The symbiotic bacterial surface factor polysaccharide A on Bacteroides fragilis inhibits IL-1β-induced inflammation in human fetal enterocytes via toll receptors 2 and 4
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Colonizing bacteria interacting with the immature, unlike the mature, human intestine favors inflammation over immune homeostasis. As a result, ten percent of premature infants under 1500 grams weight develop an inflammatory necrosis of the intestine after birth, e.g., necrotizing enterocolitis (NEC). NEC is a major health problem in this population causing extensive morbidity and mortality and an enormous expenditure of health care dollars. NEC can be prevented by giving preterm infants their mother's expressed breast milk or ingesting selective probiotic organisms. Vaginally delivered, breast fed newborns develop health promoting bacteria ("pioneer" bacteria) which preferentially stimulate intestinal host defense and anti-inflammation. One such "pioneer" organism is Bacteroides fragilis with a polysaccharide (PSA) on its capsule. B. fragilis has been shown developmentally in intestinal lymphocytes and dendritic cells to produce a balanced T-helper cell (TH1/TH2) response and to reduce intestinal inflammation by activity through the TLR2 receptor stimulating IL-10 which inhibits IL-17 causing inflammation. No studies have been done on the role of B. fragilis PSA on fetal enterocytes and its increased inflammation. Accordingly, using human and mouse fetal intestinal models, we have shown that B. fragilis with PSA and PSA alone inhibits IL-1β-induced IL-8 inflammation in fetal and NEC intestine. We have also begun to define the mechanism for this unique inflammation noted in fetal intestine. We have shown that B. fragilis PSA anti-inflammation requires both the TLR2 and TLR4 receptor and is in part mediated by the AP1 transcription factor (TLR2) which is developmentally regulated. These observations may help to devise future preventative treatments of premature infants against NEC.
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Fetal enterocytes exposed to PSA produce lower levels of IL-1β-induced IL-8, which may play a role in the development of necrotizing enterocolitis in prematurely born infants.
“Jiang et al. recently reported that fetal enterocytes exposed to PSA produce lower levels of the IL-1β-induced, pro-inflammatory cytokine IL-8, which may play a role in the development of necrotizing enterocolitis in prematurely born infants (Jiang et al., 2017).”
From Understanding the Holobiont: How Microbial Metabolites Affect Human Health and Shape the Immune System (2017) · cites this paper as Jiang et al., 2017
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Khryanin, А. А., Bocharova, V. K., & Pushkarev, E. V. (2024) · Экспериментальная и клиническая гастроэнтерология · doi:10.31146/1682-8658-ecg-217-9-195-200
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Jiang, X., Chen, B., Wang, Q., Liu, Y., Li, N., & Zhang, L. (2026) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2026.1765801
- Authors
- Jiang, F., Meng, D., Weng, M., Zhu, W., Wu, W., Kasper, D., & Walker, W. A.
- Affiliations
- Harvard University (US)
- China Agricultural University (CN)
- Corresponding author
- Walker, W. Allan
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2017-03-09
- Volume
- 12
- Issue
- 3
- Pages
- e0172738
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC5344356
- OpenAlex
- W2592395492
- Cited by
- 60
- References
- 36
- Citations by year
- 2026: 1 · 2025: 6 · 2024: 8 · 2023: 5 · 2022: 7 · 2021: 5 · 2020: 7 · 2019: 9 · 2018: 9 · 2017: 2 · 2012: 1
- FWCI
- 6.14
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute of Child Health and Human Development (R01HD01237, PO1-DK033506)
- National Institutes of Digestive Disease and Kidney DIsease (P01HD059126, P30DK040561)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Infant Nutrition and Health
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Keywords
- Bacteroides fragilis, polysaccharide A, necrotizing enterocolitis, preterm infants, IL-1β-induced inflammation, interleukin-8, TLR2, TLR4, AP-1 transcription factor, intestinal inflammation
- MeSH terms
- Animals, Bacteroides fragilis, Cells, Cultured, Disease Models, Animal, Fetus, Humans, Inflammation, Mice, Inbred C57BL, Polysaccharides, Interleukin-8, Interleukin-10, Mice, Knockout, Th1 Cells, Th2 Cells, Enterocolitis, Necrotizing, Interleukin-17, Enterocytes, RNA Interference, Toll-Like Receptor 2, Toll-Like Receptor 4, Mice, Interleukin-1beta
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