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These results demonstrated the role of the developmental stage of host embryos that arguably may be even more important than optimal combinations of ES cell and host embryo strains [25], [45].
Thus, as in the case of mammalian skin, TG-dependent protein crosslinking may be involved in the initial stage of host defense in the sub-cuticular epidermis of arthropods.
Character displacement at early stage of host colonisation should make infection more efficient by preventing competition for habitat between strains [ 49, 50].
Haustorium-forming fungi and oomycetes secrete many proteins from the haustoria into the extrahaustorial matrix during the parasitic stage of host infection, subsequently, a subset of proteins are further transported into the host cell [ 37].
Symbiotic bacteria (endosymbionts) are transmitted maternally to the offsprings and, at an early stage of host embryogenesis, these bacteria induce the differentiation of specialized host cells (the bacteriocytes) that house the bacteria, protect them from the host immune system [ 4, 5], and form a symbiotic organ (the bacteriome) that persists throughout the larval stages [ 6].
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Especially at this stage of host-pathogen interaction studies, many things are still unknown; therefore we can not easily get a conclusion that some compartments that seem not obvious to directly interact with pathogens are wrong and needed to be removed.
We have successfully established a novel leptospirosis guinea pig model through epicutaneous inoculations route, which replicates a natural course of infection and appears to be an alternative way to investigate the pathogenesis of leptospirosis, especially in terms of early stage of host-pathogen interactions.
Accordingly, upregulation of tyrosine biosynthesis genes of the endosymbiont was detected during the pupal stage of hosts and Blochmannia may thus supplement the host with tyrosine [ 19].
Bacterial counts were obtained from freshly collected blood samples, thus representing immediate snapshots of the early stages of host invasion.
We focused our study on the first 24 h of induction, to observe the changes that L. interrogans promoters undergo during the early stages of host invasion.
VirB is activated in the early stages of host cell infection, and blocking early acidification inhibits both expression of virB and Brucella survival [9].
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Justyna Jupowicz-Kozak
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