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A Broad-Spectrum Chemokine Inhibitor Blocks Inflammation-Induced Myometrial Myocyte-Macrophage Crosstalk and Myometrial Contraction. | LitMetric

A Broad-Spectrum Chemokine Inhibitor Blocks Inflammation-Induced Myometrial Myocyte-Macrophage Crosstalk and Myometrial Contraction.

Cells

Lunenfeld Tanenbaum Research Institute, Mount Sinai Hospital, 25 Orde Street, Suite 6-1017, Toronto, ON M5G 1X5, Canada.

Published: December 2021

AI Article Synopsis

  • The broad-spectrum chemokine inhibitor FX125L has been shown to prevent preterm birth and reduce uterine contractions in animal models of bacterial infection.
  • This study investigated how BSCI affects human uterine muscle cells, hypothesizing that it prevents infection-related contractions by reducing inflammatory cytokine secretion.
  • Results demonstrated that BSCI inhibits various processes involved in inflammation and contraction, suggesting it could be a new treatment option for preventing inflammation-induced preterm birth in women.

Article Abstract

Prophylactic administration of the broad-spectrum chemokine inhibitor (BSCI) FX125L has been shown to suppress uterine contraction, prevent preterm birth (PTB) induced by Group B Streptococcus in nonhuman primates, and inhibit uterine cytokine/chemokine expression in a murine model of bacterial endotoxin (LPS)-induced PTB. This study aimed to determine the mechanism(s) of BSCI action on human myometrial smooth muscle cells. We hypothesized that BSCI prevents infection-induced contraction of uterine myocytes by inhibiting the secretion of pro-inflammatory cytokines, the expression of contraction-associated proteins and disruption of myocyte interaction with tissue macrophages. Myometrial biopsies and peripheral blood were collected from women at term (not in labour) undergoing an elective caesarean section. Myocytes were isolated and treated with LPS with/out BSCI; conditioned media was collected; cytokine secretion was analyzed by ELISA; and protein expression was detected by immunoblotting and immunocytochemistry. Functional gap junction formation was assessed by parachute assay. Collagen lattices were used to examine myocyte contraction with/out blood-derived macrophages and BSCI. We found that BSCI inhibited (1) LPS-induced activation of transcription factor NF-kB; (2) secretion of chemokines (MCP-1/CCL2 and IL-8/CXCL8); (3) Connexin43-mediated intercellular connectivity, thereby preventing myocyte-macrophage crosstalk; and (4) myocyte contraction. BSCI represents novel therapeutics for prevention of inflammation-induced PTB in women.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8750067PMC
http://dx.doi.org/10.3390/cells11010128DOI Listing

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