Previous studies have suggested that increased nitric oxide (NO)-mediated products are found in the livers of subjects with primary biliary cirrhosis (PBC), but the mechanisms involved remain enigmatic. We took advantage of immunohistochemistry and several unique monoclonal antibodies to study inflammatory cells responsible for the generation of NO, the enzymes responsible for NO production, the expression of 3-nitrotyrosine, and the presence of CD68(+) and/or myeloperoxidase (MPO)(+) cells. We examined a total of 113 liver specimens, including 64 with PBC, 19 with primary sclerosing cholangitis (PSC), 6 with non-A, non-B hepatitis, 6 with alcoholic liver disease, 4 with cryptogenic cirrhosis, 4 with biliary atresia, and 10 normal subjects. Twenty-two percent of PBC had elevated expression of 3-nitrotyrosine in their bile duct epithelial cells (BECs) (P =.0316). Furthermore, the BECs in PBC also demonstrated apoptotic changes. MPO-positive inflammatory cells were also noted adjacent to the basement membrane. In contrast, the liver of normal subjects showed few apoptotic changes in the bile ducts, with no evidence of MPO staining in the portal area. Furthermore, sections from livers of subjects with stage I or stage II PBC demonstrated significantly increased inflammatory cell infiltration (P =.0064) and elevated 3-nitrotyrosine expression in BECs (P =.0246) compared with stage III and IV. The presence of 3-nitrotyrosine was closely associated with infiltrating CD68- and/or MPO-positive cells. There was also a stage-associated difference in the presence of bile duct infiltrating cells and 3-nitrotyrosine in PBC with an increase dominant in early stage disease. In conclusion, NO and reactive oxygen species, collectively determined as 3-nitrotyrosine, are associated with bile duct destruction in PBC and are particularly prevalent in early stage disease.

Heat shock protein (Hsp) 60 has been implicated in the pathogenesis of various inflammatory and autoimmune diseases. This study aimed to investigate synovial fluid and serum concentrations of Hsp60 and anti-Hsp60 and their relationship with juvenile idiopathic arthritis (JIA). Forty-eight patients with JIA, including 22 oligo-articular, 19 poly-articular, and 7 systemic diseases, and 33 normal controls were enrolled in this study. Synovial fluid and serum Hsp60 and anti-Hsp60 concentrations were measured via ELISA. Serum concentrations of Hsp60 of active and inactive oligo- and poly-articular JIA were significantly higher than those of normal controls. Serum concentration of anti-Hsp60 in active oligo-articular JIA was higher than that of normal controls (49.25 vs. 35.76 ng/mL, p = 0.059). Similarly, serum concentration of anti-Hsp60 in active poly-articular JIA was significantly higher than that of inactive samples (65.05 vs. 26.54 ng/mL, p = 0.008). In addition, serum concentration of Hsp60 correlated with the time required for remission from flare-ups in patients with JIA. Serum concentration of Hsp60 correlated well with time required for remission from flare-ups in patients with JIA, representing a potential disease marker to monitor disease activity.

Children aged 2-4 years old have higher sensitivity to egg white, ovalbumin, and ovomucoid. Children with egg white and ovalbumin sensitization have a higher risk for atopic dermatitis, and ovalbumin has a more important contribution. Furthermore, we suggested that in children with atopic dermatitis, if they are aged 2-4 years old and are having egg white and ovalbumin sensitization, avoiding eating raw or slightly heated eggs might have a beneficial effect.