Infection and Immunity, June 2009, p. 2241, Vol. 77, No. 6
0019-9567/09/$08.00+0 doi:10.1128/IAI.00412-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
| SPOTLIGHT |
Articles of Significant Interest Selected from This Issue by the Editors
Salmonella Colitis Is Possible without the Lipopolysaccharide O AntigenLipopolysaccharide is the major constituent of the outer membrane of gram-negative bacteria. This large glycolipid contains the O antigen, a long chain of oligosaccharide repeats. O-antigen mutants are viable, but pathogens with a deficiency in O-antigen biosynthesis are generally avirulent. This is attributable to higher complement susceptibility and (presumably) to malfunctioning of proteins anchored in the outer membrane. However, Ilg et al. (p. 2568-2575) observed that an O-antigen-deficient Salmonella enterica serovar Typhimurium mutant can invade host cells and cause colitis in mice. This surprising finding shows that the O antigen is not essential for two phenotypes attributed to the Salmonella pathogenicity island 1 type III secretion system.
Approaching a Vaccine against Placental Malaria by Induction of Parasite Adhesion-Inhibitory Antibodies
Malaria during pregnancy is a major cause of maternal anemia, stillbirth, and delivery of low-birth-weight children. The malaria parasite Plasmodium falciparum adheres in the placenta through an interaction between a very large parasite protein (VAR2CSA) expressed on erythrocytes and chondroitin sulfate A (CSA) present in the placenta. Naturally acquired immunity is mediated by anti-VAR2CSA antibodies which inhibit the binding of parasites to CSA in the placenta. Nielsen et al. (p. 2482-2487) generated rat antibodies against a large panel of recombinant VAR2CSA proteins and identified a single domain of VAR2CSA which induced antibodies that strongly blocked parasite adhesion. These antibodies also effectively blocked the adhesion of heterologous P. falciparum parasites to CSA. The data demonstrate that it is feasible to develop an adhesion-blocking vaccine based on a small recombinant part of VAR2CSA.
Bacterial Nuclear Effector Regulates Host Cell Gene Expression
Intracellular bacteria survive within defense cells largely dependent on their ability to modulate the host's defense response. While interactions of bacteria with host cells can alter signaling pathways and host response, interactions mediated by bacterial effectors translocated into the host cell also lead to transcriptional and functional alterations. Garcia-Garcia et al. (p. 2385-2391) show that the nuclear effector AnkA of Anaplasma phagocytophilum interacts with AT-rich sequences of the host chromatin to alter host gene expression. Chromatin alterations associated with effector binding suggest that bacteria can regulate host cell gene expression by epigenetic mechanisms.
Infection and Immunity, June 2009, p. 2241, Vol. 77, No. 6
0019-9567/09/$08.00+0 doi:10.1128/IAI.00412-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
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