The pathogenesis of streptococcal infections: from Tooth decay to meningitis

Mitchell, Tim

doi:10.1038/nrmicro771

Cited by 249 publications

(238 citation statements)

References 148 publications

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“…Pathogenic streptococci exploit surface-exposed proteins to achieve adhesion to mucosal surfaces and escape host defenses 4 . Among the 28 S. pneumoniae virulence-related genes coding surface-exposed proteins, only 4 have orthologs in S. thermophilus (Supplementary Table 7 online).…”

Section: Absence Of Virulence-related Genes In S Thermophilusmentioning

confidence: 99%

“…The dairy streptococcus must have followed a divergent evolutionary path from that of its pathogenic congeners, as it has adapted to a rather narrow, well-defined and constant ecological niche, milk. To obtain insight into this path and to assess the potential for virulence of this bacterium, we sequenced the genomes of two yogurt strains of S. thermophilus, and compared them to those of previously sequenced pathogenic streptococci [4][5][6][7][8][9] .…”

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Complete sequence and comparative genome analysis of the dairy bacterium Streptococcus thermophilus

et al. 2004

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The lactic acid bacterium Streptococcus thermophilus is widely used for the manufacture of yogurt and cheese. This dairy species of major economic importance is phylogenetically close to pathogenic streptococci, raising the possibility that it has a potential for virulence. Here we report the genome sequences of two yogurt strains of S. thermophilus . We found a striking level of gene decay (10% pseudogenes) in both microorganisms. Many genes involved in carbon utilization are nonfunctional, in line with the paucity of carbon sources in milk. Notably, most streptococcal virulence-related genes that are not involved in basic cellular processes are either inactivated or absent in the dairy streptococcus. Adaptation to the constant milk environment appears to have resulted in the stabilization of the genome structure. We conclude that S. thermophilus has evolved mainly through loss-of-function events that remarkably mirror the environment of the dairy niche resulting in a severely diminished pathogenic potential. Supplementary information The online version of this article (doi:10.1038/nbt1034) contains supplementary material, which is available to authorized users.

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Section: Absence Of Virulence-related Genes In S Thermophilusmentioning

confidence: 99%

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confidence: 99%

Complete sequence and comparative genome analysis of the dairy bacterium Streptococcus thermophilus

et al. 2004

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“…One of these CD46-binding microorganisms is the Gram-positive bacterium Streptococcus pyogenes (group A streptococcus), a human pathogen causing multiple diseases, including pharyngitis, skin infections, the streptococcal toxic shock syndrome, and postinfectious rheumatic fever (15). The major virulence factor of S. pyogenes is the M protein, an antiphagocytic surface molecule (16) that also binds human CD46 (17,18), a property that may promote bacterial adhesion.…”

Section: Induction Of a Regulatory Phenotype In Human Cd4 ؉ T Cells Bmentioning

confidence: 99%

Induction of a Regulatory Phenotype in Human CD4+ T Cells by Streptococcal M Protein

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Schaumburg

Sandin

et al. 2005

The Journal of Immunology

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Regulatory T cells (Tregs) participate in the control of the immune response. In the human system, an IL-10-secreting, T regulatory type 1 cell (Tr1)-like subset of Tregs can be induced by concurrent cross-linking of the TCR and CD46 on naive CD4+ T cells. Because many viral and bacterial pathogens, including the major human pathogen Streptococcus pyogenes, bind to CD46, we asked whether this bacterium can directly induce Tr1-like cells through the streptococcal ligand for CD46, the M protein. The M5 and M22 proteins were found to induce T cells to develop into the IL-10-producing Tr1-like phenotype. Moreover, whole M5-expressing bacteria, but not isogenic M-negative bacteria, led to proliferation and IL-10 secretion by T cells. The interaction between the M5 protein and T cells was dependent on CD46 and the conserved C repeat region of M5. Supernatants derived from T cells stimulated with M proteins or M protein-expressing bacteria suppressed bystander T cell proliferation through IL-10 secretion. In addition, activation of CD46 through streptococcal M protein induced the expression of granzyme B, providing a second means for these cells to regulate an immune response. These findings suggest that binding to CD46 and exploiting its signaling pathway may represent a strategy employed by a number of important human pathogens to induce directly an immunosuppressive/regulatory phenotype in T cells.

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“…For example, bacterial adhesins and invasins that manipulate host cells to facilitate entry of the bacteria can be membrane-bound proteins (e.g. Streptococcus pyogenes (Streptococcus A); Mitchell 2003 (Donnenberg 2000) and (together with another bacterial protein, IpgD) induce cytoskeletal rearrangements, pore formation and surface extensions (filopodia and lamilliopodia), which facilitate cell entry by an endocytic vacuole. This surface change formation can be blocked by Rac-GDP.…”

Section: The Diversity Of Immune Evasion Mechanismsmentioning

confidence: 99%

Immune defence, parasite evasion strategies and their relevance for ‘macroscopic phenomena’ such as virulence

Schmid‐Hempel

2008

Phil. Trans. R. Soc. B

207

177

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The discussion of host-parasite interactions, and of parasite virulence more specifically, has so far, with a few exceptions, not focused much attention on the accumulating evidence that immune evasion by parasites is not only almost universal but also often linked to pathogenesis, i.e. the appearance of virulence. Now, the immune evasion hypothesis offers a deeper insight into the evolution of virulence than previous hypotheses. Sensitivity analysis for parasite fitness and life-history theory shows promise to generate a more general evolutionary theory of virulence by including a major element, immune evasion to prevent parasite clearance from the host. Also, the study of dose-response relationships and multiple infections should be particularly illuminating to understand the evolution of virulence. Taking into account immune evasion brings immunological processes to the core of understanding the evolution of parasite virulence and for a range of related issues such as dose, host specificity or immunopathology. The aim of this review is to highlight the mechanism underlying immune evasion and to discuss possible consequences for the evolutionary ecology analysis of host-parasite interactions.

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The pathogenesis of streptococcal infections: from Tooth decay to meningitis

Cited by 249 publications

References 148 publications

Complete sequence and comparative genome analysis of the dairy bacterium Streptococcus thermophilus

Complete sequence and comparative genome analysis of the dairy bacterium Streptococcus thermophilus

Induction of a Regulatory Phenotype in Human CD4+ T Cells by Streptococcal M Protein

Immune defence, parasite evasion strategies and their relevance for ‘macroscopic phenomena’ such as virulence

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