Literature DB >> 30586203

Repeated lipopolysaccharide exposure leads to placental endotoxin tolerance.

Maureen L Kim1,2, Caroline Maloney1,3, Natalia Klimova1,4, Ellen Gurzenda1, Xinhua Lin1, Yuko Arita1, Treasure Walker5, Melissa J Fazzari6, Nazeeh Hanna1,2.   

Abstract

PROBLEM: Placental infection induces increased levels of pro-inflammatory cytokines, which have been implicated in the pathogenesis of pre-term labor. Endotoxin tolerance is a phenomenon in which exposure to a dose of endotoxin makes tissue less responsive to subsequent exposures. The objective of our study was to determine whether repeated exposure to endotoxin will induce a tolerant phenotype in normal human second-trimester placental tissue. METHODS OF STUDY: Human second-trimester placental explants from elective termination of pregnancy were cultured and exposed to endotoxin (LPS). After 24 hours, the media was collected for analysis, and the explants were re-exposed to LPS after adding fresh media for another 24 hours. This process was repeated for a total of 4 LPS doses. The media was collected from each day and analyzed for cytokine levels.
RESULTS: The first LPS treatment stimulated the secretion of the pro-inflammatory cytokines IL-1β and TNF-α. However, their production was significantly diminished with repeated LPS doses. Production of the anti-inflammatory cytokines, IL-1ra and IL-10, was also stimulated by the first LPS treatment, but secretion was more gradually and moderately decreased with repeated LPS doses compared to the pro-inflammatory cytokines. The ratios of the anti-inflammatory/pro-inflammatory mediators (IL-1ra/IL-1β and IL-10/TNF-α) indicate a progressively more anti-inflammatory milieu with repeated LPS doses.
CONCLUSION: Repeated LPS exposure of human second-trimester placental tissues induced endotoxin tolerance. We speculate that endotoxin tolerance at the maternal-fetal interface will protect the fetus from exaggerated inflammatory responses after repeated infectious exposure.
© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Entities:  

Keywords:  LPS; endotoxin tolerance; inflammation; placenta; pre-term labor

Mesh:

Substances:

Year:  2019        PMID: 30586203     DOI: 10.1111/aji.13080

Source DB:  PubMed          Journal:  Am J Reprod Immunol        ISSN: 1046-7408            Impact factor:   3.886


  7 in total

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Journal:  J Med Virol       Date:  2021-05-24       Impact factor: 20.693

Review 2.  MicroRNA-Mediated Control of Inflammation and Tolerance in Pregnancy.

Authors:  Ranjith Kamity; Surendra Sharma; Nazeeh Hanna
Journal:  Front Immunol       Date:  2019-04-05       Impact factor: 7.561

3.  Circulating miRNAs as Epigenetic Mediators of Periodontitis and Preeclampsia Association.

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Journal:  Dis Markers       Date:  2022-07-11       Impact factor: 3.464

4.  Maternal siRNA silencing of placental SAA2 mitigates preterm birth following intrauterine inflammation.

Authors:  Yang Liu; Jin Liu; Anguo Liu; Hillary Yin; Irina Burd; Jun Lei
Journal:  Front Immunol       Date:  2022-09-23       Impact factor: 8.786

5.  Placental extracellular vesicles-associated microRNA-519c mediates endotoxin adaptation in pregnancy.

Authors:  Caterina Tiozzo; Mark Bustoros; Xinhua Lin; Claudia Manzano De Mejia; Ellen Gurzenda; Martin Chavez; Iman Hanna; Paola Aguiari; Laura Perin; Nazeeh Hanna
Journal:  Am J Obstet Gynecol       Date:  2021-06-26       Impact factor: 8.661

6.  Immune Tolerance as the Physiologic Counterpart of Chronic Inflammation.

Authors:  Vladimir Rogovskii
Journal:  Front Immunol       Date:  2020-09-30       Impact factor: 7.561

Review 7.  Is pregnancy an immunological contributor to severe or controlled COVID-19 disease?

Authors:  Nazeeh Hanna; Monica Hanna; Surendra Sharma
Journal:  Am J Reprod Immunol       Date:  2020-08-20       Impact factor: 3.777

  7 in total

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