» Articles » PMID: 10848506

Inhibition of Cyclooxygenase-2 Prevents Inflammation-mediated Preterm Labor in the Mouse

Overview
Specialty Physiology
Date 2000 Jun 10
PMID 10848506
Citations 51
Authors
Affiliations
Soon will be listed here.
Abstract

Prostaglandins (PGs) have proven important during parturition, but inhibition of PG production treating preterm labor (PTL) results in significant maternal and fetal side effects. We hypothesize that specific inhibition of either cyclooxygenase (COX)-1 or -2 may result in separation of therapeutic and toxic effects. We demonstrate that COX-2, but not COX-1, is induced during inflammation-mediated PTL caused by lipopolysaccharide (LPS) administration. A two- to threefold increase in uterine and ovarian PG concentrations coincides with this induction of COX-2. The COX-2-selective inhibitor SC-236 proved effective in stopping preterm delivery and the increases in PGs. The COX-1-selective inhibitor SC-560 also attenuated uterine and ovarian PG production after LPS but did not inhibit PTL as efficiently as SC-236. COX-1-deficient mice, which show delay in the onset of term labor, exhibited no delay in onset of PTL after LPS. These findings suggest that the mechanisms for initiation of inflammation-mediated PTL and term labor differ and that selective COX-2 inhibition may provide a means of stopping inflammation-induced PTL in humans.

Citing Articles

Unlocking the Cervix: Biological Mechanisms and Research Gaps in Preterm Birth.

Felix J, Bartosch C, Matias A Cureus. 2024; 16(11):e72835.

PMID: 39618778 PMC: 11608575. DOI: 10.7759/cureus.72835.


Integration of transcriptomics and metabolomics reveals the responses of the maternal circulation and maternal-fetal interface to LPS-induced preterm birth in mice.

Cao X, Zhou X, Chen S, Xu C Front Immunol. 2023; 14:1213902.

PMID: 37649476 PMC: 10464907. DOI: 10.3389/fimmu.2023.1213902.


The great obstetrical syndromes and the placenta.

Hoffman M BJOG. 2023; 130 Suppl 3:8-15.

PMID: 37530495 PMC: 10834844. DOI: 10.1111/1471-0528.17613.


The adrenal stress response is an essential host response against therapy-induced lethal immune activation.

Guo L, Wang W, Wang Q, Hao D, Ito M, Huang B Sci Signal. 2023; 16(777):eadd4900.

PMID: 36943922 PMC: 10091512. DOI: 10.1126/scisignal.add4900.


Circumvention of luteolysis reveals parturition pathways in mice dependent upon innate type 2 immunity.

Siewiera J, McIntyre T, Cautivo K, Mahiddine K, Rideaux D, Molofsky A Immunity. 2023; 56(3):606-619.e7.

PMID: 36750100 PMC: 10023352. DOI: 10.1016/j.immuni.2023.01.005.