Atherosclerosis is strongly modulated by inflammatory components. Furthermore, arterial blood flow is an important modulator of plaque location and plaque progression. The connection between blood flow and plaque progression is found in shear stress, i.e. the frictional force induced by the blood flow, exerted on the endothelium. If shear stress and inflammation play an important role in atherosclerosis, both factors may influence each other. In this review, the role of shear stress on inflammation is evaluated. Because low shear stress has been associated with plaque formation, we specifically sought how low shear stress affects inflammation. By reviewing the literature, we were able to formulate important mechanisms in which low shear stress might interfere with monocyte accumulation. These mechanisms will be discussed in details in the present review.