Abstract : M2-macrophage is abundant in tumour microenvironment. However, the relationship between lymphovascular invasion with M2-macrophage, the secreted cytokine and receptor remained unclear. Haematoxylin and eosin (H&E) and immunohistochemical (IHC) staining on six consecutive sections of 99 formalin fixed-paraffin embedded (FFPE) breast carcinoma samples were carried out. D2-40, CD34, CD163, IL-1β, and ICAM-1 were used to stain lymphatic vessel, blood vessel, M2-macrophage, IL-1β, and ICAM-1 receptor respectively. Results show that although the mean value of blood vessel density (BVD) is higher than lymphatic vessel density (LVD) (p<0.0001), the lymphatic vessel invasion (LVI) is higher than blood vessel invasion (BVI) (p=0.008). Increase of intra-tumoural LVI significantly increases IL-1β expression (p=0.009). High M2-macrophage count is significantly related with increases IL-1β expression (p=0.03). In conclusion, IL-1β might be responsible in tumour metastasis via lymphatic vessel. The infiltration of M2- macrophage might enhance the secretion of IL-1β intra-tumourally in breast carcinoma. Therefore, IL-1β could be the targeted molecules in reducing tumour metastasis rate