Persistent infections by microorganisms that are difficult to eradicate, such as mycobacteria and certain viruses, fungi, and parasites. These organisms often evoke an immune reaction called delayed-type hypersensitivity (Chapter 5). The inflammatory response sometimes takes a specific pattern called granulomatous inflammation (discussed later). In other cases, unresolved acute inflammation evolves into chronic inflammation, such as when an acute bacterial infection of the lung progresses to a chronic lung abscess.
Hypersensitivity diseases. Chronic inflammation plays an important role in a group of diseases that are caused by excessive and inappropriate activation of the immune system (Chapter 5). In autoimmune diseases, self (auto) antigens evoke a self-perpetuating immune reaction that results in chronic inflammation and tissue damage; examples of such diseases are rheumatoid arthritis and multiple sclerosis. In allergic diseases, chronic inflammation is the result of excessive immune responses against common environmental substances, as in bronchial asthma. Because these autoimmune and allergic reactions are triggered against antigens that are normally harmless, the reactions serve no useful purpose and only cause disease. Such diseases may show morphologic patterns of mixed acute and chronic inflammation because they are characterized by repeated bouts of inflammation. Fibrosis may dominate the late stages.
Prolonged exposure to potentially toxic agents, either exogenous or endogenous. An example of an exogenous agent is particulate silica, a nondegradable inanimate material that, when inhaled for prolonged periods, results in an inflammatory lung disease called silicosis (Chapter 13). Atherosclerosis (Chapter 10) is a chronic inflammatory process affecting the arterial wall that is thought to be induced, at least in part, by excessive production and tissue deposition of endogenous cholesterol and other lipids.
Some forms of chronic inflammation may be important in the pathogenesis of diseases that are not convention ally thought of as inflammatory disorders. These include neurodegenerative diseases such as Alzheimer disease, metabolic syndrome and the associated type 2 diabetes, and certain cancers in which inflammatory reactions promote tumor development. The role of inflammation in these conditions is discussed in the relevant chapters.
In contrast to acute inflammation, which is manifested by vascular changes, edema, and predominantly neutrophilic infiltration, chronic inflammation is characterized by the following:
Infiltration with mononuclear cells, which include macrophages, lymphocytes, and plasma cells (
Fig. 3.17
Tissue destruction, induced by the persistent offending agent or by the inflammatory cells
Attempts at healing by connective tissue replacement of damaged tissue, accomplished by angiogenesis (proliferation of small blood vessels) and, in particular,
Fig. 3.17 (A) Chronic inflammation in the lung, showing all three characteristic histologic features: (1) collection of chronic inflammatory cells (*), (2) destruction of parenchyma (normal alveoli are replaced by spaces lined by cuboidal epithelium, arrowheads), and (3) replacement by connective tissue (fibrosis, arrows). (B) In contrast, in acute inflammation of the lung (acute bronchopneumonia), neutrophils fill the alveolar spaces and blood vessels are congested.
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Because angiogenesis and fibrosis are also components of wound healing and repair, they are discussed later, in the context of tissue repair.
Cells and Mediators of Chronic Inflammation
The combination of leukocyte infiltration, tissue damage, and fibrosis that characterize chronic inflammation is the result of the local activation of several cell types and the production of mediators.
Role of Macrophages