ArticleThe Journal of biological chemistry2009
Invasion of endothelial cells by tissue-invasive M3 type group A streptococci requires Src kinase and activation of Rac1 by a phosphatidylinositol 3-kinase-independent mechanism.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 33 citations in OpenAlex.
- Interplay between group AMicrobiology and molecular biology reviews : MMBR · 2024Review
- Expanding the genetic toolbox for the obligate human pathogenFrontiers in bioengineering and biotechnology · 2024Article
- Epidemiological and Clinical Features ofPathogens (Basel, Switzerland) · 2023Article
- Intracellular Invasion byMicrobiology spectrum · 2019Review
- Differential mechanisms of adenosine- and ATPγS-induced microvascular endothelial barrier strengthening.Journal of cellular physiology · 2019Article
- Group AMicrobiology spectrum · 2019Article
- Article
- The M1 protein of Streptococcus pyogenes triggers an innate uptake mechanism into polarized human endothelial cells.Journal of innate immunity · 2014Article
- CCCTC-binding factor controls its own nuclear transport via regulating the expression of importin 13.Molecules and cells · 2013Article
- The FbaB-type fibronectin-binding protein of Streptococcus pyogenes promotes specific invasion into endothelial cells.Cellular microbiology · 2011Article
- [Necrotizing fasciitis. 2011 update].Der Unfallchirurg · 2011Article
- Invasion of eukaryotic cells by Borrelia burgdorferi requires β(1) integrins and Src kinase activity.Infection and immunity · 2011Article
- Polymeric immunoglobulin receptor-mediated invasion of Streptococcus pneumoniae into host cells requires a coordinate signaling of SRC family of protein-tyrosine kinases, ERK, and c-Jun N-terminal kinase.The Journal of biological chemistry · 2010Article
- The CXC chemokine-degrading protease SpyCep of Streptococcus pyogenes promotes its uptake into endothelial cells.The Journal of biological chemistry · 2010Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Streptococcus pyogenes can cause invasive diseases in humans, such as sepsis or necrotizing fasciitis. Among the various M serotypes of group A streptococci (GAS), M3 GAS lacks the major epithelial invasins SfbI/PrtF1 and M1 protein but has a high potential to cause invasive disease. We examined the uptake of M3 GAS into human endothelial cells and identified host signaling factors required to initiate streptococcal uptake. Bacterial uptake is accompanied by local F-actin accumulation and formation of membrane protrusions at the entry site. We found that Src kinases and Rac1 but not phosphatidylinositol 3-kinases (PI3Ks) are essential to mediate S. pyogenes internalization. Pharmacological inhibition of Src activity reduced bacterial uptake and abolished the formation of membrane protrusions and actin accumulation in the vicinity of adherent streptococci. We found that Src kinases are activated in a time-dependent manner in response to M3 GAS. We also demonstrated that PI3K is dispensable for internalization of M3 streptococci and the formation of F-actin accumulations at the entry site. Furthermore, Rac1 was activated in infected cells and accumulated with F-actin in a PI3K-independent manner at bacterial entry sites. Genetic interference with Rac1 function inhibited streptococcal internalization, demonstrating an essential role of Rac1 for the uptake process of streptococci into endothelial cells. In addition, we demonstrated for the first time accumulation of the actin nucleation complex Arp2/3 at the entry port of invading M3 streptococci.
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