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STAT3 Deficiency Alters the Macrophage Activation Pattern and Enhances Matrix Metalloproteinase 9 Expression during
Susan Farmand1,2, Vicky Sender1,3, Jens Karlsson1,3
1Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Journal of Immunology (Baltimore, Md. : 1950)
|November 20, 2023
Summary
STAT3 deficiency in myeloid cells exacerbates inflammation during Staphylococcus aureus pneumonia but does not impair pathogen clearance. This heightened inflammatory response, involving matrix metalloproteinase 9 and miR-155, may contribute to lung tissue damage in susceptible patients.
Area of Science:
- Immunology
- Cell Biology
- Pulmonary Medicine
Background:
- Staphylococcus aureus causes severe lung infections, particularly in individuals with STAT3 deficiency.
- Macrophages play a critical role in host defense and inflammation during bacterial pneumonia.
Purpose of the Study:
- To investigate the role of myeloid STAT3 in macrophage response to S. aureus infection.
- To determine the effect of murine myeloid STAT3 deficiency on inflammation and pathogen clearance in staphylococcal pneumonia.
Main Methods:
- Murine bone marrow-derived macrophages (BMDM) from STAT3 knockout and wild-type mice were stimulated with S. aureus.
- Analysis of pro- and anti-inflammatory responses, polarization, and activation markers in vitro.
- Intratracheal S. aureus infection in mice, followed by analysis of bronchoalveolar lavage and lung tissue.
Main Results:
- STAT3-deficient BMDM exhibited increased pro-inflammatory cytokine release and enhanced upregulation of MHC class II and CD86 upon S. aureus challenge.
- Murine myeloid STAT3 deficiency did not impact S. aureus clearance in vitro or in vivo.
- Matrix metalloproteinase 9 and miR-155 expression were upregulated in STAT3-deficient macrophages and lung tissues during S. aureus infection.
Conclusions:
- Murine myeloid STAT3 deficiency leads to enhanced inflammatory responses and matrix metalloproteinase 9 and miR-155 upregulation during S. aureus infection.
- These findings suggest a potential mechanism for lung tissue damage observed in STAT3-deficient patients with staphylococcal pneumonia.
