Journal
GUT MICROBES
Volume 11, Issue 2, Pages 217-230Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/19490976.2019.1629236
Keywords
Gut vascular barrier; gut lymphatic barrier; bacterial translocation; autoimmunity; enterococcus; microbiota; intestinal permeability; tight junctions; vancomycin resistance; TLR7; lupus; autoimmune liver disease
Categories
Funding
- National Institutes of Health (NIH) [K08AI095318, R01AI118855, T32AI07019, T32DK007017-39]
- Yale Rheumatic Diseases Research Core (NIH) [P30 AR053495]
- Yale Liver Center (NIH) [P30 DK34989]
- Women's Health Research at Yale
- O'Brien Center at Yale (NIH) [P30DK079310]
- Arthritis National Research Foundation
- Arthritis Foundation
- Lupus Research Institute
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Humans and other mammalian hosts have evolved mechanisms to control the bacteria colonizing their mucosal barriers to prevent invasion. While the breach of barriers by bacteria typically leads to overt infection, increasing evidence supports a role for translocation of commensal bacteria across an impaired gut barrier to extraintestinal sites in the pathogenesis of autoimmune and other chronic, non-infectious diseases. Whether gut commensal translocation is a cause or consequence of the disease is incompletely defined. Here we discuss factors that lead to translocation of live bacteria across the gut barrier. We expand upon our recently published demonstration that translocation of the gut pathobiont Enterococcus gallinarum can induce autoimmunity in susceptible hosts and postulate on the role of Enterococcus species as instigators of chronic, non-infectious diseases.
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