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Together, the metabolic host cell responses triggered by bacterial pathogens that are determined by the core response genes aim primarily at increasing antimicrobial activities and decreasing metabolic reactions that may provide essential nutrients to the pathogens, thus inhibiting their proliferation (termed nutriprive mechanisms) (Appelberg, However, bacterial pathogens may also trigger infection-promoting metabolic host responses that counteract these latter antimicrobial reactions of the host and provide protection and/or increased nutrient supply to the pathogen

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Germ-free and SURV-experiment mice did not exhibit enhanced IL-12/23p40 protein levels from B12 supplementation as observed in EPC-experiment mice