TY - JOUR
T1 - miR-21 differentially regulates IL-1β and IL-10 expression in human decidual cells infected with streptococcus B
AU - Castro-Leyva, Violeta
AU - Arenas-Huertero, Francisco
AU - Espejel-Núñez, Aurora
AU - Giono Cerezo, Silvia
AU - Flores-Pliego, Arturo
AU - Espino y Sosa, Salvador
AU - Reyes-Muñoz, Enrique
AU - Vadillo-Ortega, Felipe
AU - Borboa-Olivares, Héctor
AU - Camacho-Arroyo, Ignacio
AU - Estrada-Gutierrez, Guadalupe
N1 - Publisher Copyright:
© 2022 The Authors
PY - 2022/3
Y1 - 2022/3
N2 - Intrauterine infections caused by bacteria like group B streptococcus (GBS) and the subsequent activation of the maternal inflammatory response have been long suspected to be the underlying cause of preterm labor. The inflammatory network triggered by maternal decidua has been widely described and includes the secretion of pro- and anti-inflammatory cytokines as IL-1β and IL-10; however, the mechanisms that regulate their secretion have not been completely elucidated. MicroRNAs (miRNAs) are critical modulators of the inflammatory response by regulating cytokine expression in several cell types. Here, we explored the role of miR-21 in the expression of IL-1β and IL-10 in human decidual stromal cells (DSCs) exposed in vitro to GBS. We observed that IL1B and IL10 expression at the mRNA level was increased in DSCs after GBS infection. IL-10 but not IL-1β secretion was detected in the culture supernatants. We found a higher miR-21 expression (22-fold) in infected DSCs as compared with non-infected cells. miR-21 functional analysis revealed that DSCs transfected with an antagomiR vs. miR-21 significantly increased the secretion of IL-1β but decreased that of IL-10 in DSCs cells infected with GBS. Our results suggest that miR-21 participates in balancing the inflammatory response in infected decidua through at least IL-1β and IL-10 regulation. This is the first study attributing a functional role of miR-21 in the regulation of key molecules involved in the inflammatory response in infected DSCs, providing new insights into the epigenetic control of human decidual inflammation.
AB - Intrauterine infections caused by bacteria like group B streptococcus (GBS) and the subsequent activation of the maternal inflammatory response have been long suspected to be the underlying cause of preterm labor. The inflammatory network triggered by maternal decidua has been widely described and includes the secretion of pro- and anti-inflammatory cytokines as IL-1β and IL-10; however, the mechanisms that regulate their secretion have not been completely elucidated. MicroRNAs (miRNAs) are critical modulators of the inflammatory response by regulating cytokine expression in several cell types. Here, we explored the role of miR-21 in the expression of IL-1β and IL-10 in human decidual stromal cells (DSCs) exposed in vitro to GBS. We observed that IL1B and IL10 expression at the mRNA level was increased in DSCs after GBS infection. IL-10 but not IL-1β secretion was detected in the culture supernatants. We found a higher miR-21 expression (22-fold) in infected DSCs as compared with non-infected cells. miR-21 functional analysis revealed that DSCs transfected with an antagomiR vs. miR-21 significantly increased the secretion of IL-1β but decreased that of IL-10 in DSCs cells infected with GBS. Our results suggest that miR-21 participates in balancing the inflammatory response in infected decidua through at least IL-1β and IL-10 regulation. This is the first study attributing a functional role of miR-21 in the regulation of key molecules involved in the inflammatory response in infected DSCs, providing new insights into the epigenetic control of human decidual inflammation.
KW - Decidual inflammation
KW - Intrauterine infection
KW - Pregnancy
KW - Preterm labor
KW - microRNAs
UR - http://www.scopus.com/inward/record.url?scp=85122613648&partnerID=8YFLogxK
U2 - 10.1016/j.repbio.2022.100604
DO - 10.1016/j.repbio.2022.100604
M3 - Artículo
C2 - 35033900
AN - SCOPUS:85122613648
SN - 1642-431X
VL - 22
JO - Reproductive Biology
JF - Reproductive Biology
IS - 1
M1 - 100604
ER -