[Investigations on the etiology of sepsis by using an experimental mouse model with leukocytopenia. 2. The role of the reticuloendothelial system in the etiology of bacteremia].
It has been recognized by clinical data that most of sepsis occurring in the immunocompromised host are endogenous infection. In recent years, we have investigated the mechanism of these bacteremia and sepsis by experimental studies using neutropenic mice treated with cyclophosphamide. And we evidenced that most pathogens causing bacteremia originated in the intestinal flora of the host. It has been shown that bacteria causing bacteremia were divided into two main groups, causing systemic bacteremia and causing portal bacteremia. Pseudomonas aeruginosa and Morganella morganii belonged to the former, on the other hand, Escherichia coli, Enterobacter cloacae and some other bacteria belonged to the latter. In this study, we studied the role of the reticuloendothelial system (RES) in the etiology of bacteremia or sepsis, using various kinds of bacteria isolated from bacteremic mice. As a result, the following facts were revealed. 1. It was suggested that the low blood clearance rate of the bacteria was one of the great risk factor of systemic bacteremia, since the blood clearance rate of bacteria causing systemic bacteremia was significantly lower than those of bacteria causing portal bacteremia. 2. Bacteria in the blood were eliminated by the RES, mainly by the liver, and the level of bacterial clearance by the liver was relative to the type of bacteremia which was systemic or portal. 3. It was suggested that the bacterial clearance by the liver mainly reflected the phagocytosis by Kupffer cells, and especially the adherence of these cells to bacteria as the first step of phagocytosis.
Hirakata
Y
Y
Yamaguchi
K
K
Tomono
K
K
Shimoguchi
K
K
Tateda
K
K
Nouda
K
K
Sugahara
K
K
Kohno
S
S
Hirota
M
M
Hara
K
K
D000818:Animals; D004195:Disease Models, Animal; D008099:Liver / Q000503:physiopathology; D008297:Male; D051379:Mice; D012157:Mononuclear Phagocyte System / Q000503:physiopathology*; D018805:Sepsis / Q000209:etiology*