The pathophysiology of sepsis is not completely understood. Bacteria are the main cause of sepsis. Activated receptors of the innate immune system lead to an exaggerated immune response. Immune cells including activated neutrophils and macrophages express and are controlled by a variety of cytokines, chemokines, complement factors and other mediators. These proinflammatory factors induce the expression of secondary mediators such as lipids and reactive oxygen species leading to further amplification of inflammation. Due to loss of control mechanisms in sepsis the immune response causes damage of the own organism. The early phase of sepsis is characterized by a proinflammatory response. In contrast, in the late stage of sepsis an anti-inflammatory milieu is observed that can cause severe immunosuppression. An overview will be given on the recent advances in understanding the interaction of different pathophysiological mechanisms and potential therapeutic interventions in the complex and dynamic syndrome of sepsis.