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Streptococcus pyogenes induces epithelial inflammatory responses through NF-kappaB/MAPK signaling pathways.
Pei-Jane Tsai1, Ying-Huei Chen, Chieh-Hsing Hsueh
1Graduate Institutes of Medical Biotechnology, Department of Laboratory Medicine and Biotechnology, Medical College, Tzu-Chi University, 701, Chung Yan Road Section 3, Hualien 970, Taiwan. pjtsai@mail.tcu.edu.tw
Microbes and Infection
|May 17, 2006
Summary
Streptococcus pyogenes infection triggers epithelial cells to release inflammatory signals, attracting immune cells. This response involves key signaling pathways like NF-kappaB and MAP kinase, crucial for innate immunity.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Innate immunity orchestrates inflammatory responses via chemokines and cytokines.
- Epithelial cells play a critical role in initiating immune responses to pathogens.
- Streptococcus pyogenes is a significant human pathogen that can infect respiratory epithelial cells.
Purpose of the Study:
- To investigate the epithelial inflammatory response to Streptococcus pyogenes infection.
- To identify the signaling pathways involved in S. pyogenes-induced inflammation in respiratory epithelial cells.
- To determine the role of epithelial cells in initiating innate immune responses during S. pyogenes infection.
Main Methods:
- Culturing human respiratory epithelial HEp-2 cells and infecting them with S. pyogenes.
- Analyzing cell-free supernatants for monocyte chemotaxis.
- Measuring mRNA and protein expression of interleukin-8 (IL-8) and IL-6.
- Utilizing electrophoretic mobility shift assays (EMSA) and reporter-gene assays to assess transcription factor activation (NF-kappaB, AP-1).
- Employing mitogen-activated protein (MAP) kinase inhibitors and NF-kappaB inhibitors to study signaling pathways.
Main Results:
- Supernatants from S. pyogenes-infected HEp-2 cells significantly increased monocyte chemotaxis.
- Infection led to significantly increased mRNA and protein levels of IL-8 and IL-6.
- NF-kappaB and AP-1 transcription factors were activated following S. pyogenes infection.
- MAP kinase signaling pathways were involved in the activation of NF-kappaB and AP-1.
- Inhibitors of NF-kappaB and MAP kinase abrogated the upregulation of IL-8 and IL-6 mRNA.
Conclusions:
- S. pyogenes infection of epithelial cells induces pro-inflammatory chemokine and cytokine secretion.
- The NF-kappaB and MAP kinase signaling pathways are critical mediators of this response.
- These early innate immune responses by infected epithelial cells contribute to immune cell recruitment and inflammation in the airways.