To determine the role of systemic effects of inflammation at traumatic brain disease caused by severe traumatic brain injury. The study is performed on 65 white outbred male rats. TBI is applied with one blow on animal’s cranial vaults with blow energy of 0.52 J. The rate of mortality within the first 5 days after the injury is 87%. Experimental animals have got severe closed TBI. Blood contents of circulating immune complexes, C-reactive protein, ceruloplasmin, proinflammatory - interleukins(IL-1b, IL-6, IL-8 and tumor necrosis factor a -TNF-a) are investigated. The circulating immune complexes levels are increased 3.1 times in 24 hours and 4.4 times on the 5th days of trauma reflecting the progressive accumulation of metabolites and toxins in brain tissue and in the blood of injured animals. Blood levels of C-reactive protein are markedly increased in all periods of observation exceeding the control levels 3.5 times in 3 hours and 21.3 times after 5th day of trauma. Thus the study results suggest that the acute phase of systemic inflammation sets at the end of the 1st day after the trauma and it progresses in the course of traumatic brain disease. Blood contents of IL-1b increases continuously: 4.7 times in 3 hours; 7.6 times in 24 hours; and 17.4 times on the 5th day after trauma. The other interleukins levels are also increased but to a lesser extent. The coherence of changes in levels of circulating immune complexes, acute-phase proteins and interleukins indicates a pathogenic pattern of the acute period of traumatic disease at traumatic brain injury: spreading of damage processes with the involvement of body organs and tissues and the establishment of a systemic inflammatory reaction stage from the second day of posttraumatic period.