title: Expression of proinflammatory cytokines and their inhibitors during the course of spontaneous bacterial peritonitis.
abstract: The aim of this work was the evaluation, in cirrhotic patients with noninfected ascites and with spontaneous bacterial peritonitis (SBP), of serum and ascitic fluid levels of proinflammatory cytokines [interleukin (IL) 1-beta, tumor necrosis factor alpha (TNF-alpha), and IL6] and antiinflammatory compounds [IL10, soluble IL-1 receptor antagonist (sIL-1Ra), soluble receptors of TNF p55 and p75 (sTNFR55 and sTNFR75), and soluble receptor of IL6 (sIL6R)], as well as their relationship with the outcome of the infection in those with SBP. These molecules were assayed by ELISA in noninfected cirrhotic controls (n = 15), patients with SBP (n = 32), and healthy controls (n = 20). Serum levels of IL6 and of the majority of antiinflammatory mediators, sIL1Ra, sTNFR75, and sIL6R, were higher in control cirrhotic patients compared to healthy subjects. SBP was associated with significantly elevated ascitic fluid levels of every one of the proinflammatory cytokines compared to those in cirrhotic controls. Also, serum levels of IL10 and both TNF receptors and ascitic fluid levels of sIL1Ra and sTNFR55 were higher in patients with SBP compared to cirrhotic controls. Ascitic fluid levels of proinflammatory cytokines decreased rapidly after resolution of the infection; however, nonsignificant changes were detected in ascitic fluid concentrations of antiinflammatory molecules. Thus, elevated levels of antiinflammatory compounds both in noninfected cirrhotic patients and in patients with SBP suggest a regulatory control of the inflammatory process by these molecules in liver cirrhosis patients.
authors.affiliation: Digestive Diseases, Hospital Universitario Puerta del Mar, Cádiz, Spain.
authors.forename: C
authors.initials: C
authors.lastname: Rodríguez-Ramos
authors.forename: F
authors.initials: F
authors.lastname: Galan
authors.forename: F
authors.initials: F
authors.lastname: Díaz
authors.forename: J
authors.initials: J
authors.lastname: Elvira
authors.forename: L
authors.initials: L
authors.lastname: Martín-Herrera
authors.forename: J A
authors.initials: JA
authors.lastname: Girón-González
mesh_terms: D015703:Antigens, CD / Q000032:analysis; D001202:Ascitic Fluid / Q000737:chemistry; D001424:Bacterial Infections / Q000150:complications / Q000378:metabolism*; D016207:Cytokines / Q000032:analysis* / Q000037:antagonists & inhibitors; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis* / Q000037:antagonists & inhibitors; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000032:analysis; D016753:Interleukin-10 / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D008103:Liver Cirrhosis / Q000150:complications; D008297:Male; D008875:Middle Aged; D010538:Peritonitis / Q000150:complications / Q000378:metabolism*; D018124:Receptors, Tumor Necrosis Factor / Q000032:analysis; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D012795:Sialoglycoproteins / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D015703:Antigens, CD; D016207:Cytokines; C507763:IL1RN protein, human; D018836:Inflammation Mediators; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D015850:Interleukin-6; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10