RESUMO
White fat cells secrete adipokines that induce inflammation and obesity has been reported to be characterized by high serum levels of inflammatory cytokines such as IL-6 and TNF-alpha. Rheumatoid arthritis (RA) is a prototype of inflammatory arthritis, but the relationship between RA and obesity is controversial. We made an obese inflammatory arthritis model: obese collagen-induced arthritis (CIA). C57BL/6 mice were fed a 60-kcal high fat diet (HFD) from the age of 4 weeks and they were immunized twice with type II collagen (CII). After immunization, the obese CIA mice showed higher arthritis index scores and histology scores and a more increased incidence of developing arthritis than did the lean CIA mice. After treatment with CII, mixed lymphocyte reaction also showed CII-specific response more intensely in the obese CIA mice than lean CIA. The anti-CII IgG and anti-CII IgG2a levels in the sera of the obese CIA mice were higher than those of the lean CIA mice. The number of Th17 cells was higher and the IL-17 mRNA expression of the splenocytes in the obese CIA mice was higher than that of the lean CIA mice. Obese CIA mice also showed high IL-17 expression on synovium in immunohistochemistry. Although obesity may not play a pathogenic role in initiating arthritis, it could play an important role in amplifying the inflammation of arthritis through the Th1/Th17 response. The obese CIA murine model will be an important tool when we investigate the effect of several therapeutic target molecules to treat RA.
Assuntos
Animais , Humanos , Camundongos , Adipocinas/imunologia , Artrite Experimental/genética , Diferenciação Celular/genética , Colágeno Tipo II/administração & dosagem , Modelos Animais de Doenças , Expressão Gênica , Inflamação/induzido quimicamente , Interleucina-17/metabolismo , Interleucina-6/sangue , Articulações/imunologia , Camundongos Endogâmicos C57BL , Obesidade/genética , Células Th17/imunologia , Fator de Necrose Tumoral alfa/sangueRESUMO
The present study was designed to compare the amount of resistin hormone released by explants of human adipose tissue in primary culture either from the visceral fat compartment or from posterior subcutaneous abdominal adipose tissue mass [PSAATM]. Visceral omental and abdominal subcutaneous adipose tissues, representing group I and II respectively, were obtained from 30 women undergoing abdominoplasty with concomitant procedures necessitating opening of the peritoneal cavity. Isolation of fat cells from adipose tissue was done according to the method of Fain et al At the end of the isolation, each group was further subdivided into 4 subgroups [a-d] according to the separation method which were [a] represented explants of adipose tissue, [b] represented adipose tissue debris remaining after digestion of minced adipose tissue, [c] represented non-fat [Stromal-Vascular [SV]] cells, and [d] represented fat cells. Resistin was assayed in each of the 8 subgroups at 24 hours and 48 hours. The release of resistin over 24 h was about half that seen at 48 h by all subgroups. There was a significant greater release of resistin by explants of adipose tissue, adipose tissue debris, SV cells, and fat cells subgroups of omental adipose tissue when compared to the subgroups of subcutaneous adipose tissue explants. It could be concluded that resistin is made and released at much higher levels by the omental adipose tissues than subcutaneous adipose tissues. Whether or not resistin is produced by: the fat cells or non-fat cells of human adipose tissue, needs further investigations