Pathological inflammatory states

We have prepared pure dog Hp by our method for human Hp type 1-1. Rabbit-antidog Hp serum was easily obtained. It was found to cross-react with human Hp. The Hp-level in dog plasma increases after injection of endotoxin or turpentine (G7), and, as in humans, it increases after surgical trauma (A9) and disappears after Hb injection (VI). In rats, guinea pigs, and rabbits the plasma Hp level rises markedly after induction of different types of inflammatory states (II, M5, R3), but the absolute values never reach the high level seen in pathological conditions in man. 

Increased cytokine production may also play a role in silica-induced autoimmune vascular disease. Adhesion molecule expression is elevated on vascular endothelial cells in response to TNF-a and IL-1. Adhesion molecules such as endothelial leukocyte adhesion molecule-1 (ELAM-1) and intercellular adhesion molecule-1 (ICAM-1) recruit inflammatory cells to specific sites on the vascular endothelium, and it has been hypothesized that vascular pathology following silica exposure may be the result of this interaction (Nowack et al., 1998). IFN-y is expressed at elevated levels by lymphocytes in silicotic thoracic lymph nodes and may be responsible for the long-lasting inducible nitric oxide synthase (iNOS) expression in these tissues (Friedetzky et al., 2002). The increase in IFN-y may also cause a shift towards a dominant Thl response, contributing to the maintenance of a chronic inflammatory state in silica-containing lymph nodes (Gam et al., 2000). 

Differentiation of hip joint disorders from paraarticular pathologies is of the utmost importance because their treatment and prognosis are different. While advanced inflammatory states and degenerative conditions limit joint motion and are readily evident on standard radiographs, therapy is more effective if started early, before the occurrence of advanced joint damage. In general, physical examination of patients with disorders affecting the hip joint is characterized by stiffness and local pain-... 

The wide range of inflammation-related factors that adipocytes secrete is linked to the inflammatory response that the tissue exhibits in obesity [1]. Obesity in general, like an increasing number of other diseases, is characterised by a state of mild chronic inflammation, and adipose tissue plays a central role in this. The production of most inflammation-related adipokines increases markedly in obesity and there is an elevated circulating level of a number of these factors as well as of other inflammatory markers such as C-reactive protein (CRP). The increased production of inflammatory adipokines (and decreased production of adiponectin with its anti-inflammatory action) in the obese is considered to play a critical role in the development of the obesity-associated pathologies, particularly type 2 diabetes and the metabolic syndrome [1]. 

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