Abstract
A major cause of preterm labor in pregnant women is intra-amniotic infection, which is mediated by an inflammatory process. Hydrogen sulfide (H2S), a gaseous transmitter, has been implicated to be involved in inflammatory responses. We sought to investigate whether H2S affects infectious preterm birth using the mouse model of lipopolysaccharides (LPS)-induced preterm birth. Administration of LPS at 0.4 mg/kg with two injections intraperitoneally (i.p.) on gestational day 14.5 induced preterm labor. LPS significantly increased leukocyte infiltration in uterus, stimulated the expression of pro-inflammatory cytokines interleukin 1β (IL-1β), IL-6, tumor necrosis factor α (TNF-α), CCL2 and CXCL15 in myometrium. Administration of NaHS (i.p.) delayed the onset of labor induced by LPS in a dose-dependent manner. NaHS prevented leukocyte infiltration into intrauterine tissues and inhibited the production of pro-inflammatory cytokines in myometrium and decreased the levels of these cytokines in maternal circulation. H2S also decreased LPS-activated extracellular signal-regulated kinase (ERK) 1/2/ nuclear factor (NF)-κB signaling pathways in myometrium. This study provides new in vivo evidence for the roles of H2S in attenuating inflammation, and a potential novel therapeutic strategy for infection-related preterm labor.
Highlights
Preterm birth (PTB) occurs in 5–15% of all pregnancies worldwide, and is the leading cause of infant morbidity and mortality [1, 2]
The animals received two injections of normal saline (NS) delivered by 124.38±6.76 hrs after the first injection (Table 1), which is comparable to the normal delivery time of mice
We demonstrated that H2S significantly delayed LPS-induced preterm labor and suppressed LPS-induced inflammation in myometrium
Summary
Preterm birth (PTB) occurs in 5–15% of all pregnancies worldwide, and is the leading cause of infant morbidity and mortality [1, 2]. Of the survivors of PTB, 25% will have at least one developmental delay such as cerebral palsy and long term vision, hearing and respiratory problems [3]. Half of PTB is of unknown aetiology, while maternal genito-urinary infections account for up to 30% to 40% of all PTB [4]. PLOS ONE | DOI:10.1371/journal.pone.0152838 April 1, 2016
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