4.5 Article

STAT3-dependent CXC chemokine formation and neutrophil migration in streptococcal M1 protein-induced acute lung inflammation

Journal

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00324.2014

Keywords

adhesion; inflammation; leukocytes; sepsis

Funding

  1. Swedish Medical Research Council [2012-3685]
  2. Crafoordska stiftelsen
  3. Einar och Inga Nilssons stiftelse
  4. Harald och Greta Jaenssons stiftelse
  5. Greta och Johan Kocks stiftelser
  6. Froken Agnes Nilssons stiftelse
  7. Franke och Margareta Bergqvists stiftelse for framjande av cancerforskning
  8. Magnus Bergvalls stiftelse
  9. Mossfelts stiftelse
  10. Nanna Svartz stiftelse
  11. Ruth och Richard Julins stiftelse
  12. Svenska Lakaresallskapet
  13. Allmana sjukhusets i Malmo stiftelse for bekampande av cancer
  14. MAS fonder
  15. Malmo University Hospital
  16. Lund University

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Streptococcus pyogenes cause infections ranging from mild pharyngitis to severe streptococcal toxic shock syndrome (STSS). The M1 serotype of Streptococcus pyogenes is most frequently associated with STSS. Herein, it was hypothesized that STAT3 signaling might be involved in M1 protein-evoked lung inflammation. The STAT3 inhibitor, S3I-201, was administered to male C57Bl/6 mice before iv challenge with M1 protein. Bronchoalveolar fluid and lung tissue were harvested for quantification of STAT3 activity, neutrophil recruitment, edema, and CXC chemokine formation. Neutrophil expression of Mac-1 was quantified by use of flow cytometry. Levels of IL-6 and HMGB1 were determined in plasma. CXCL2-induced neutrophil chemotaxis was studied in vitro. Administration of S3I-201 markedly reduced M1 protein-provoked STAT3 activity, neutrophil recruitment, edema formation, and inflammatory changes in the lung. In addition, M1 protein significantly increased Mac-1 expression on neutrophils and CXC chemokine levels in the lung. Treatment with S3I-201 had no effect on M1 protein-induced expression of Mac-1 on neutrophils. In contrast, inhibition of STAT3 activity greatly reduced M1 protein-induced formation of CXC chemokines in the lung. Interestingly, STAT3 inhibition markedly decreased plasma levels of IL-6 and HMGB1 in animals exposed to M1 protein. Moreover, we found that S3I-201 abolished CXCL2-induced neutrophil migration in vitro. In conclusion, these novel findings indicate that STAT3 signaling plays a key role in mediating CXC chemokine production and neutrophil infiltration in M1 protein-induced acute lung inflammation.

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