IFN-I is critical in immune reactions, influencing innate and adaptive immune systems. It affects dendritic cell activation T-cell responses and supports regulatory T-cell function.
IFN-I production occurs upon detection of microbial products, and depending on the context of microbial exposure, IFN-I can contribute to either pro-inflammatory or anti-inflammatory responses:
- IFN-I response to microbial pathogens induces a robust antimicrobial and anti-inflammatory reaction.
- IFN-I response to products from commensal bacteria sustains anti-inflammatory reactions, with commensal bacteria being normal inhabitants of the body without causing diseases.
Researchers from the University of California’s Pathology Department demonstrated that commensal bacteria play a crucial role in maintaining IFN-I production in the intestines, ensuring the normal functioning of the intestinal mucosa and protecting against inflammation.
Experiments Confirm the Necessity of Commensal Bacteria for IFN-I Production
A series of experiments conducted on mice revealed that the absence of intestinal microbiota reduced IFN-I-related gene expression in the mouse colon tissue. Activation of interferon-stimulated genes required the presence of commensal bacteria. Colonizing mice without microbiota with the commensal bacterium B. fragilis partially restored the expression of interferon-associated genes in the colon.
During simulated infections, mice with normal microbiota exhibited significantly increased IFN-I production in the colon. In contrast, microbiota-depleted mice showed no IFN response. Analysis of the immune system cells further indicated impaired interferon signal transmission in microbiota-depleted mice. Colonization with the commensal bacterium B. fragilis restored interferon signal transmission.
Commensal Bacteria Influence Immunological Tolerance and Anti-Inflammatory Responses
Immunological tolerance is crucial for the body’s normal functioning, allowing the immune system to distinguish healthy tissues and beneficial bacteria from pathogens. Dendritic cells, producing interferon, contribute to creating and maintaining the immune environment in the intestines by analyzing its contents, including bacteria. Different bacteria influence IFN production differently; stimulation of dendritic cells by B. fragilis and other Bacteroides species initiates significant IFN-beta production, while pathogens induce higher IFN-beta levels than B. fragilis and other commensal bacteria.
The production of IFN-I by dendritic cells depends on the regulation of IL-27. Stimulation of IL-27 production by commensal bacteria initiates the production of anti-inflammatory IL-10 by Treg cells. Consequently, commensal bacteria influence the IFN response and contribute to immunological tolerance, safeguarding the intestine from inflammation.
Conclusion
Intestinal dendritic cells produce type I interferons in response to the microbiota. Disruption of the microbiota can lead to a reduction in type I interferon production. Various commensal bacteria, including B. fragilis, stimulate IFN-beta production in the colon. The transmission of interferon signals is vital for anti-inflammatory reactions in the intestines.
Useful article, necessary information? Share it!
Someone will also find it useful and necessary:
Reference
Commensal bacteria promote type I interferon signaling to maintain immune tolerance in mice
