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Notch Signaling Pathway Is Activated by Sulfate Reducing Bacteria
Sudha B Singh1, Cristina N Coffman1, Amanda Carroll-Portillo2
1Biomedical Research Institute of New Mexico, New Mexico VA Health Care System, Albuquerque, NM, United States.
Frontiers in Cellular and Infection Microbiology
|August 2, 2021
Summary
Sulfate-reducing bacteria (SRB) blooms in the gut activate the Notch signaling pathway in host cells. This newly discovered mechanism may contribute to inflammation and offers a potential therapeutic target.
Area of Science:
- Microbiology and Immunology
- Cellular Signaling
Background:
- Sulfate-reducing bacteria (SRB) are linked to inflammatory conditions like Inflammatory Bowel Disease (IBD).
- The mechanisms connecting SRB blooms to host inflammation are not well understood.
- Notch signaling is a crucial pathway in cell communication, often dysregulated in inflammation.
Purpose of the Study:
- To investigate if Desulfovibrio, a dominant gut SRB genus, activates Notch signaling in host cells.
- To explore the downstream effects of SRB-induced Notch activation.
Main Methods:
- RAW 264.7 macrophages were infected with Desulfovibrio vulgaris (DSV).
- Expression of Notch pathway proteins, pro-IL1β, and SOCS3 was analyzed.
- Inhibition studies using DAPT (gamma secretase inhibitor) and Notch siRNA were performed.
- TLR4 involvement was assessed using a TLR4 antagonist (C34).
Main Results:
- DSV infection dose- and time-dependently increased Notch1, NICD, and p21 expression.
- DSV induced pro-IL1β and SOCS3 expression, which were reduced by DAPT or Notch siRNA.
- DSV-induced Notch activation was independent of TLR4 signaling.
- DSV activated Notch signaling in human epithelial cells (HCT116) and mouse small intestine.
Conclusions:
- Desulfovibrio activates the Notch signaling pathway in host cells, representing a novel interaction mechanism.
- This SRB-mediated Notch activation may contribute to inflammation in conditions with SRB blooms.
- Targeting the Notch pathway could be a potential therapeutic strategy for SRB-associated inflammatory diseases.
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