Wound-healing response

Chronic inflammation is a leading component and contributing event to the pathogenesis of fibrotic disease, where a normal inflammatory response to injury becomes a chronic, pathologic wound-healing response. 

Consumption of fish oil in excess can generate immunotoxic effects in laboratory animals. Rats fed a 17% fish oil diet had reduced wound-healing responses when compared to com oil [59], In a mouse model of bacterial resistance to S. typhimurium, lower survival rates were reported for those animals that ingested a 20% fish oil diet over 15 days [59], Similar fish oil-induced effects in guinea pigs were noted in a study of experimental tuberculosis leading the authors to conclude that this treatment resulted in decreased resistance to infectious disease. The consumption of fish oil has also been reported to result in alterations of hemostatic parameters such as platelet production and function. However, there is no indication that at doses normally consumed by humans, immunotoxicity will occur. 

The acute inflammatory process is associated initially with increased HA levels, the result of the cytokines released by the polymorphonuclear leukocytes, the predominant cells of the acute inflammatory process. The erythema, swelling, and warmth of the acute process are followed later by the characteristic dry appearance and the formation of wrinkles. The precise mechanisms are unknown, but may relate to the differences between acute and chronic inflammatory cells and the attendant chemical mediators released by such cells. Alternatively, initiation of a wound healing response, with collagen deposition, may be a mechanism invoked for the premature aged appearance of the skin in chronic inflammation. 

Hepatic fibrosis is seen with chronic exposure to hepatoxicants that cause increasing damage to hepatocytes and is part of the wound healing response. Chronic fibrosis leads to severe disruption of the liver architecture by the deposition of extracellular matrix (ECM). Advanced fibrosis disrupts the proper blood flow and results in scarring of the liver that can lead to irreversible liver damage known as cirrhosis. Chronic exposure to the hepatoxins CCI4, monocrotaline, and alcohol are examples of compounds that cause excessive fibrosis. 

Local and systematic factors may play a role in the wound healing response to biomaterials or implants. Local factors include the site (tissue or organ) of implantation, the adequacy of blood supply, and the potential for infection. Systematic factors may include nutrition, hematologic derangements, gluco-cortical steroids, and preexisting disease such as atherosclerosis, diabetes, and infection. 

Nath LK, Dutta SK (1992) Wound healing response of the proteolytic enzyme curcain. Ind J Pharmacol 24 114-115... 

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