The containment of fertilized eggs within the maternal body in the presence of a placenta offers a protected environment for the embryo and later fetus to develop, grow and mature in. The ability of the offspring to suit its developmental trajectory to the maternal environment provides evolutionary advantages and requires functional adaptations. The mother, however, is exposed to a plethora of external factors, including common infections, air-pollution and other compounds that stress her immune system. Maternal inflammation requires the fetus to adapt to a temporally altered maternal environment, in which the placenta may not entirely mitigate transfer of an inflammatory signal to the fetus and maternally-derived nutrients may be temporarily decreased. This can acutely result in fetal tissue specific adaptations, but also dysfunction of the placenta or fetal organs, when adaptation is no longer possible. Such adaptations and dysfunctions, even as a result of a brief maternal immune activation (MIA) may result in susceptibility to a wide spectre of diseases postnatally, including neurodevelopmental and psychiatric disorders and cardiovascular diseases. How the decidua, placenta and the fetus respond to acute MIA over time is unknown. As part of this Ph.D. project, I have characterized the response to acute maternal pulmonary inflammation induced by lipopolysaccharide (LPS) across the first 24 h after exposure, across maternal and fetal organs using e.g. RNA-seq, phosphoproteomics and lipidomics. I found that unlike maternal lungs and liver which mounted strong innate immune responses, the decidua and placenta during the first 12 h after MIA, instead upregulated tissue-integrity genes, likely to prevent fetal exposure to an inflammatory signal, and simultaneously downregulated growth-associated genes. Subsequently, 12 - 24 h after exposure, the placenta upregulated biosynthesis and endoplasmic reticulum stress genes in order to return to homeostasis. These decidual and placental responses likely protected the fetus, since I detected no immune response in the fetal liver. Instead, likely due to decreased levels of maternally-derived nutrients, the fetal liver displayed metabolic adaptations, including increases in lipids containing docosahexaenoic acid (DHA), crucial for fat deposits and neonatal brain development. My study shows, for the first time, the acute temporal response to pulmonary MIA across maternal and fetal organs, and sets out exciting paths for future research on mechanisms for placental protection and fetal metabolic plasticity.