Mannheimia haemolytica and Its Leukotoxin Cause Neutrophil Extracellular Trap Formation by Bovine Neutrophils
Activated neutrophils can release a DNA matrix studded with antimicrobial proteins known as neutrophil extracellular traps (NETs). Aulik et al. (p. 4454-4466) show that bovine neutrophils form NETs in response to the respiratory pathogen Mannheimia haemolytica and its leukotoxin. NET formation is dependent on the interaction between the leukotoxin and CD18, its receptor on bovine leukocytes. M. haemolytica cells are trapped within bovine NETs, and a portion of the trapped cells are killed extracellularly. These observations provide a new perspective on the participation of neutrophils in the pathogenesis of bovine respiratory disease.
Role of Host Phosphoinositide 3-Kinase in Internalization of Listeria Is Partly Elucidated
Many microbial pathogens induce their internalization into human cells by subverting a host enzyme called phosphoinositide (PI) 3-kinase. Microbes that exploit PI 3-kinase include Ebola virus, the parasite Trypanosoma cruzi, and the bacteria Chlamydia pneumoniae, Yersinia pseudotuberculosis, and Listeria monocytogenes. How PI 3-kinase promotes pathogen uptake remains poorly understood. Gavicherla et al. (p. 4532-4541) show that entry of Listeria requires the host signaling protein ARAP2, which is a known downstream effector of PI 3-kinase. ARAP2 promotes Listeria uptake, in part, by inactivating the human GTPase Arf6. These findings reveal a critical mechanism through which PI 3-kinase stimulates internalization of microbes.
Adhesion, Invasion, and Agglutination Mediated by Two Trimeric Autotransporters in the Human Uropathogen Proteus mirabilis
Adherence to host uroepithelium and formation of biofilms, hallmarks of infection of the urinary tract by Proteus mirabilis, have thus far been attributed only to fimbriae synthesized by this bacterium. In this study, Alamuri et al. (p. 4882-4894) used in silico analyses to identify two trimeric autotransporters, TaaP and AipA, and combined in vitro and in vivo mutant analyses to characterize their structure-function relationship in mediating autoagglutination, adhesion, and invasion. Each protein contributes to successful colonization of the murine urinary tract. This is the first study where nonfimbrial surface proteins of P. mirabilis were shown to mediate such interactions in vitro or in vivo.
Bacteria Help Candida albicans To Colonize Oral Cavity Surfaces
Candida albicans is a dimorphic fungus associated with a range of mucosal and systemic infections. Silverman et al. (p. 4644-4652) show that one of the hypha-specific cell wall proteins (designated Als3) is recognized by an antigen I/II family adhesin (SspB) found on the surface of Streptococcus gordonii, a common inhabitant of the oral cavity. Lactococcus lactis cells expressing heterologous SspB bind Saccharomyces cerevisiae cells engineered to express Als3p, indicating direct protein-protein interaction. The authors suggest that this interaction drives the formation of mixed-species biofilms that promote colonization and infection by C. albicans.
The Shiga Toxin Receptor Globotriaosylceramide Is Present on Human Colonic Epithelial Cells
The identification of the Shiga toxin (Stx) receptor globotriaosylceramide (Gb3) in the late 1980s created an intriguing conundrum because subsequent work indicated that the receptor for the toxin was apparently absent at the site of initial toxin penetration, the colonic epithelium. Zumbrun et al. (p. 4488-4499) demonstrate that Gb3 appears to be present on both human colonic tissue sections and cultured colonic cells. Detection of the Gb3 receptor on human colonic tissue provides new insight into the pathogenesis of Stx-producing Escherichia coli. Stxs may induce localized damage to intestinal cells that express Gb3. As a consequence of the injury to some colonic epithelial cells, further systemic dissemination of the toxin may occur, leading to the development of hemolytic-uremic syndrome.
Promotion of Early T Cell Actions by Interleukin-7 Improves the Host Immune Response to Sepsis
Following an initial hyperinflammatory phase, septic patients become profoundly immune suppressed. Such immunosuppression leaves sepsis patients susceptible to existing as well as new infections. Thus, a major challenge is to find therapies that boost immunologic function without promoting hyperinflammation. Kasten et al. (p. 4714-4722) demonstrate a novel mechanism by which the T cell-specific cytokine interleukin-7 (IL-7) protects mice from sepsis. They show that IL-7 promotes gamma-delta T cell production of IL-17, which accelerates neutrophil recruitment and enhances bacterial clearance. These data show an early, complex interplay between innate and adaptive immune responses and suggest IL-7 as a potent antisepsis therapy.
- Copyright © 2010 American Society for Microbiology
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- Article
- Mannheimia haemolytica and Its Leukotoxin Cause Neutrophil Extracellular Trap Formation by Bovine Neutrophils
- Role of Host Phosphoinositide 3-Kinase in Internalization of Listeria Is Partly Elucidated
- Adhesion, Invasion, and Agglutination Mediated by Two Trimeric Autotransporters in the Human Uropathogen Proteus mirabilis
- Bacteria Help Candida albicans To Colonize Oral Cavity Surfaces
- The Shiga Toxin Receptor Globotriaosylceramide Is Present on Human Colonic Epithelial Cells
- Promotion of Early T Cell Actions by Interleukin-7 Improves the Host Immune Response to Sepsis
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