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Several strategies have been proposed to create refractory mosquitoes, including silencing the expression of essential molecules through RNAi in host cells invaded by the parasite, expression of toxins or single chain antibodies in close proximity to the invading parasite, and production of peptides to out-compete parasite binding to host epithelial receptors[2], [12], [13], [14], [15], [16].
Among these apical organelle associated proteins, P1 and P30 have been previously shown by us and others to elicit immunological responses in human and are also involved in binding to host epithelial receptors [ 17- 21].
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Other unidentified factors are also probably required for the intimate binding of SFBs to host epithelial cells, and many of such factors may be encoded by SFB-specific genes, most of which are of unknown function (Fig. 4).
In addition to mere binding to host cells, CEACAM engagement triggers endocytosis of the bacteria into epithelial cells and transcytosis of microorganisms through intact epithelial layers [ 53, 58, 59].
In addition, this was an in vitro study and increased attachment to host epithelial cells would need to be validated in vivo.
The pilus-associated adhesin PilC1 plays a critical role in mediating attachment to host epithelial target cells [22], [23].
CagA is then able to interact with phosphatidylserine and gain entry to host epithelial cells [ 9].
The key event in these infections is the adhesion of C. glabrata to host epithelial cells via epithelial adhesin (EPA) genes.
For example, parasite surface receptors that promote adherence to host epithelial cells may be key factors in pathogenesis.
Knock-down of CEACAM1 interferes with binding to lung epithelial cells, whereas chemical or pharmacological disruption of host protein glycosylation does not abrogate CEACAM1 recognition by non-opaque meningococci.
Meningococcal pathogenesis relies on the ability of the bacteria to break host epithelial or endothelial cellular barriers.
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