Macrophages play a significant role in the initiation and perpetuation of innate and adaptive immune responses. In this role, they perform multiple functions, including the uptake, processing and presentation of antigen, microbial killing, phagocytosis of apoptotic cells, and the secretion of cytokines, chemokines and chemical mediators . The expression and secretion of immune modulators imparts the macrophage the ability to orchestrate immune responses, skewing them toward the pro-inflammatory, anti-inflammatory or regulatory arms of immunity. While pro-inflammatory responses are crucial to the elimination of pathogens, they are also central to the pathogenesis of autoimmune (for example type 1 diabetes, multiple sclerosis and rheumatoid arthritis) and pro-inflammatory (for example sepsis) diseases. Accordingly, much research has focused on understanding the responses of macrophages to pro-inflammatory conditions. These investigations often use murine bone marrow derived macrophages (BMDM), as a model mammalian macrophage system [2–4]. This is because BMDMs exhibit phenotypic and functional homogeneity and closely resemble ex vivo primary cells, thereby making them the preferable model, as opposed to other sources of primary macrophages or cell lines. Immortalised cell lines differ significantly in phenotype/function to primary murine macrophages. Primary resident macrophages of the peritoneum or lung are not naïve, and, therefore, differ phenotypically/functionally according to their previous immune experiences. Moreover, these cells are obtained in lower numbers, as compared to yields derived from bone marrow.