Infection and Immunity, December 2008, p. 5437, Vol. 76, No. 12
0019-9567/08/$08.00+0 doi:10.1128/IAI.01271-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.
| SPOTLIGHT |
Articles of Significant Interest Selected from This Issue by the Editors
Modification of Lipooligosaccharide Enhances Meningococcal Adhesion to Human Endothelial and Epithelial CellsAlthough many pathogenic mechanisms of Neisseria meningitidis, a gram-negative agent of septicemia and meningitis, have been elucidated, the biological role of phosphoethanolamine (PEA) modification of lipooligosaccharide (LOS) remains unclear. Takahashi et al. (p. 5777-5789) show that disruption of the lptA gene encoding the PEA transferase for 4' lipid A results in decreased adherence to human endothelial and epithelial cells. The effect of LptA was independent of other identified adhesins, such as pili and Opc. This study elucidates a new physiological role of modification of LOS with PEA by LptA that enhances N. meningitidis adhesion to host cells.
T Helper 2 Responses Drive Pulmonary Pathology in Nippostrongylus brasiliensis Infection
Nematode infections are characterized by interleukin-4 (IL-4)-promoted T helper 2 (TH2) responses, believed to be beneficial for host defense mechanisms. CD4+ T-cell-specific IL-4R
-deficient mice, established using the Cre/loxP system, were infected with the rodent hookworm Nippostrongylus brasiliensis in a loss-of-function in vivo approach. Mearns et al. (p. 5535-5542) show that impairment of IL-4-promoted TH2 differentiation had no influence on worm expulsion. However, pulmonary pathology caused by larval migration through the lung was ameliorated in infected CD4+ T-cell-specific IL-4R-deficient mice, as demonstrated by reduced goblet cell hyperplasia, eosinophil and lymphocyte recruitment, lymphocyte localization, and TH2 cytokine production.
The Cytosolic Pathogen Francisella tularensis Takes Advantage of the Early Phagosomal Environment To Enhance Expression of Its Virulence Attributes
Francisella tularensis relies on intracellular proliferation within the cytosol of host cells to cause tularemia. Phagosomal escape is an early and essential step in the Francisella intracellular cycle, but the underlying mechanisms of this process remain unknown. Chong et al. (p. 5488-5499) show that trafficking of Francisella through an early, acidified phagosome provides cues that potentiate the phagosomal escape process and induce the expression of proteins encoded by the Francisella pathogenicity island, a chromosomal locus required for intracellular growth. This study highlights how efficiently this pathogen responds to its intracellular environment, a feature essential to its high level of virulence.
Targeted Mutagenesis in Pathogenic Leptospira Species
Leptospirosis is a spirochetal zoonosis that has emerged to become a major cause of hemorrhagic fever worldwide. The lack of tools to genetically manipulate the Leptospira agent has been a barrier to understanding the pathogenesis of this disease. Croda et al. (p. 5826-5833) used allelic exchange in Leptospira interrogans to construct mutations of the ligB gene, which encodes a member of the superfamily of bacterial immunoglobulin-like proteins. Gene disruption was not associated with loss-of-virulence phenotypes in animal models of infection. However, the work provides the first evidence for site-directed homologous recombination in pathogenic Leptospira species and makes it feasible to identify virulence factors in this pathogen.
Infection and Immunity, December 2008, p. 5437, Vol. 76, No. 12
0019-9567/08/$08.00+0 doi:10.1128/IAI.01271-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.
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