Splanchnic sympathectomy prevents translocation and spreading of E coli but not S aureus in liver cirrhosis.
BACKGROUND
Spontaneous bacterial peritonitis (SBP) is mainly caused by bacterial translocation of enteric Gram-negative bacteria, predominantly Escherichia coli. The sympathetic nervous system (SNS) is activated in advanced cirrhosis, particularly in the splanchic circulation, and exerts potent immunosuppressive actions. However, the role of splanchnic SNS activity in bacterial translocation and bacterial spreading in cirrhosis remains unclear.


METHODS
E coli or Stapylococcus aureus (10(6) CFU) were given intraperitoneally. After 6 h, mesenteric lymph nodes (MLN), liver, spleen, lung and peripheral blood were harvested from ascitic cirrhotic rats (LC) and healthy controls with and without splanchnic sympathectomy (SE). The bacterial tissue burden was determined by standard microbiological culture techniques. In vitro phagocytic activity of peritoneal polymorphonuclear leucocytes was assessed by FACS analysis.


RESULTS
Under basal conditions SE reduced bacterial translocation to MLN in LC rats from 45% to 17%. LC rats had a marked increase in bacteraemia after E coli and S aureus challenge and an increased incidence and degree of E coli translocation to MLN, liver, spleen and lung compared with control rats. SE prevented bacteraemia in LC rats after E coli but not after S aureus challenge. Prior SE abolished the difference in incidence as well as the bacterial tissue burden in each organ after E coli application in LC rats, being no longer significantly different from control rats with or without SE. The protective effects of SE against E coli were associated with a greater influx of mononuclear cells into the peritoneal cavity and increased phagocytic activity of peritoneal polymorphonuclear leucocytes.


CONCLUSIONS
In cirrhosis with bacterial peritonitis, hyperactivity of the splanchnic sympathetic nervous system contributes to the translocation of E coli but not S aureus to MLN and extraintestinal sites. This indicates a key role for sympathetic drive in the impairment in host defence against Gram-negative bacteria in cirrhosis.
Department of Internal Medicine, School of Medicine, University Hospital, Regensburg, Germany.
M
M
Worlicek
K
K
Knebel
H J
HJ
Linde
L
L
Moleda
J
J
Schölmerich
R H
RH
Straub
R
R
Wiest
D000818:Animals; D018988:Bacterial Translocation / Q000502:physiology*; D002478:Cells, Cultured; D004926:Escherichia coli / Q000502:physiology*; D004927:Escherichia coli Infections / Q000382:microbiology / Q000503:physiopathology; D007421:Intestine, Small / Q000294:innervation; D008106:Liver Cirrhosis, Experimental / Q000276:immunology / Q000382:microbiology* / Q000503:physiopathology; D008297:Male; D020556:Neutrophil Infiltration / Q000502:physiology; D009504:Neutrophils / Q000276:immunology; D010529:Peritoneal Cavity / Q000166:cytology; D010538:Peritonitis / Q000276:immunology / Q000382:microbiology* / Q000503:physiopathology; D010587:Phagocytosis / Q000276:immunology; D051381:Rats; D013153:Splanchnic Nerves / Q000503:physiopathology*; D013203:Staphylococcal Infections / Q000382:microbiology / Q000503:physiopathology; D013211:Staphylococcus aureus / Q000502:physiology*; D013562:Sympathectomy