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Kenzel, Sybille; Mergen, Miriam; von Süßkind-Schwendi, Julius; Wennekamp, Julia; Deshmukh, Sachin D.; Haeffner, Monika; Triantafyllopoulou, Antigoni; Fuchs, Sebastian; Farmand, Susan; Santos-Sierra, Sandra; Seufert, Jochen; van den Berg, Timo K.; Kuijpers, Taco W.; Henneke, Philipp

Insulin Modulates the Inflammatory Granulocyte Response to Streptococci via Phosphatidylinositol 3-Kinase

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  • Media type: E-Article
  • Title: Insulin Modulates the Inflammatory Granulocyte Response to Streptococci via Phosphatidylinositol 3-Kinase
  • Contributor: Kenzel, Sybille; Mergen, Miriam; von Süßkind-Schwendi, Julius; Wennekamp, Julia; Deshmukh, Sachin D.; Haeffner, Monika; Triantafyllopoulou, Antigoni; Fuchs, Sebastian; Farmand, Susan; Santos-Sierra, Sandra; Seufert, Jochen; van den Berg, Timo K.; Kuijpers, Taco W.; Henneke, Philipp
  • Published: The American Association of Immunologists, 2012
  • Published in: The Journal of Immunology, 189 (2012) 9, Seite 4582-4591
  • Language: English
  • DOI: 10.4049/jimmunol.1200205
  • ISSN: 1550-6606; 0022-1767
  • Origination:
  • Footnote:
  • Description: Abstract Group B streptococci (GBS; Streptococcus agalactiae) are a major cause of invasive infections in newborn infants and in patients with type 2 diabetes. Both patient groups exhibit peripheral insulin resistance and alterations in polymorphonuclear leukocyte (PML) function. In this investigation, we studied the PML response repertoire to GBS with a focus on TLR signaling and the modulation of this response by insulin in mice and humans. We found that GBS-induced, MyD88-dependent chemokine formation of PML was specifically downmodulated by insulin via insulin receptor-mediated induction of PI3K. PI3K inhibited transcription of chemokine genes on the level of NF-κB activation and binding. Insulin specifically modulated the chemokine response of PML to whole bacteria, but affected neither activation by purified TLR agonists nor antimicrobial properties, such as migration, phagocytosis, bacterial killing, and formation of reactive oxygen species. The targeted modulation of bacteria-induced chemokine formation by insulin via PI3K may form a basis for the development of novel targets of adjunctive sepsis therapy.
  • Access State: Open Access