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Next we wanted to investigate if bacterial surface component(s) and/or bacterial active process(s) are required to be present for cellular uptake.
Adhesion is mediated by a bacterial surface component called MSCRAMM (microbial surface components recognizing adhesive matrix molecules) [ 31].
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While the exact mechanism for escaping phagocytosis is unclear, it may occur because capsules make bacterial surface components more slippery, helping the bacterium to escape engulfment by phagocytic cells.
Under the same conditions discussed above, the effects of bacterial surface components LPS and LTA on the activity of antibiotics were investigated.
In all, these data suggest that other bacterial surface components, in addition to HCP are present under these growth conditions that promote cytokine production (Fig. 8A and B).
The binding of free bacterial surface components (e.g. LPS and LTA) to polycationic antibiotics like polymyxin B may be beneficial to the host in terms of suppressing inflammation however it will compromise the antibacterial effect of the antibiotic.
More recent ex vivo and in vitro studies have ascribed additional functions to M protein, including epithelial cell adhesion [8], [9], formation of toxic soluble complexes with fibrinogen (Fg) [10], induction of T-regulatory cells [11], acquisition of surface-localized plasmin activity [12], and camouflaging of other bacterial surface components [13].
The pathogenicity of Staphylococcus aureus depends on various bacterial surface components and extracellular proteins.
Adhesion associated PFAMs were identified by searching the PFAM database release 26.0 [ 61] entries with various keywords related to adhesion, host tissue components, and bacterial surface components, and by manual examination of the literature.
Since formaldehyde fixed L. casei had the same inhibitory effect on IP-10 secretion as live bacteria, active interaction between bacteria and IEC is not necessary for the inhibitory effect, suggesting a bacterial cell surface component as the effective probiotic structure.
SpA can prevent phagocytosis by binding the complement binding portion (Fcγ) of functional antibodies thus hindering the antibody binding to bacterial cell surface components and subsequent complement dependent uptake of bacteria by phagocytic cells.
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