Inflammation/inflammatory response

Human bodies are constantly exposed to a plethora of bacteria, viruses, and other inflammatory substances. To combat these infections and toxic agents, the body has developed a carefully regulated inflammatory response system. Part of that response is the orderly migration of leukocytes to sites of inflammation. Leukocytes literally roll along the vascular wall and into the tissue site of inflammation. This rolling movement is mediated by reversible adhesive interactions between the leukocytes and the vascular surface. 

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]. 

The objectives of the inflammatory response can be viewed as a hierarchical ordered panel of events. The most successful consequence of an inflammatory response is the complete restoration of function and structure of the affected tissue, also denoted as resolution. If this is not possible, inflammation aims for healing by repair and replacement of lost tissue by scar tissue. 

Fig. 4.1 Hypothetical model of pathogenesis of pain in DSP. (1) Injury of peripheral nerve fibers due to multifocal inflammation and secreted macrophage activation products results in abnormal spontaneous activity of neighboring uninjured nociceptive fibers ( peripheral sensitization ). (2) Furthermore, the aberrant inflammatory response in DRG leads to alterations in neuronal sodium and calcium channel expression and ectopic impulse generation. (3) This results in central remodeling within the dorsal horn due to A-fiber sprouting and synaptic formation with pain fibers in lamina 11, and maintenance of neuropathic pain ( central sensitization ). Reproduced with permission from (Keswani et al. 2002)...

Inflammation is a non-specific reaction which can be induced by a variety of agents apart fiom microorganisms. Lymphokines and derivatives of arachidonic acid, including prostaglandins, leukotrienes and thromboxanes are probable mediators of the inflammatory response. The release of vasoactive amines such as histamine and serotonin (5-hydroxytryptamine) firm activated or damaged cells also contribute to inflammation. 

Tea extracts have been demonstrated to inhibit a wide range of inflammatory responses and may be useful in treating chronic inflammatory states. For example, rheumatoid arthritis is an inflammatory disease that causes pain, swelling, stiffness and loss of function in the joints. The antioxidants in green tea may prevent or reduce the severity of these symptoms by reducing inflammation and slowing cartilage breakdown (Adcocks et al, 2002 Haqqi et al, 1999). 

Colorectal cancer is a well-established complication of ulcerative colitis (Lennard-Jones era/., 1990 Ekbom et al., 1990). It has been shown that inflammation enhances the formation of colonic tumours in experimental animals given known carcint ens (Chester etal., 1986) and it is tempting to speculate that the longterm inflammatory response is respronsible for the increased risk of malignancy in ulcerative colitis. However, there is very little direct evidence to support this. It has also been postulated that free radicals may play a part in the development of sporadic cancers (Babbs,... 

---