Meeting Abstract
Marsupials and placental mammals have diverged substantially in life history: marsupials produce highly altricial young which complete development attached to the mother’s nipple, whereas placental mammals have evolved the potential for extended pregnancy. The traditional explanation for this pattern is that marsupials are constrained by a rejection-like immune response upon contact of fetal and maternal tissues that is incompatible with prolonged gestation. Indeed, transcriptomic and histological studies of the opossum Monodelphis domestica have shown that an inflammatory phase of pregnancy begins after intrauterine hatching from the shell coat and progresses until birth. However, it has remained unclear whether this phenomenon is defensive inflammation, a tissue damage response, or a modified pregnancy-specific derivative of inflammation. If the constraint model for marsupial pregnancy is accurate, we would expect that inflammation proceeds as in a normal defensive immune response of host to pathogen, and that the fetus is expelled because it is not masked from the maternal immune system. Predictions of this model were tested by identifying the cellular origin of inflammatory signals in opossum pregnancy using immunohistochemistry and in situ hybridization. In at least two key pathways, prostaglandin synthesis and the cytokine interleukin-17, pro-inflammatory signals were found to originate from both the fetus and the mother, rather than the mother alone. We therefore reject that opossum parturition is a maternal attack upon the fetus, and instead propose that inflammation has been evolutionarily stabilized in this marsupial, potentially as a way for the fetus to effect its own birth. We name this new model cooperative inflammation and shall discuss its implications for the evolutionary narrative of mammalian viviparity.
