Metabolic Diversity in Campylobacter jejuni Enhances Specific Tissue Colonization

Abstract

Campylobacter jejuni is a leading cause of foodborne illness in industrialized countries. This pathogen exhibits significant strain-to-strain variability, which results in differences in virulence potential and clinical presentations. Here, we report that acquisition of the capacity to utilize specific nutrients enhanced the ability of a highly pathogenic strain of C. jejuni to colonize specific tissues. The acquisition of a gene encoding a gamma-glutamyltranspeptidase enabled this strain to utilize glutamine and glutathione and enhanced its ability to colonize the intestine. Furthermore, the acquisition of a DNA segment, which added a sec-dependent secretion signal to an otherwise cytoplasmic asparaginase, allowed this pathogen to utilize asparagine and to more efficiently colonize the liver. Our results reveal that subtle genetic changes in a bacterial pathogen result in significant changes in its ability to colonize specific tissues. In addition, these studies revealed remarkably specific nutritional requirements for a pathogen to effectively colonize different tissues.

ppGpp Conjures Bacterial Virulence

“…A physiological switch within host cells is thought to occur, such as a shift in respiration, which allows C. jejuni to adapt to its intracellular niche. Consistent with this, C. jejuni has evolved significant metabolic diversity that influences host colonization and tissue tropism (90).…”

Nucleases Encoded by the Integrated Elements CJIE2 and CJIE4 Inhibit Natural Transformation of Campylobacter jejuni

“…Besides the incomplete DRGH motif, the inactive C. jejuni proteins also appear to contain a degenerated signal peptide sequence which may hamper transport to the periplasm. Changes in protein localization (from cytoplasmic to periplasmic) can be beneficial to a host for some properties (17). However, we consider it unlikely that nucleases from DNase Ϫ strains are functionally expressed in the cytoplasm, as induced high-level expression in E. coli resulted in the cessation of growth (unpublished observation).…”

Amino Acid Homeostasis Modulates Salicylic Acid–Associated Redox Status and Defense Responses inArabidopsis

“…The Gln depletion in infected host tissues might also be due to the specific acquisition and usage of amino acids by the pathogen, as revealed in human pathosystems (Hofreuter et al, 2008;Blume et al, 2009), although it appears that this direct pathogen drain might contribute only partially to this depletion, especially during the early stages of infection. Interestingly, expression of plastidic GS2, the major isoform of GS for Gln biosynthesis in leaves, was found to be downregulated during pathogen infection and senescence, which, in turn, causes a Gln deficiency in the chloroplast, a major site for Gln biosynthesis in normal plants.…”