PMC |
| http://dx.doi.org/10.3389/fmicb.2018.02283 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
CSFV restricts necroptosis to sustain infection by inducing autophagy/mitophagy-targeted degradation of RIPK3.
Microbiol Spectr
January 2024
College of Veterinary Medicine, South China Agricultural University, Guangzhou, China.
CSFV infection in pigs causes persistent high fever, hemorrhagic necrotizing multi-organ inflammation, and high mortality, which seriously threatens the global swine industry. Cell death is an essential immune response of the host against pathogen invasion, and lymphopenia is the most typical clinical feature in the acute phase of CSFV infection, which affects the initial host antiviral immunity. As an "old" virus, CSFV has evolved mechanisms to evade host immune response after a long genetic evolution.
View Article and Find Full Text PDFInteraction among inflammasome, PANoptosise, and innate immune cells in infection of influenza virus: Updated review.
Immun Inflamm Dis
September 2023
Intensive Care Unit, Huzhou Third Municipal hospital, The Affiliated hospital of Huzhou University, Huzhou, China.
Background: Influenza virus (IV) is a leading cause of respiratory tract infections, eliciting responses from key innate immune cells such as Macrophages (MQs), Neutrophils, and Dendritic Cells (DCs). These cells employ diverse mechanisms to combat IV, with Inflammasomes playing a pivotal role in viral infection control. Cellular death mechanisms, including Pyroptosis, Apoptosis, and Necroptosis (collectively called PANoptosis), significantly contribute to the innate immune response.
View Article and Find Full Text PDFeffector SopF regulates PANoptosis of intestinal epithelial cells to aggravate systemic infection.
Gut Microbes
February 2023
Department of Medical Microbiology, School of Biology and Basic Medical Science, Suzhou Medical College of Soochow University, Suzhou, China.
SopF, a newly discovered effector secreted by pathogenicity island-1 type III secretion system (T3SS1), was reported to target phosphoinositide on host cell membrane and aggravate systemic infection, while its functional relevance and underlying mechanisms have yet to be elucidated. PANoptosis (pyroptosis, apoptosis, and necroptosis) of intestinal epithelial cells (IECs) has been characterized as a pivotal host defense to limit the dissemination of foodborne pathogens, whereas the effect of SopF on IECs PANoptosis induced by is rather limited. Here, we show that SopF can attenuate intestinal inflammation and suppress IECs expulsion to promote bacterial dissemination in mice infected with serovar Typhimurium (.
View Article and Find Full Text PDFProgrammed Cell Death-Dependent Host Defense in Ocular Herpes Simplex Virus Infection.
Front Microbiol
April 2022
Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA, United States.
Herpes simplex virus type 1 (HSV1) remains one of the most ubiquitous human pathogens on earth. The classical presentation of HSV1 infection occurs as a recurrent lesions of the oral mucosa commonly refer to as the common cold sore. However, HSV1 also is responsible for a range of ocular diseases in immunocompetent persons that are of medical importance, causing vision loss that may result in blindness.
View Article and Find Full Text PDFActivation and manipulation of inflammasomes and pyroptosis during bacterial infections.
Biochem J
April 2022
Department of Biochemistry, University of Lausanne, Epalinges, Switzerland.
Following detection of pathogen infection and disrupted cellular homeostasis, cells can activate a range of cell death pathways, such as apoptosis, necroptosis and pyroptosis, as part of their defence strategy. The initiation of pro-inflammatory, lytic pyroptosis is controlled by inflammasomes, which respond to a range of cellular perturbations. As is true for many host defence pathways, pathogens have evolved multiple mechanisms to subvert this pathway, many of which have only recently been described.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!