Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add more filters










Database
Language
Publication year range
1.
Viruses ; 13(7)2021 07 01.
Article in English | MEDLINE | ID: mdl-34372495

ABSTRACT

The enteric human adenoviruses of species F (HAdVs-F), which comprise HAdV-F40 and HAdV-F41, are significant pathogens that cause acute gastroenteritis in children worldwide. The early transcription unit 3 (E3) of HAdVs-F is markedly different from that of all other HAdV species. To date, the E3 proteins unique to HAdVs-F have not been characterized and the mechanism by which HAdVs-F evade immune defenses in the gastrointestinal (GI) tract is poorly understood. Here, we show that HAdV-F41 infection of human intestinal HCT116 cells upregulated the expression of MHC class I-related chain A (MIC A) and MIC B relative to uninfected cells. Our results also showed that, for MIC B, this response did not however result in a significant increase of MIC B on the cell surface. Instead, MIC B was largely sequestered intracellularly. Thus, although HAdV-F41 infection of HCT116 cells upregulated MIC B expression, the ligand remained inside infected cells. A similar observation could not be made for MIC A in these cells. Our preliminary findings represent a novel function of HAdVs-F that may enable these viruses to evade immune surveillance by natural killer (NK) cells in the infected gut, thereby paving the way for the future investigation of their unique E3 proteins.


Subject(s)
Adenoviridae/pathogenicity , Growth Differentiation Factor 15/classification , Growth Differentiation Factor 15/genetics , Intercellular Signaling Peptides and Proteins/genetics , Adenoviridae/immunology , GPI-Linked Proteins/genetics , HCT116 Cells , Humans , Phylogeny , Sequence Analysis, DNA
2.
Dev Comp Immunol ; 109: 103698, 2020 08.
Article in English | MEDLINE | ID: mdl-32289326

ABSTRACT

GDF15 is frequently detected in patients suffering from various diseases, especially those associated with pro-inflammatory processes and/or metabolic disorders. Accordingly, sepsis, whose major complications are related to metabolic alterations and systemic inflammation, significantly increases the secretion of GDF15. Indeed, this cytokine could be considered a marker of sepsis severity. However, until the last several years, the involvement of GDF15 in these disorders had not been widely characterized. In mice, GDF15 was recently described as a pivotal inducer of sepsis tolerance by mediating metabolic alterations that reduce tissue damage. In this work we describe a zebrafish gdf15 gene. We found that gdf15 follows an expression pattern similar to that observed in mammals, being highly expressed in the liver and kidney and induced after pro-inflammatory stimuli. Moreover, larvae overexpressing gdf15 were more resistant to bacterial and viral challenges without affecting the pathogen load. Consequently, Gdf15 also protected zebrafish larvae against LPS-induced mortality. As in mice, zebrafish Gdf15 seems to induce sepsis tolerance by altering the metabolic parameters of the individuals.


Subject(s)
Disease Models, Animal , Growth Differentiation Factor 15/genetics , Sepsis/genetics , Zebrafish Proteins/genetics , Aeromonas hydrophila/physiology , Amino Acid Sequence , Animals , Base Sequence , Gene Expression Profiling/methods , Growth Differentiation Factor 15/classification , Growth Differentiation Factor 15/metabolism , Host-Pathogen Interactions , Humans , Larva/genetics , Larva/metabolism , Larva/microbiology , Lipopolysaccharides , Mice , Phylogeny , Sepsis/chemically induced , Sepsis/microbiology , Survival Analysis , Zebrafish Proteins/classification , Zebrafish Proteins/metabolism
SELECTION OF CITATIONS
SEARCH DETAIL
...