Bacterial translocation, microcirculation injury and sepsis.
Sepsis is the result from a complex bacterial-host interaction, which is an often-fatal response when host protective molecular mechanisms designed to fight invading bacteria surpass the beneficial intensity to the point of causing injury to the host. Increasing evidences have implicated the bacterial translocation (BT) as the main source for the induction of sepsis, although the beneficial effect of BT process has been related to the development of the intestinal immune response by physiological interaction between bacteria and host. In this article, we examined evolving concepts concerning to BT and discussed about its potential role in the promotion of microcirculation injury, moreover, its possible participation in the sepsis induction. According to our data obtained from in-vivo BT animal-model, both bacterial overgrowth and bacterial pathogenic determinants seem to be major predisposing factors for the induction of BT. Besides, translocation of luminal bacteria through the lymphatic via elicits the activation of the GALT inflammatory response contributing to microcirculation injuries, and the haematological via of BT was responsible to the systemic bacterial spread. On other hand, the combination of BT process to the pre-existing host systemic infection played a crucial role in the worsening of the clinical outcome. In our understanding, studies concerning to intestinal immune response and the pathophysiology of bacterial-host interaction, under normal and disease conditions, seems to be the key elements to the development of therapeutic approaches towards sepsis.
Koh
I H J
IH
Department of Surgery of Escola Paulista de Medicina, Federal University of São Paulo, São Paulo, Brazil. ivankoh@terra.com.br
Liberatore
A M A
AM
Menchaca-Diaz
J L
JL
Ruiz-Silva
M
M
Vilela-Oliveira
L
L
Watanabe
A Y
AY
Salomao
R
R
Fagundes-Neto
U
U
Silva
R M
RM
D000818:Animals; D018988:Bacterial Translocation / Q000502:physiology*; D006801:Humans; D007422:Intestines / Q000098:blood supply / Q000276:immunology / Q000382:microbiology; D008833:Microcirculation / Q000276:immunology / Q000293:injuries* / Q000382:microbiology*; D018805:Sepsis / Q000276:immunology / Q000382:microbiology*