Serum amyloid A inhibits RANKL-induced osteoclast formation

When mouse bone marrow-derived macrophages were stimulated with serum amyloid A (SAA), which is a major acute-phase protein, there was strong inhibition of osteoclast formation induced by the receptor activator of nuclear factor kappaB ligand. SAA not only markedly blocked the expression of several osteoclast-associated genes (TNF receptor-associated factor 6 and osteoclast-associated receptor) but also strongly induced the expression of negative regulators (MafB and interferon regulatory factor 8). Moreover, SAA decreased c-fms expression on the cell surface via shedding of the c-fms extracellular domain. SAA also restrained the fusion of osteoclast precursors by blocking intracellular ATP release. This inhibitory response of SAA is not mediated by the well-known SAA receptors (formyl peptide receptor 2, Toll-like receptor 2 (TLR2) or TLR4). These findings provide insight into a novel inhibitory role of SAA in osteoclastogenesis and suggest that SAA is an important endogenous modulator that regulates bone homeostasis.

Inflammatory Hepatic Adenoma / 대한소화기학회지

No abstract available.

Intestinal Amyloidosis with Intractable Diarrhea and Intestinal Pseudo-obstruction / 대한소화기학회지

We report herein a case of intestinal amyloidosis with grave prognosis that caused intractable diarrhea and intestinal pseudo-obstruction, alternately in spite of intensive conservative treatment. A 44-year-old woman was admitted for fever, diarrhea, and crampy abdominal pain which had been continuned during 6 months. Abdomen CT scan showed edematous wall thickening of the small bowel and right colon, and colonoscopic biopsy revealed amyloid deposition in the mucosa. Monoclonal light chains in serum and/or urine were not detected and highly elevated serum amyloid A was shown. In spite of intensive treatment including oral prednisolone and colchicine, diarrhea and intestinal pseudo-obstruction developed alternately, general status rapidly got worsened and died after two months.

Lysophosphatidylglycerol inhibits formyl peptide receptor like-1-stimulated chemotactic migration and IL-1beta production from human phagocytes

In this study, we observed that lysophosphatidylglycerol (LPG) completely inhibited a formyl peptide receptor like-1 (FPRL1) agonist (MMK-1)-stimulated chemotactic migration in human phagocytes, such as neutrophils and monocytes. LPG also dramatically inhibited IL-1beta production by another FPRL1 agonist serum amyloid A (SAA) in human phagocytes. However, LPG itself induced intracellular calcium increase and superoxide anion production in human phagocytes. Keeping in mind that phagocytes migration and IL-1beta production by FPRL1 are important for the induction of inflammatory response, our data suggest that LPG can be regarded as a useful material for the modulation of inflammatory response induced by FPRL1 activation.

Capacidade dos biomarcadores inflamatórios em predizer a síndrome metabólica / Inflammation biomarkers capacity in predicting the metabolic syndrome

O processo inflamatório é o elo entre a síndrome metabólica e as doenças cardiovasculares. Para medir o grau da inflamação subclínica, vários biomarcadores inflamatórios têm sido propostos. Este trabalho tem como objetivo revisar as recentes pesquisas das associações entre os biomarcadores inflamatórios e a síndrome metabólica, bem como a capacidade daqueles em predizer a síndrome metabólica. Estes biomarcadores incluem as citocinas pró-inflamatórias, citocinas antiinflamatórias, adipocinas, chemocinas, marcadores de inflamação derivados de hepatócitos, marcadores de conseqüência da inflamação e enzimas. Com esta revisão pode-se integrar o novo conhecimento referente às interações possíveis de mediadores inflamatórios com a síndrome metabólica, visto que estes biomarcadores desempenham vários papéis e seguem diversos caminhos metabólicos.

The inflammatory process is the link between metabolic syndrome and cardiovascular diseases. To measure the degree of subclinical inflammation some inflammatory biomarkers have been considered. This work reviews the recent researches of the associations between inflammatory biomarkers and metabolic syndrome, as well as the capacity in predicting the metabolic syndrome. These biomarkers include pro-inflammatory cytokines, anti-inflammatory cytokines, adipokines, chemokines, inflammation markers derived from hepatocites, the consequence markers of inflammation and enzymes. This review integrates the new knowledge of inflammatory mediators interactions with metabolic syndrome, since these biomarkers play different roles and follow diverse metabolic ways.

Biologic effects of serum amyloid A in rheumatoid arthritis

A-SAA closely reflects measures of disease activity in patients with inflammatory arthritis. A-SAA, like TNF; can induce many of the proinflammatory activities associated with pannus formation and joint destruction in inflammatory arthritis.