Rheumatoid Arthritis: Castellino G

Corallini F, Bossi F, Gonelli A, Tripodo C, Castellino G, Mollnes TE, Tedesco F, Rizzi L, Trotta F, Zauli G, Secchiero P. · Interdepartmental Center of Molecular Medicine, University of Trieste, Trieste, Italy. · Rheumatology (Oxford). · Pubmed #19168833 No free full text.

Abstract: OBJECTIVE: Complement activation products contribute to a large number of inflammatory diseases, including RA. We have investigated whether osteoprotegerin (OPG) may concur with the soluble terminal complement complex (SC5b-9) to the inflammatory cascade characterizing RA. METHODS: Levels of SC5b-9 and OPG in the plasma and SF of patients with active RA were determined by ELISA. The presence of SC5b-9 and OPG in RA synovial lesions was analysed by immunohistochemistry. Cultured endothelial cells were used for in vitro leucocyte/endothelial cell adhesion assays. In addition, endothelial cells were exposed to SC5b-9 in order to evaluate the effects on the production of OPG protein, as well as the activation of the OPG promoter. RESULTS: Patients affected by active RA are characterized by elevated levels of both SC5b-9 and OPG in plasma and/or SF. Of note, we have observed a co-localization of SC5b-9 and OPG in endothelial cells of post-capillary venules of RA synovial lesions. Data on endothelial cell cultures showed that exposure to SC5b-9 induced the up-regulation of OPG expression/release, stimulating the transcriptional activity of the OPG promoter, and synergized with TNF-alpha in up-regulating OPG production. CONCLUSIONS: Our findings demonstrate that SC5b-9 induces OPG production by endothelial cells and we propose that the SC5b-9-mediated up-regulation of OPG may be an important mechanism whereby complement contributes in promoting and/or enhancing the inflammation in RA.

Brucato A, Doria A, Frassi M, Castellino G, Franceschini F, Faden D, Pisoni MP, Solerte L, Muscarà M, Lojacono A, Motta M, Cavazzana I, Ghirardello A, Vescovi F, Tombini V, Cimaz R, Gambari PF, Meroni PL, Canesi B, Tincani A. · · Lupus. · Pubmed #12475001 No free full text.

Abstract: Anti-Ro/SSA antibodies are associated with neonatal lupus but are also considered a possible cause for unexplained pregnancy loss and adverse pregnancy outcome. In a large multicentres cohort study we have prospectively followed 100 anti-Ro/SSA positive women (53 systemic lupus erythematosus (SLE)) during their 122 pregnancies and 107 anti-Ro/SSA negative women (58 SLE) (140 pregnancies). Anti-Ro/SSA antibodies were tested by immunoblot and counterimunoelectrophoresis. Mean gestational age at delivery (38 vs 37.9 weeks), prevalence of pregnancy loss (9.9 vs 18.6%), preterm birth (21.3 vs 13.9%), cesarean sections (49.2 vs 53.4%), premature rupture of membranes (4.9 vs 8.1%), preeclampsia (6.6 vs 8%), intrauterine growth retardation (0 vs 2.3%)and newborns small for gestational age (11.5 vs 5.8%) were similar in anti-Ro/SSA positive and negative SLE mothers; findings were similar in non-SLE women. Two cases of congenital heart block were observed out of 100 anti-Ro/SSA positive women. In conclusion, anti-Ro/SSA antibodies are responsible for congenital heart block but do not affect other pregnancy outcomes, both in SLE and in non-SLE women. The general outcome of these pregnancies is now very good, ifprospectively followed by multidisciplinary teams with ample experience in this field.

Castellino G, Corallini F, Trotta F, Secchiero P. · No affiliation provided · Ann Rheum Dis. · Pubmed #18621972 No free full text.

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Castellino G, Govoni M, Padovan M, Rizzo N, Trotta F. · No affiliation provided · Ann Rheum Dis. · Pubmed #15769929 links to  free full text

This publication has no abstract.

Castellino G, Govoni M, Trotta F. · No affiliation provided · Rheumatology (Oxford). · Pubmed #11085812 links to  free full text

This publication has no abstract.