Articles of Significant Interest Selected from This Issue by the Editors

doi:10.1128/IAI.06344-11

DOI: 10.1128/IAI.06344-11

Novel Mechanism Used by an Encapsulated Bacterial Pathogen To Avoid Phagocytosis

Bacterial capsular polysaccharides (CPSs) have been hitherto considered a physical barrier that protects bacteria from destruction by immune cells. Houde et al. (p. 506–517) demonstrate in the zoonotic agent Streptococcus suis type 2 that the sialic acid-rich CPS plays a more dynamic role than simply acting as a protective coat. In fact, S. suis CPS actively disrupts essential cellular processes involved in phagocytosis. This work defines a novel mechanism, disruption of lipid microdomains by bacterial CPS, that prevents the recognition of bacterial patterns by signaling platforms at the interaction points of the bacterium with the macrophage membrane.

Evidence for an Additional Human Complement Factor H-Dependent Mechanism of Evasion of Innate Immunity by Meningococci

Neisseria meningitidis binds the complement downregulating protein factor H (fH), which enables the organism to evade host defenses. Two fH ligands, factor H binding protein (fHbp) and neisserial surface protein A (NspA), are known to bind specifically to human fH. Vu et al. (p. 643–650) developed a human fH transgenic infant rat model to investigate the effect of human fH on meningococcal bacteremia. Surprisingly, human fH transgenic rats developed bacteremia after challenge with both the wild type and an isogenic ΔfHbp ΔNspA mutant. While both strains were killed by normal rat serum, the addition of human fH permitted survival. The results imply the existence of an additional human fH-dependent mechanism of evasion of innate immunity.

Toll-Like Receptor 9-Dependent Activation of Bone Marrow-Derived Dendritic Cells by URA5 DNA from Cryptococcus neoformans

Toll-like receptor 9 (TLR9) is involved in the recognition of microbial DNA by immune cells. Cryptococcus neoformans DNA is sensed by dendritic cells (DCs) using this molecule, resulting in the activation of immune response and protection from this infection. Tanaka et al. (p. 778–786) demonstrate that a PCR-amplified URA5 gene fragment from C. neoformans induces interleukin-12 p40 production and CD40 expression by bone marrow-derived DCs and finds DNA motifs responsible for this activity, which are different from a canonical CpG motif in some features. These results suggest that the C. neoformans URA5 gene activates immune cells through a TLR9-mediated signaling pathway using a mechanism that may be independent of the CpG motif.

Prolonged In Vivo Growth Drives Bacterial Adaptation to Host Environments

During asymptomatic bacteriuria (ABU), Escherichia coli stably colonizes the urinary tract in a manner closely resembling commensalism. The prototype ABU strain 83972 has a smaller genome than uropathogenic E. coli that contains deletions or point mutations in several virulence genes, suggesting programmed reductive evolution within human hosts. Salvador and colleagues (p. 668–678) extend this concept by analysis of community-acquired ABU strains isolated during a population-based screen and hospital strains using extensive genotyping and phenotyping. Typical virulence traits were frequently attenuated, supporting loss of expression or decay of virulence genes as an adaptation to host environments.