Infection and Immunity, July 2009, p. 2589, Vol. 77, No. 7
0019-9567/09/$08.00+0 doi:10.1128/IAI.00549-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
| SPOTLIGHT |
Articles of Significant Interest Selected from This Issue by the Editors
The K5 Capsule of the Probiotic Escherichia coli Strain Nissle 1917 Mediates Interactions with Epithelial Cells and Induces ChemokinesThe probiotic Escherichia coli strain Nissle 1917 expresses a K5 capsule. Hafez et al. (p. 2995-3003) demonstrate that the K5 capsule mediates interactions between Nissle 1917 and intestinal epithelial cells. The loss of the K5 capsule significantly reduced chemokine induction by Nissle 1917. Chemokine induction could be restored by addition of purified K5 to the mutant lacking the capsule, indicating that the K5 polysaccharide was mediating interactions between Nissle 1917 and intestinal epithelial cells. Maximal chemokine induction was generated by interactions between Nissle 1917 and the basolateral surfaces of epithelial cells, suggesting that Nissle 1917 is most effective in inducing chemokines where the epithelial barrier is disrupted.
Membrane Contact Induces Type III Secretion and Recruitment of IpaC to the Shigella flexneri Type III Secretion Apparatus Needle Tip
Shigella flexneri infection requires a type III secretion system that delivers invasion effectors into target cells. IpaD, at the tip of the Shigella type III secretion apparatus (TTSA) needle, senses environmental ligands to recruit the translocator IpaB to the needle tip. Epler et al. (p. 2754-2761) show that final induction of type III secretion occurs when IpaC is transported to the TTSA needle tip following bacterial contact with membranes rich in sphingomyelin and cholesterol. Thus, Shigella type III secretion induction occurs when IpaB and IpaC are inserted into the host cell membrane from a position at the TTSA needle tip.
Plasmodium falciparum-Induced Cellular Responses as Correlates of Immunity
Cellular cytokine responses may contribute to both immunity and risk of clinical malaria in Plasmodium falciparum infections. In a cohort study of children residing in a region of Papua New Guinea where malaria is endemic, Robinson et al. (p. 3033-3043) show that in vitro parasite-induced early tumor necrosis factor and gamma interferon responses are associated with a reduced incidence of clinical episodes, while interleukin-6 is associated with an increased incidence of such episodes. Monocytes/macrophages and 
-T cells predominantly mediated these responses, confirming an important role for early-intermediate cellular responses both in risk of disease and in development of immunity to symptomatic malaria.
Salmonella enterica Serovar Typhimurium Type III Secretion System Translocases Mediate Intimate Attachment to Nonphagocytic Cells
Type III secretion systems (TTSS) are central to the virulence of several pathogens, including Salmonella enterica serovar Typhimurium. TTSS deliver bacterial proteins into host cells, a process that requires the intimate association of bacteria with those cells. Lara-Tejero and Galán (p. 2635-2642) show that the protein translocases SipB, SipC, and SipD are required for this association. They also show that SipD is on the bacterial surface prior to contact with host cells, while SipB and SipC become surface exposed upon bacterial contact with target cells. They conclude that the coordinated deployment of the protein translocases mediates the TTSS-dependent intimate association of S. Typhimurium with host cells.
Prevention of Staphylococcus aureus Pneumonia by Novel Anti-Alpha-Hemolysin Antibodies
Staphylococcus aureus pneumonia is among the most common severe invasive diseases caused by this human pathogen. Vaccine-based targeting of the pore-forming cytotoxin alpha-hemolysin is a recently described strategy to prevent this disease, as the toxin is essential for pathogenesis in experimental infection. Extending these observations, Ragle and Bubeck Wardenburg (p. 2712-2718) describe two novel mouse monoclonal antibodies that target the N terminus of alpha-hemolysin, conferring protection against lethal S. aureus pneumonia. These antibodies prevent toxin oligomerization on the host cell membrane, defining a potent mechanism of inhibition that may be exploited for the future development of human immunotherapeutics.
Infection and Immunity, July 2009, p. 2589, Vol. 77, No. 7
0019-9567/09/$08.00+0 doi:10.1128/IAI.00549-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
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