Previous Article | Next Article 
Infection and Immunity, September 2009, p. 3520-3521, Vol. 77, No. 9
0019-9567/09/$08.00+0 doi:10.1128/IAI.00803-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
| SPOTLIGHT |
Articles of Significant Interest Selected from This Issue by the Editors
Antibiotics Trigger Clostridium difficile Disease and TransmissionClostridium difficile, a major cause of antibiotic-associated diarrhea, produces highly resistant spores that contaminate hospital environments and facilitate efficient disease transmission. Antibiotic treatment that spares C. difficile but suppresses the intestinal microbiota allows C. difficile to proliferate, thereby potentially leading to intestinal inflammation and clinical disease. Here Lawley et al. (p. 3661-3669) show that antibiotics trigger C. difficile disease in colonized mice by reducing the intestinal microbiota diversity. Surprisingly, antibiotic treatment also resulted in mice releasing large numbers of spores into the environment, leading to extremely efficient host transmission. Stringent disinfection regimens with sporicidal agents are required to block C. difficile transmission.
Cellular Immunity Induced by a Recombinant Vaccine Confers Protection from Amebiasis
An effective vaccine is a desirable and feasible goal to prevent Entamoeba histolytica infection. With an intestinal amebiasis model, Guo et al. (p. 3909-3918) show that a recombinant antigen derived from E. histolytica surface lectin effectively protects the mouse from amebiasis with a range of human-appropriate adjuvants and routes. Unexpectedly, they find that T cells and gamma interferon (IFN-
) play a critical role in vaccine-elicited protection while serum antibody does not. The frequency of antigen-specific IFN- or IFN--, tumor necrosis factor alpha-, and interleukin-2-producing blood CD4 cells is a predictive marker for alum-based vaccine protection. This study lays a path for future vaccine development of amebiasis through optimization of cell-mediated responses.
Watching Macrophages in Action in Zebrafish Infected with Listeria monocytogenes
Although Listeria monocytogenes is one of the best-studied bacterial pathogens, it remains the cause of a significant number of abortions and deadly meningitis. Interactions of L. monocytogenes with phagocytes, critical for its virulence, have been thoroughly studied in vitro, and Levraud et al. (p. 3651-3660) now report in vivo studies using zebrafish larvae. In this optically accessible vertebrate, they imaged macrophages trapping bacteria from the bloodstream and subsequent behavior. Key virulence factors, such as listeriolysin and the actA product required for phagosome escape and actin-based motility, respectively, were found to have conserved functions in this host, demonstrating its relevance to the human infection.
The RD1 Locus in the Mycobacterium tuberculosis Genome Contributes to Activation of Caspase-1
A genomic locus known as region of difference 1 (RD1) in Mycobacterium tuberculosis has been shown to contribute to the generation of host protective immunity and bacterial virulence. To gain insight into the underlying molecular mechanism, Kurenuma et al. (p. 3992-4001) investigated the role of RD1 in the production of inflammatory cytokines. The results implicate RD1 as assuming a role in the induction of caspase-1 activation via potassium ion efflux and facilitating the production of interleukin-18 (IL-18) and IL-1β. Cytokine production and caspase-1 activation were induced independently of a P2X7 purinergic receptor and type I interferon receptor.
CD137 Aggravates Polymicrobial Sepsis
Recent studies have revealed that CD137 (4-1BB) plays important roles in various innate immune responses as well as in T-cell responses. Using KO mice and antagonistic antibody, Nguyen et al. (p. 3932-3938) show that blocking CD137 signaling improves the survival of mice with polymicrobial sepsis. They also show that stimulation of CD137 aggravates sepsis in mice. These latest studies build on previous reports by the same group showing that CD137 is expressed on murine neutrophils and that CD137 activation using agonistic anti-CD137 antibodies completely protected mice from lethal infection with the gram-positive intracellular bacterium Listeria monocytogenes.
Mechanism for In Vivo Activation of Vibrio cholerae Virulence Gene Expression
Vibrio cholerae causes cholera by producing two major virulence factors, cholera toxin (CT) and toxin-coregulated pilus (TCP). Bicarbonate is present at a high concentration in the human duodenum where V. cholerae colonizes and has been shown to induce CT and TCP expression in vitro. Abuaita and Withey (p. 4111-4120) provide evidence that bicarbonate enhances activity of ToxT, the transcription factor that directly activates CT and TCP expression. Bicarbonate does not affect expression or stability of ToxT, but CT and TCP production are greatly enhanced by bicarbonate. Thus, bicarbonate may be the major signal that induces V. cholerae virulence in humans.
Infection and Immunity, September 2009, p. 3520-3521, Vol. 77, No. 9
0019-9567/09/$08.00+0 doi:10.1128/IAI.00803-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
| ||||||||||||||||||||||||||||||||
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»