Soluble interleukin-6 receptor, interleukin-10 and granulocyte colony-stimulating factor in acute pyelonephritis: relationship to markers of bacterial virulence and renal function.
BACKGROUND
Cytokines and cytokine receptors are involved in the systemic and local inflammatory response in patients with urinary tract infections.


METHODS
We examined urine and serum concentrations of soluble IL-6 receptor (sIL-6R), IL-10 and granulocyte colony-stimulating factor (G-CSF) in 29 women with acute pyelonephritis caused by Escherichia coli 2 weeks after the infection, during the subsequent episode of cystitis or asymptomatic bacteriuria and also later when the same patients were free from bacteriuria. Concentrations of sIL-6R, IL-10 and G-CSF were related to the expression of five virulence markers of E. coli and to glomerular filtration rate (GFR) after pyelonephritis.


RESULTS
On admission because of acute pyelonephritis the serum concentration of sIL-6R was similar to that of 12 healthy controls. Two weeks after the infection when all patients had received antibiotic treatment, the serum concentration of sIL-6R was significantly higher compared to that on admission (p < 0.001) and also higher compared to healthy controls (p = 0.001). Patients with increased concentrations of sIL-6R in serum 2 weeks after infection had significantly lower GFR at follow-up (p < 0.05). Patients with acute pyelonephritis had higher concentrations of G-CSF and IL-10 in serum compared to healthy subjects (p < 0.001 and p = 0.06, respectively). G-CSF in serum was higher in patients infected by E. coli producing cytotoxic necrotizing factor (p < 0.05). Patients infected by strains producing hemolysin had lower concentrations of sIL-6R (p < 0.001). Patients with detectable levels of the anti-inflammatory cytokine IL-10 in serum had significantly higher concentrations of IL-6 and the soluble tumor necrosis factor receptors I and II in serum as compared to patients in whom IL-10 was not detectable (p < 0.001, p = 0.001 and p < 0.05, respectively.


CONCLUSIONS
These investigations, together with our previous findings summarized in this paper, contribute to an increased understanding of the local and systemic inflammatory response arising in response to acute pyelonephritis.
Jacobson
S H
SH
Department of Nephrology, Karolinska Hospital, Stockholm, Sweden. staco@divmed.ks.se
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Y
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Brauner
A
A
D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D000368:Aged; D004926:Escherichia coli / Q000472:pathogenicity*; D004927:Escherichia coli Infections / Q000188:drug therapy / Q000378:metabolism* / Q000652:urine; D005260:Female; D016179:Granulocyte Colony-Stimulating Factor / Q000097:blood / Q000378:metabolism* / Q000652:urine; D006801:Humans; D016753:Interleukin-10 / Q000097:blood / Q000378:metabolism* / Q000652:urine; D007668:Kidney / Q000503:physiopathology*; D008875:Middle Aged; D011704:Pyelonephritis / Q000188:drug therapy / Q000378:metabolism* / Q000652:urine; D019947:Receptors, Interleukin-6 / Q000097:blood / Q000378:metabolism*; D012995:Solubility; D014774:Virulence
D019947:Receptors, Interleukin-6; D016753:Interleukin-10; D016179:Granulocyte Colony-Stimulating Factor