Advertisement

Group A Streptococcus: A Loser in the Battle with Autophagy

  • Tamotsu YoshimoriEmail author
  • Atsuo Amano
Chapter
Part of the Current Topics in Microbiology and Immunology book series (CT MICROBIOLOGY, volume 335)

Abstract

Autophagy is an intracellular bulk degradation/recycling system for turning over cellular constituents. In one of the more remarkable findings among the recent developments in the field of autophagy, it was found that autophagy can also eliminate bacteria that invade host cells. The first evidence of this phenomenon came from an analysis of group A Streptococcus (GAS), the etiological agent underlying diverse human diseases. This bacterium is often internalized into nonphagocytic cells via the endocytic pathway, and then escapes from endosomes into the cytoplasm by secreting streptolysin O. The bacteria that escape into the cytoplasm induce and are captured by a unique membranous structure, which shares characteristics and molecular machinery with canonical autophagosomes but has some distinctions, including its large size. Subsequent fusion with lysosomes causes the death of most intracellular GAS. These findings have opened up a new field of innate immunity: the intracellular immune system against pathogens that penetrate the first defense of the endocytic pathway. The role of autophagy in Staphylococcus aureus infection is also discussed.

Keywords

Necrotizing Fasciitis Toxic Shock Syndrome Isolation Membrane Streptococcal Toxic Shock Syndrome Host Cell Death 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

References

  1. Amano A, Nakagawa I, Yoshimori T (2006) Autophagy in innate immunity against intracellular bacteria. J Biochem 140:161–166CrossRefPubMedGoogle Scholar
  2. Carapetis JR, Steer AC, Mulholland EK, Weber M (2005) The global burden of group A streptococcal diseases. Lancet Infect Dis 5:685–694CrossRefPubMedGoogle Scholar
  3. Cunningham MW (2000) Pathogenesis of group A streptococcal infections. Clin Microbiol Rev 13:470–511CrossRefPubMedGoogle Scholar
  4. Cywes C, Wessels MR (2001) Group A Streptococcus tissue invasion by CD44-mediated cell signalling. Nature 414:648–652CrossRefPubMedGoogle Scholar
  5. European Antimicrobial Resistance Surveillance System (EARSS)Management Team (2006) Antimicrobial resistance in Europe. In: EARSS annual report 2005 (eds) EARSS, Bilthoven, pp 41–65Google Scholar
  6. Finch R (2006) Gram-positive infections: lessons learnt and novel solutions. Clin Microbiol Infect 12 (Suppl 8): 3–8CrossRefGoogle Scholar
  7. Hynes W (2004) Virulence factors of the group A streptococci and genes that regulate their expression. Front Biosci 9:3399–3433CrossRefPubMedGoogle Scholar
  8. Kabeya Y, Mizushima N, Ueno T, Yamamoto A, Kirisako T, Noda T, Kominami E, Ohsumi Y, Yoshimori T (2000) LC3, a mammalian homolog of yeast Apg8p, is localized in autophagosome membranes after processing. EMBO J 19:5720–5728CrossRefPubMedGoogle Scholar
  9. Kollef MH, Micek ST (2006) Methicillin-resistant Staphylococcus aureus: a new community-acquired pathogen? Curr Opin Infect Dis 19:161–168PubMedGoogle Scholar
  10. Krut O, Utermöhlen O, Schlossherr X, Krönke M (2003) Strain-specific association of cytotoxic activity and virulence of clinical Staphylococcus aureus isolates. Infect Immun 71:2716–2723CrossRefPubMedGoogle Scholar
  11. Mizushima N, Yamamoto A, Hatano M, Kobayashi Y, Kabeya Y, Tokuhisa T, Ohsumi Y, Yoshimori T (2001) Dissection of autophagosome formation using Apg5-deficient mouse embryonic stem cells. J Cell Biol 152:657–667CrossRefPubMedGoogle Scholar
  12. Molinari G, Rohde M, Guzman CA, Chhatwal GS (2000) Two distinct pathways for the invasion of Streptococcus pyogenes in non-phagocytic cells. Cell Microbiol 2:145–154CrossRefPubMedGoogle Scholar
  13. Nakagawa I, Nakata M, Kawabata S, Hamada S (2001) Cytochrome c-mediated caspase-9 activation triggers apoptosis in Streptococcus pyogenes-infected epithelial cells. Cell Microbiol 3:395–405CrossRefPubMedGoogle Scholar
  14. Nakagawa I, Nakata M, Kawabata S, Hamada S (2004a) Transcriptome analysis and gene expression profiles of early apoptosis-related genes in Streptococcus pyogenes-infected epithelial cells. Cell Microbiol 6:939–952CrossRefPubMedGoogle Scholar
  15. Nakagawa I, Amano A, Mizushima N, Yamamoto A, Yamaguchi H, Kamimoto T, Nara A, Funao J, Nakata M, Tsuda K, Hamada S, Yoshimori T (2004b) Autophagy defenses cells against invading group A Streptococcus. Science 306:1037–1040CrossRefPubMedGoogle Scholar
  16. Novick RP (2003) Autoinduction and signal transduction in the regulation of staphylococcal virulence. Mol Microbiol 48:1429–1449CrossRefPubMedGoogle Scholar
  17. Schnaith A, Kashkar H, Leggio SA, Addicks K, Krönke M, Krut O (2007) Staphylococcus aureus subvert autophagy for induction of caspase-independent host cell death. J Biol Chem 282:2695–2706CrossRefPubMedGoogle Scholar
  18. Sinha B, Herrmann M (2005) Mechanism and consequences of invasion of endothelial cells by Staphylococcus aureus. Thromb Haemostasis 94:266–277Google Scholar
  19. Smith A, Lamagni TL, Oliver I, Efstratiou A, George RC, Stuart JM (2005) Invasive group A streptococcal disease: should close contacts routinely receive antibiotic prophylaxis? Lancet Infect Dis 5:494–500CrossRefPubMedGoogle Scholar
  20. Sumby P, Whitney AR, Graviss EA, DeLeo FR, Musser JM (2006) Genome-wide analysis of group A streptococci reveals a mutation that modulates global phenotype and disease specificity. PLoS Pathog 2:41–49CrossRefGoogle Scholar
  21. Tomasini-Johansson BR, Kaufman NR, Ensenberger MG, Ozeri V, Hanski E, Mosher DF (2001) A 49-residue peptide from adhesin F1 of Streptococcus pyogenes inhibits fibronectin matrix assembly. J Biol Chem 276:23430–23439CrossRefPubMedGoogle Scholar
  22. Vieira OV, Botelho RJ, Grinstein S (2002) Phagosome maturation: aging gracefully. Biochem J 366:689–704PubMedGoogle Scholar
  23. Wisplinghoff H, Bischoff T, Tallent SM, Seifert H, Wenzel RP, Edmond MB (2004) Nosocomial bloodstream infections in US hospitals: analysis of 24,179 cases from a prospective nationwide surveillance study. Clin Infect Dis 39:309–317CrossRefPubMedGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2009

Authors and Affiliations

  1. 1.Department of Cell Regulation, Research Institute for Microbial DiseasesOsaka UniversitySuita-OsakaJapan
  2. 2.Department of Oral Frontier BiologyOsaka University Graduate School of DentistrySuita-OsakaJapan

Personalised recommendations