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On a global basis, leptospirosis is the most widespread bacterial infection that humans can acquire from animals. The mechanisms that the pathogenic leptospires use to cause infection and disease remain poorly understood, but binding to the extracellular matrix has been thoroughly documented. A new study by Breiner et al. (p. 5528-5536) shows for the first time that pathogenic leptospires bind more efficiently to mammalian cells than to the extracellular matrix. This attachment is mediated in part by proteoglycans. This work provides new insights and avenues for further investigations into how pathogenic leptospires cause the tissue damage seen in leptospirosis.
The outcome of urinary tract infection depends on a balance between bacterial virulence and the host immune response. Lloyd et al. (p. 5322-5333) demonstrate that sisA and sisB from uropathogenic Escherichia coli (UPEC) strain CFT073, homologs of shiA of Shigella flexneri, function to suppress the host inflammatory response during urinary tract infection. Deletion of these genes resulted in a hyperinflammatory phenotype in the kidneys of mice, which was suppressed to wild-type levels by complementation with either sisA or sisB. sisA was expressed by UPEC in vivo in 70% of women during naturally occurring urinary tract infection, while sisB was not common among UPEC isolates.
Ehrlichia chaffeensis, an intracellular bacterium, causes human monocytotropic ehrlichiosis, an emerging tick-borne disease with the highest incidence in people aged 50 years or older. This suggests the possibility that childhood and/or young adult exposure to Ehrlichia elicits an incomplete or defective memory immune response. Using murine models of ehrlichiosis, Thirumalapura et al. (p. 5682-5689) demonstrate that persistence of ehrlichial infection contributes to protection against other ehrlichial species (heterologous immunity) by maintaining memory T-cell responses and possibly by inducing transforming growth factor β and T regulatory cells to suppress immune-mediated pathology.
Lipopolysaccharide-mediated resistance against antimicrobial host defense and invasion of nonphagocytic cells are two major virulence traits of Salmonella enterica. Both mechanisms depend on the proper organization of the cell envelope. The study by Hölzer and colleagues (p. 5458-5470) reveals that synthesis of short, long, and very long O-antigen species fulfills this requirement in an elegant manner: the presence of three O-antigen variants allows sufficient invasion without affecting the protective properties of the lipopolysaccharide. This study highlights how a pathogen coordinates various virulence functions in order to be perfectly adapted to host environments.