Central Nervous System cells exhibit significant diversity and specialization, not only between cell types and functions, but also regarding their morphology. Such morphological and functional polarization complexity is due to the uneven distribution of proteins at a subcellular level. This distribution can be obtained either by protein transport to a specific cell site, or by mRNA transport and in site translation in a stimulus dependent manner, allowing cells to react to environmental changes, mechanism called local protein synthesis or local translation. Local protein synthesis has been long known to happen in neurons. However, evidence suggests that oligodendrocytes, astrocytes, and radial glia also rely on local translation to maintain protein homeostasis and functional integrity. Local translation in microglia has been observed, but its specific relationship to pathology remains unclear. Given the scant evidence, our study aims to investigate the existence of local translation in microglial peripheral processes (PeMPs) and unravel its functional significance in response to inflammation. Using primary microglia cultures and bacterial lipopolysaccharides (LPS), we have seen that Actb mRNA polarizes to PeMPs and is locally translated upon LPS exposure. Interestingly, downregulation of the Actb binding protein IMP1/ZBP1 impaires Actb mRNA polarization and its localized translation, and leads to defects in PeMP motility, directed migration and phagocytosis in microglia. We also conducted immunohistochemical and in situ hybridization analyses following intraperitoneal LPS injections in 1 month old mice. Results suggest that LPS enhances local protein synthesis in vivo, as phosphorylation levels of ribosomal protein Rsp6 increase in cortical PeMPs. We analyzed Actb mRNA levels in mice and observed an increase in cortical growth cone (GC)-like PeMPs and in phagocytic pouches in the dentate gyrus in response to LPS. Interestingly, IMP1 expression increases in primary PeMPs in the cortex and in phagocytic pouches in response to LPS. Indeed, we observed a significant positive correlation between Actb and IMP1 in phagocytic microglia suggesting IMP1 drives Actb localization in vivo. Altogether, our study confirms local translation in PeMPs and that it is enhanced in microglial inflammatory response with LPS suggesting a functional relevance of this molecular mechanism in response to inflammation. This adds to the evidence supporting mRNA localization and localized translation in microglia, offering mechanistic insights into their crucial role in responding to inflammation.