In the case of sepsis, the role and participation of platelets in this condition was determined based on the decreased activity resulting from the deficiency of their GPIbβ receptor - a fibrinogen-specific marker, which is manifested by a weaker interaction of platelets/neutrophils and platelets/monocytes, including reduced synthesis of proinflammatory factors such as: TNF-α (Tumour necrosis factor-α), MCP-1, IL-6 and MIP-1β, which in turn reduces the immune status of the macroorganism and increases susceptibility to infection (34, 76, 78). Here, CCL2 is linked to infection.