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This auxin production is hypothesised to be a component of a bacterial colonisation mechanism whereby the auxin-induced stimulation of root growth and branching leads to an increase in the area available for bacterial colonisation and so increased C supply [ 19].
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While the knowledge of the molecular mechanism of colonisation has helped to understand special aspects of the infection, like the explicit tropism of gonococci for human tissues, the long-term consequences of engaging these receptors are still unknown.
We also examined its effect on gut microbiota, faecal calprotectin levels, and E coli colonisation, all implicated in the mechanism of disease.
The uropygial gland function as a defence mechanism to avoid colonisation and maintenance of pathogenic microorganisms on feathers, and thus protect birds from infections and feather degradation [ 20, 21, 25, 26].
To understand the selective forces responsible for phase shifting in these bacteria, which are not invariably pathogenic, it is important to consider its relevance to the commensal existence of these bacteria at an epidemiological level, as a mechanism to facilitate colonisation of genetically and immunologically diverse hosts.
Using hunting-based knowledge on colonization history and an information-theoretic approach, we evaluated support to four a priori hypotheses explaining mechanisms of wild boar colonisation in an agro-ecosystem: natural forested landscape as recolonization mechanism, and cultivated landscape, propagule pressure and climate change as invasion mechanisms.
For example, the contrasting life histories of birds and mammals may result in differences in the mechanisms of microbial colonisation.
Other essential mechanisms for the colonisation of the gastric mucosa participate in pH homeostasis [ 18]: H. bizzozeronii CIII-1 contains the periplasmic α-carbonic anhydrase orthologue HBZC1_14670, which contributes to the urease-dependent response to acidity in H. pylori [ 19], but lacks an orthologue for the β-carbonic anhydrase.
We also hypothesise that the intervention group compared to the control group will have (at one month): more diverse gut microbiota, lower faecal calprotectin levels, and less E. coli colonisation, thereby suggesting a potential pathophysiological mechanism in infant colic.
Previous work demonstrated host specificity in mice and begun to determine the mechanisms by which gut colonisation and host restriction is achieved.
48 Future work on the identification of the bacterial factor(s) responsible for PKC activation will give additional insights into the mechanisms of gastric mucosa colonisation by H pylori and could provide a comprehensive picture of host microbial interaction.
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