AI Article Synopsis
- Infection-induced inflammation and proinflammatory cytokines are linked to preterm birth, highlighting the role of the immune system in this process.
- A study found that mice lacking the cannabinoid receptor 2 (CB2) were resistant to preterm birth induced by lipopolysaccharide (LPS) and did not experience a drop in serum progesterone levels.
- The absence of CB2 led to increased IL-10 and decreased IL-6 after LPS exposure, suggesting that augmented cAMP accumulation in these mice could be a potential mechanism for their resistance to preterm birth, which may have important clinical implications.
Article Abstract
Infection-induced inflammation, frequently associated with increased production of proinflammatory cytokines, is considered a significant contributor to preterm birth. A G protein-coupled cannabinoid receptor 2 (CB2), encoded by Cnr2, is expressed in various immune cells and was shown to modulate immune responses. We show here that Cnr2, but not Cnr1, deficient mice are resistant to lipopolysaccharide (LPS)-driven preterm birth and suppression of serum progesterone levels. After LPS challenge, Cnr2(-/-) mice exhibited increased serum levels of IL-10 with decreased IL-6 levels. These changes were associated with reduced LPS-induced Ptgs2 expression at the maternal-conceptus interface on day 16 of pregnancy. LPS stimulation of Cnr2(-/-) dendritic cells in vitro resulted in increased IL-10 with reduced IL-6 production and correlated with increased cAMP accumulation. Collectively, our results suggest that increased IL-10 production occurring via augmented cAMP accumulation represents a potential mechanism for the resistance of Cnr2(-/-) mice to LPS-induced preterm birth. These results may have clinical relevance, because currently, there are limited options to prevent preterm birth.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4164934 | PMC |
| http://dx.doi.org/10.1210/en.2014-1387 | DOI Listing |
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