Infection and Immunity, November 2006, p. 6025-6026, Vol. 74, No. 11
0019-9567/06/$08.00+0 doi:10.1128/IAI.01476-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
| SPOTLIGHT |
Articles of Significant Interest Selected from This Issue by the Editors
Zebrafish Model for Unraveling the Basis of Mycobacterial PersistenceThe understanding of Mycobacterium tuberculosis physiology and antibiotic tolerance during chronic infection has been hampered by a lack of facile animal models that faithfully recapitulate human disease. Swaim et al. (p. 6108-6117) describe a Mycobacterium marinum-zebrafish model of tuberculosis that develops caseating granulomas similar to human tuberculosis lesions. Moreover, they demonstrate that adaptive immunity plays the same critical role in controlling fish tuberculosis as it does in mammalian systems. Zebrafish are amenable to large-scale genetic and small molecule screens and should facilitate both the understanding of mycobacterial physiology in the host and the discovery of new antimycobacterial agents.
Role of Inflammation on Tight Junctions during Bacterial Infections
Tight junctions are highly modified during attaching and effacing (A/E) bacterial infections. These structures are also thought to be altered by inflammation. To investigate the impact of the inflammatory response during in vivo A/E bacterial infection, Guttman et al. (p. 6075-6084) utilized the A/E pathogen Citrobacter rodentium and demonstrate that tight junction transmembrane proteins, ultrastructural morphology, and barrier function are unaltered during inflammation. Any observed tight junction modifications required the intimate attachment of bacteria directly to intestinal epithelial cells. These findings indicate that intestinal inflammation during A/E bacterial infections does not impact tight junctions.
Escape from the Phagosome Enhances the Potency of Listeria monocytogenes-Specific CD8+ T Cells
Almost 20 years ago, it was established that Listeria monocytogenes strains lacking listeriolysin O (LLO) do not elicit protective immunity due to an inability to directly deliver protein into the major histocompatibility complex class I pathway. Bahjat et al. (p. 6387-6397) demonstrate that cross-presentation of antigen from L. monocytogenes lacking LLO does, in fact, lead to robust CD8+-T-cell responses. Instead, they show that phagosomal escape is required for optimal dendritic cell activation and integration of CD40 signaling in vivo, enhancing the potency of the resulting L. monocytogenes-specific CD8+ T cells. These findings highlight the importance of innate immune signaling in shaping the subsequent adaptive immune response.
African Trypanosomes Benefit from Tsetse Fly Saliva for the Onset of Infection
Upon inoculation into the mammalian host as well as during the development of a systemic infection, trypanosomes become exposed to proinflammatory immune effectors that help to control parasitemia. Caljon et al. (p. 6324-6330) demonstrate that during tsetse fly feeding, salivary components deposited together with the parasites accelerate the onset of infection. This effect is correlated with reduced local and systemic inflammatory responses. The presented findings contribute to our understanding of vector-host interactions that affect the transmission efficiency of trypanosomes by the blood-feeding tsetse fly.
To Have or Have Not: Heme and Iron Acquisition from Hemoglobin-Haptoglobin in Virulence of Haemophilus influenzae in Invasive Disease
Restriction of extracellular heme and iron availability is an important component of vertebrate innate immunity. The opportunistic human pathogen Haemophilus influenzae requires both of these micronutrients for aerobic growth and has evolved multiple, redundant mechanisms to acquire them from host sources. Seale et al. (p. 6213-6225) demonstrate that hgp genes encoding outer membrane proteins that bind hemoglobin and hemoglobin-haptoglobin along with genes of the hxu operon contribute importantly to virulence in the rat model of invasive disease and provide evidence that the virulence effects are age dependent. These findings illustrate the complex competition between bacterium and host for heme/iron during pathogenesis.
Novel Role for a Streptococcal Penicillin-Binding Protein in Evading Host Innate Immunity
Evasion of host immune defenses is critical for the progression of invasive infections caused by bacterial pathogens such as group B streptococcus (GBS). While penicillin-binding proteins are traditionally known for their role in peptidoglycan biosynthesis, Hamilton et al. (p. 6179-6187) now show that they can also promote resistance of GBS to antimicrobial peptides of the innate immune system. This represents a novel function for this class of surface proteins and adds to the growing body of literature linking resistance to antimicrobial peptides with bacterial virulence.
Infection and Immunity, November 2006, p. 6025-6026, Vol. 74, No. 11
0019-9567/06/$08.00+0 doi:10.1128/IAI.01476-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
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