Chapter 3 Inflammation: general principles
Inflammation is the complex coordinated response by vascularized tissue to injury or microorganisms, mediated by:
The word inflammation derives from the Latin for burning. Celsus, the Roman physician, in the first century AD described the four cardinal signs: calor (heat), rubor (redness), dolor (pain) and tumor (swelling). These derive from a series of events.
The suffix -itis signifies inflammation: appendicitis is inflammation of the appendix and arthritis that of joints.
Through inflammation, evolution has equipped the body with a powerful response to tissue damage and to invasion by microorganisms. However, it is a two-edged sword: it is the inflammatory processes themselves, rather than the factors that elicited the inflammation, that are responsible for the clinical features of many diseases. Furthermore, the inflammatory response may be mounted in inappropriate circumstances, for example in autoimmune diseases. Indeed, the potential for inflammation to harm is such that it needs to be tightly controlled by a large number of chemical mediators that interact with cells and with each other in complex interconnected ways (see Ch. 8).
Inflammation is divided into two types: acute and chronic. It is the time-scale that defines these two terms; acute inflammation lasts hours or days, while chronic inflammation lasts more than a few days and continues as long as the injurious agent persists. These two responses have many things in common but are characterized by different cell types and processes.
Phagocytosis and inflammation
Phagocytosis (Greek for eating and cell) is the process by which a cell engulfs and digests an extracellular particle. Although a number of different cells can exhibit phagocytosis under certain circumstances, two types are specifically adapted to phagocytic functions: neutrophils and macrophages. These are sometimes called professional phagocytes. They have important roles in the inflammatory response.
Monocytes (macrophage precursors) and neutrophils are produced in the bone marrow and circulate in the blood. At sites of inflammation, they leave the circulation and migrate to the damaged tissues by amoeboid motion. This same amoeboid ability allows the phagocyte to ingest particles such as bacteria and then digest them within a vacuole (Fig. 3.3.1). The digestive enzymes and free radicals (Fig. 3.3.2) may be released into the extracellular space rather than the phagolysosome, especially if the particle is too large to ingest; this can result in severe tissue damage via oxidation of proteins, lipids and DNA. Cells can be protected from damage by enzymes such as catalase, which promotes the breakdown of hydrogen peroxide, and antioxidants such as vitamins C and E, which free radicals convert to less-reactive derivatives. These defences are useful not only in limiting tissue damage from free radicals released in inflammatory processes but also in scavenging free radicals produced in normal cellular metabolism, ionizing radiation and chemical pollutants. Neutrophils and macrophages can act independently of the immune system and are, therefore, part of innate immunity. However, their function is greatly enhanced by the immune system.