This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content

Next Article 

Infection and Immunity, November 2007, p. 5073, Vol. 75, No. 11
0019-9567/07/$08.00+0     doi:10.1128/IAI.01262-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

SPOTLIGHT

Articles of Significant Interest Selected from This Issue by the Editors

D-Ribose is not normally used by commensal strains of Escherichia coli for growth in the mouse intestine. However, Autieri et al. (p. 5465-5475) present data suggesting that two commensal strains of E. coli switch to using D-ribose in the intestine when L-fuculose-1-phosphate, an intermediate in the metabolism of L-fucose, accumulates. These findings demonstrate that an intermediate in the metabolism of one sugar can regulate the metabolism of a second sugar, resulting in more-efficient utilization of available limiting nutrients by E. coli to maintain a growth rate sufficient to avoid washout from the intestine.

The Obligate Intracellular Pathogen Coxiella burnetii Inhibits Host Apoptosis

Coxiella burnetii, the etiological agent of Q fever, invades mammalian cells and creates a lysosome-derived vacuole inside of which the pathogen replicates. Lührmann and Roy (p. 5282-5289) demonstrate that cells infected with C. burnetii are protected against several stimuli that normally kill mammalian cells by a programmed cell death pathway called apoptosis. Inhibition of apoptosis is an active process that requires bacterial protein synthesis, suggesting there are C. burnetii proteins that can disrupt this host cell autonomous response that would otherwise prematurely terminate the replicative cycle of this intracellular pathogen.

Novel Insights into the Mode and Genetics of Systemic Translocation of Salmonella enterica

Typhoidal salmonellosis has mostly been studied in mice and is believed to involve deposition of passively sampled bacteria in blood via phagocytes. By capturing migrating bacteria by cannulation, Pullinger et al. (p. 5191-5199) report that translocation of Salmonella enterica serovar Dublin from the intestines of its natural bovine host predominantly occurs cell-free via efferent lymph. By screening tagged mutants, early translocation was found to require the type III secretion system 1 (T3SS-1) (forced uptake) but not T3SS-2 or other virulence-associated loci. Lymphatic translocation is highly relevant in cattle, since the clones arriving at distal organs are the same as those present in nodes and lymph draining the gut.

Immunological Consequences of Mosaic Structure of Antigenic Variants

Bacterial and protozoal pathogens expand their potential repertoire of antigenic variants via segmental gene conversion, in which segments from multiple donor alleles are recombined to generate expression site mosaics. Zhuang et al. (p. 5185-5190) tracked the antibody response to Anaplasma marginale variants and determined that the immunogenicity was dynamic during infection. Specifically, epitopes that initially stimulated antibody when expressed following recombination of a single donor allele were no longer immunogenic when presented in a mosaic structure. Thus, the combinatorial diversity represented by segmental gene conversion results in immune escape, consistent with its use by a wide array of pathogens.

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content