title: The IL-1 system in HIV infection: peripheral concentrations of IL-1beta, IL-1 receptor antagonist and soluble IL-1 receptor type II.
abstract: The proinflammatory cytokine IL-1beta is thought to be involved in ongoing HIV disease. Furthermore, its naturally occurring inhibitors soluble IL-1 receptor type II (sIL-1RII) and IL-1 receptor antagonist (IL-1Ra) may play a pivotal role in regulating its biological action. To investigate the involvement of the IL-1 system we determined serum levels of IL-1beta, IL-1Ra and sIL-1RII in 90 HIV- patients. The obtained values were compared with markers of disease progression such as CD4+ count, 5'-neopterin. Beta2-microglobulin and soluble tumour necrosis factor receptors (sTNF-R) p55 and p75 and then compared with C-reactive protein (CRP), granulocyte count, IL-6 and TNF-alpha. While IL-1Ra concentrations increased significantly with progressive CDC disease stages, sIL-1RII and IL-1beta were not altered in our cohort. IL-1Ra showed statistical relation to decreasing CD4+ lymphocytes and increasing 5'-neopterin, beta2-microglobulin, sTNF-R p55, sTNF-R p75. Furthermore, IL-1Ra correlated positively with serum IL-6, TNF-alpha, CRP and granulocytes. In contrast, sIL-1RII and IL-1beta tended to show an inverse correlation or showed no significant relationship to all these parameters. IL-1beta was measurable only in a limited number of samples. IL-1Ra showed a clear relationship to acute inflammatory events as well as to the different disease stages. Our data suggest a dissociation between IL-1Ra and sIL-1RII serum levels which may indicate that the two IL-1 binding proteins have different pathophysiological roles in HIV infection.
authors.affiliation: Department of Medicine, University of Bonn, Germany.
authors.forename: K A
authors.initials: KA
authors.lastname: Kreuzer
authors.forename: J M
authors.initials: JM
authors.lastname: Dayer
authors.forename: J K
authors.initials: JK
authors.lastname: Rockstroh
authors.forename: T
authors.initials: T
authors.lastname: Sauerbruch
authors.forename: U
authors.initials: U
authors.lastname: Spengler
mesh_terms: D000328:Adult; D000368:Aged; D001708:Biopterins / Q000031:analogs & derivatives / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis; D018791:CD4 Lymphocyte Count; D018450:Disease Progression; D005260:Female; D006098:Granulocytes / Q000276:immunology; D015658:HIV Infections / Q000097:blood / Q000276:immunology*; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000032:analysis / Q000276:immunology*; D015850:Interleukin-6 / Q000032:analysis; D008297:Male; D008875:Middle Aged; D019798:Neopterin; D017472:Receptors, Interleukin-1 / Q000032:analysis / Q000276:immunology*; D053574:Receptors, Interleukin-1 Type II; D018124:Receptors, Tumor Necrosis Factor / Q000032:analysis; D012795:Sialoglycoproteins / Q000032:analysis / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D001613:beta 2-Microglobulin / Q000032:analysis
chemical_list: C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D015850:Interleukin-6; D017472:Receptors, Interleukin-1; D053574:Receptors, Interleukin-1 Type II; D018124:Receptors, Tumor Necrosis Factor; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha; D001613:beta 2-Microglobulin; D001708:Biopterins; D019798:Neopterin; D002097:C-Reactive Protein