Interactions between glycans and proteins have tremendous impact in biomolecular interactions. They are important for cell-cell interactions, proliferation and much more. Here, we emphasize the glycan-mediated interactions between pathogens and host cells. , responsible for a huge number of nosocomial infections, is especially the focus when it comes to glycan-derivatives as pathoblockers. We present a microwave assisted protecting group free synthesis of glycomonomers based on lactose, melibiose and fucose. The monomers were polymerized in a precipitation polymerization in the presence of NiPAm to form crosslinked glyco-nanogels. The influence of reaction parameters like crosslinker type or stabilizer amount was investigated. The gels were characterized in lectin binding studies using model lectins and showed size and composition-dependent inhibition of lectin binding. Due to multivalent presentation of glycans in the gel, the inhibition was clearly stronger than with unmodified saccharides, which was compared after determination of the glycan loading. First studies with revealed a surprising influence on the secretion of virulence factors. Functional glycogels may be in the future potent alternatives or adjuvants for antibiotic treatment of infections based on glycan interactions between host and pathogen.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6572176 | PMC |
http://dx.doi.org/10.3390/molecules24101865 | DOI Listing |
Sci Rep
January 2025
Department of Nephrology, The First Affiliated Hospital of Zhengzhou University, No.1 East Jianshe Road, Erqi District, Zhengzhou, 450052, China.
Increasing evidence points toward an essential role for complement activation in the pathogenesis of diabetic kidney disease (DKD). However, the precise molecular mechanisms remain unclear, and the pathway predominantly contributing to complement activation in DKD is of particular interest. In this study, the glomerular proteome, especially the profiles of the complement proteins, was analyzed in kidney biopsies from 40 DKD patients and 10 normal controls using laser microdissection-assisted liquid chromatography-tandem mass spectrometry (LMD-LC-MS/MS).
View Article and Find Full Text PDFPLoS One
January 2025
Lawrence Livermore National Laboratory, Physical and Life Science Directorate, Livermore, CA, United States of America.
Post-traumatic osteoarthritis (PTOA) is a painful joint disease characterized by the degradation of bone, cartilage, and other connective tissues in the joint. PTOA is initiated by trauma to joint-stabilizing tissues, such as the anterior cruciate ligament, medial meniscus, or by intra-articular fractures. In humans, ~50% of joint injuries progress to PTOA, while the rest spontaneously resolve.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Georgia, Athens, GA, USA.
Background: Inflammatory cells play a key role in the pathophysiology of AD and other neurodegenerative disorders. Glycans are known to mediate inflammatory cell activation and migration yet very little is understood about the expression of glycans, glycoproteins, and other glycoconjugates at the CP which serves as a gateway for peripheral immune cells into the brain. In a familial AD mouse model, we observed increased expression of Siglec-F-recognized glycans on CP epithelial cells.
View Article and Find Full Text PDFBackground: Microglia are the primary immune cells of the brain and represent the main line of defense against brain environmental insults. In recent years, microglia have been implicated in Alzheimer's disease (AD) pathogenesis by having interconnected yet opposing roles: beneficial as they clear amyloid beta (Aβ) and amyloid plaques, and detrimental as being responsible for synaptic and neuronal loss. These activities are tightly regulated by microglia receptors CD33 and TREM2.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Institute of Brain Sciene, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Background: Genome-wide association studies demonstrated that immune suppressive receptor CD33 variants are associated with high susceptibility to developing Alzheimer's disease (AD). Human CD33 (hCD33) regulates microglial immune response and clearance ability. However, the differential regulation of phagocytosis by human and mouse CD33 imposes constraints on utilizing the mouse model for investigating the role of CD33 in AD.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!