Inflammation is a key process in a lot of diseases including rheumatic diseases. Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disorder that may affect many tissues and organs, but principally attacks the joints producing an inflammatory synovitis that often progresses to destruction of the articular cartilage and ankylosis of the joints.

RA is the most common form of chronic inflammatory joint disease. In its typical form RA is a symmetrical, destructive and deforming polyarthritis affecting small and large synovial joints, with associated systemic disturbance, a variety of extra-articular features and the presence of circulating antiglobulin antibodies (rheumatoid factors). Rheumatoid arthritis can also produce diffuse inflammation in the lungs, pericardium, pleura, and sclera, and also nodular lesions, most common in subcutaneous tissue under the skin.

Although the cause of rheumatoid arthritis is unknown, autoimmunity plays a pivotal role in its chronicity and progression. Characteristically, the course of the disease is prolonged with exacerbations and remissions but atypical, asymmetrical and incomplete forms are not uncommon.

An acute inflammation is characterized by vascular reaction, neutrophils and mast cells activation. The systemic changes associated with acute inflammation are collectively called the acute-phase response, or the systemic inflammatory response syndrome. These changes are reactions to cytokines whose production is stimulated by bacterial products such as LPS and by other inflammatory stimuli. Inflammation is a pattern of response to injury, in which cells and exudate accumulate in irritated tissues and tend to protect from further damage. It may be classified as acute or chronic. Chronic inflammation may result from failure of the recovery phase of acute inflammation, or may occur as a distinct process from the outset, because of the nature of the irritant. Although it shares many characteristics of the acute inflammatory response, chronic inflammation is a biologically distinct pattern of response to an irritant. It may be divided into nongranulomatous and granuloma- tous chronic inflammation; the term granuloma refers to a localized collection of activated macrophages and their derivatives. The systemic efects of inflammation are more pronounced in chronic inflammatory diseases and may contribute significantly to the clinical consequences. These systemic efects are largely mediated by cytokines, coagulation system, kinins, fibrinolytic and complement system. In addition to humoral, there are involved cellular factors too.

In clinical practice to determine the degree of inflammatory activity is often used for laboratory research, including immunology. According to the latest literature, experimental model of collagen and adjuvant-induced arthritis is increasingly used to study the mechanisms of formation of new autoimmune process.

Hence, it is important to create novel experimental animal models that allow developing new strategy for diagnostic and treatment of these diseases.

The purpose of this work was to study the enzymatic activity and protein composition of the blood serum of rats with induced inflammatory arthritis. Experimental acute and chronic arthritis in rats were induced by immunisation of collagen and caragenins respectively. Obtained data showed:

1. In blood serum of the rats with acute inflammation (animals immunized by caragenin) the elevation of alkaline phosphatase and AST activity, as well as the grow of the level of the α1- and α2-globulin fractions and decrease of the level of the γ-globulins fraction were observed.

2. In blood serum of the rats with chronic inflammation (animals immunized by bovine collagen II) the elevation of alkaline phosphatase, ALT, AST activity and growing of the level of α2- and γ-globulins in protein fractions were found. This data correlate chronic stage of inflammation activity in animals.

Keywords: collagen arthritis, carrageenan arthritis, white laboratory rats, albumin, globulins, enzymatic activity

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