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Host–Biofilm Interactions at Mucosal Surfaces and Implications in Human Health
Published in Chaminda Jayampath Seneviratne, Microbial Biofilms, 2017
Nityasri Venkiteswaran, Kassapa Ellepola, Chaminda Jayampath Seneviratne, Yuan Kun Lee, Kia Joo Puan, Siew Cheng Wong
Molecules that specifically interact with ECM components such as fibronectin, collagen, laminin and elastin are commonly described as ‘microbial surface components recognising adhesive matrix molecules (MSCRAMMs)’ [87]. The expression of fibronectin-binding proteins could increase bacterial aggregation, suggesting that these proteins can promote the initiation of biofilm development. For example, mutant S. aureus lacking surface expression of fibronectin binding proteins (FnBPA and FnBPB) are defective in adhering to fibronectin-coated surfaces to form biofilms [88,89]. Similarly, two surface adhesins of E. faecium, SgrA and EcbA, showed binding to ECM components such as nidogen 1, nidogen 2, fibrinogen and collagen type V found in the basal lamina of mucosal surfaces [90]. In H. influenzae, an adhesin designated protein E was shown to bind vitronectin [91–93]. Mucin, a major glycoprotein component in mucus, could promote P. aeruginosa attachment and biofilm formation in vitro [94]. Glycoprotein-340 is another mucin-like protein found adsorbed to mucosal surfaces that could mediate the attachment of S. mutans and Streptococcus gordonii via surface adhesin SpaP [95,96] and SspA and SspB [97] respectively [98].
The extracellular matrix of the blood–brain barrier: structural and functional roles in health, aging, and Alzheimer’s disease
Published in Tissue Barriers, 2019
May J. Reed, Mamatha Damodarasamy, William A. Banks
Nidogens function in neural plasticity and one would predict levels of these glycoproteins are reduced in normal aging, which is characterized by decreased plasticity in most organs.122 Indeed, results from Western blotting and immunocytochemistry experiments showed a significant reduction in nidogen 2 in the cortex and striatum during normal aging in mice.91 In contrast, studies in humans showed an increase in nidogen 2 with age that might reflect differences in techniques, regions and concurrent presence of CAA.90
Spatial composition and turnover of the main molecules in the adult glomerular basement membrane
Published in Tissue Barriers, 2023
David W. Smith, Azin Azadi, Chang-Joon Lee, Bruce S. Gardiner
After 12 weeks, we note that nidogen 1 and nidogen 2 had N-14 contents of 9% and 31%, respectively,77 suggesting half-lives of around 24 days and 49 days, respectively. These data are consistent with nidogen 2 being produced mainly by podocytes (diffusion across the lamina densa would presumably explain its somewhat longer half-life), and nidogen 1 being produced by endothelial cells.