Abstract:
PROBLEM:Exposure to systemic maternal inflammation (i.e., maternal sepsis, influenza, human immunodeficiency virus, or pyelonephritis) and intrauterine (IU) inflammation (i.e., chorioamnionitis or preterm labor) have been associated with adverse perinatal sequelae. Whether systemic and localized inflammation leading to adverse outcomes have similar placental mechanisms remain unclear. METHOD OF STUDY:We conducted a study by murine modeling systemic and localized IU inflammation with injections of either intraperitoneal (IP) or IU interleukin-1β (IL-1β) and compared fetoplacental hemodynamic changes, cytokine/chemokine expression, and fetal loss. RESULTS:IU IL-1β exposure reduced offspring survival by 31.1% and IP IL-1β exposure by 34.5% when compared with control pups. Despite this similar outcome in offspring survival, Doppler analysis revealed a stark difference: IU group displayed worsened fetoplacental hemodynamic changes while no differences were found between IP and control groups. While both IU and IP groups had increases in pro-inflammatory cytokines and chemokines, specific gene expression trends differed between the two groups, once again highlighting their mechanistic differences. CONCLUSION:While both IP and IU IL-1β exposure similarly affected pup survival, only IU inflammation resulted in fetoplacental hemodynamic changes. We speculate that exposure to maternal systemic and IU inflammation plays a key role in fetal injury by utilizing different placental inflammatory pathways and mechanisms.
journal_name
J Reprod Immunoljournal_title
Journal of reproductive immunologyauthors
Lee JY,Shin NE,Na Q,Dong J,Chudnovets A,Li S,Novak CM,McLane MW,Lei J,Burd Idoi
10.1016/j.jri.2019.06.004subject
Has Abstractpub_date
2019-06-01 00:00:00pages
52-62eissn
0165-0378issn
1872-7603pii
S0165-0378(19)30093-2journal_volume
133pub_type
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