Viral infection-induced inflammation during pregnancy has been associated to malformations of the fetal brain. Microglia, the brain-resident macrophages, respond to inflammatory signals and at the same time are actively involved in various aspects of brain development. We know surprisingly little about how microglia balance the different demands during human embryonic development and which functional consequences an inflammatory environment has on neuronal organization and connectivity. Human induced pluripotent stem cells (hiPSC) provide a unique opportunity to investigate this relationship.Here, we differentiate hiPSC into functional microglia-like cells (iMG) and retinal organoids (RO) and generate microglia-assembled retinal organoids (iMG-RO) to overcome the limitation that organoids commonly lack microglia. We observed that iMG successfully integrated into 2D-dissociated retinal organoid cultures where they remove cellular debris and actively phagocytose ganglion cells. Then, we applied poly(I:C) to mimic a fetal viral infection. The established microglia-dependent inflammatory response resulted in an increased proliferation rate and elevated the calcium peak amplitude of retinal cell types. To modify the poly(I:C)-mediated effects, we applied the anti-inflammatory drug Ibuprofen, which can be taken during the first half of pregnancy. The treatment ameliorated the inflammatory response concurrently rescued the poly(I:C) mediated consequences on retinal development. Our results provide first insights into how inflammation during pregnancy might lead to neurological phenotypes in human and give a first intuition how these might increase occurrence of mental health issues in adult.