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SPOTLIGHT

Articles of Significant Interest Selected from This Issue by the Editors

The pathogenesis of melioidosis, an important cause of sepsis in Southeast Asia, is still largely unknown. Wiersinga et al. (p. 3739-3746) now demonstrate the important role of interleukin-18 (IL-18) in host defense against this dangerous pathogen. In patients with melioidosis, levels of IL-18 and IL-18 binding protein are elevated and correlate with mortality. Using a mouse model of melioidosis, the authors demonstrate that IL-18 gene-deficient mice show accelerated mortality accompanied by enhanced bacterial growth in their organs. These findings indicate that the enhanced production of IL-18 is an essential part of a protective immune response to this severe infection.

Biofilm Production in Acute Infections Independent of Cell-to-Cell Signaling

Biofilms have been studied intensely in the context of bacterial pathogenesis and play important roles in persistence and antibiotic resistance in chronic infections. Bacterial cell-to-cell communication, or quorum sensing, is thought to facilitate coordinated biofilm production. Schaber et al. (p. 3715-3721) demonstrate that the opportunistic pathogen Pseudomonas aeruginosa forms biofilms in a acute-infection murine model as soon as 8 h after infection despite the lack of a functional quorum-sensing system. These findings indicate that biofilms are not unique to chronic infections and can form extremely rapidly in vivo independent of quorum sensing.

Different Types of T Cells Are Associated with Recombinant Adenovirus 35 Tuberculosis Vaccine-Induced Protection against Tuberculosis

The correlate of protection in tuberculosis is not resolved. Whether gamma interferon-producing CD4 or CD8 T cells are the major player in the protection has been a matter of numerous debates. Using identified T-cell epitopes as a readout in two mouse strains, Radoevi et al. (p. 4105-4115) demonstrate that both CD4 and CD8 T cells are associated with the protective ability of a recombinant adenovirus 35 tuberculosis vaccine. The finding that protection is achieved with different T cells in animals of different genetic backgrounds is promising when considering the vaccination of a heterogenous human population.

Clonal Invasion and Abscess Formation by Yersinia enterocolitica

Yersinia enterocolitica is a common cause of food-borne gastrointestinal disease. In the oral-infection mouse model, yersiniae replicate in the small intestine, invade Peyer's patches of the distal ileum, and disseminate to the liver and spleen where they replicate extracellularly and form microabscesses. Oellerich et al. (p. 3802-3811) demonstrate that these microabscesses in Peyer's patches, liver, and spleen are exclusively monoclonal, indicating that a single bacterium is able to initiate abscess formation. Very few clonal microabscesses are found in Peyer's patches, indicating that only a very small number of yersiniae invade and establish abscesses in Peyer's patches. The requirement for only a very few yersiniae in the process is due to both Yersinia- and host-specific factors.

Biofilms Protect Mycoplasmas from Innate Immunity

As mycoplasmas lack a cell wall, they might be expected to be sensitive to the lytic effects of complement and antimicrobial peptides, such as gramicidin. Simmons and Dybvig (p. 3696-3699) show that mycoplasmal cells become resistant to complement and gramicidin when they are encased in a biofilm. The resistant cells were densely packed into the tower structures of the biofilm. In contrast, sensitive mycoplasmas were located in regions of the biofilms where they were freely accessible to complement or gramicidin. These results suggest that the mycoplasmas may shield themselves from the immune system by forming tight associations with each other.

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