If the condition causing acute inflammation is not resolved, the inflammation may pass to a longer term chronic phase. Also, some pathogies by their nature tend to directly provoke chronic rather than acute inflammation. Many of the features of acute inflammation continue as the inflammation becomes chronic, including increased blood flow and increased capillary permeability. Accumulation of white blood cells also continues, but the composition of the cells changes.
As the last page describes, neutrophils quickly enter the infected tissue, and these short-lived cells predominate initially. However, soon macrophages and lymphocytes begin to be recruited. The sequence by which they bind to cell adhesion molecules and pass through the endothelium is the same as for neutrophils. Thus, the primary cells of chronic inflammation are macrophages and lymphocytes.
Macrophages live far longer than neutrophils. As their name suggests, macrophages phagocytize pathogens and other material at the site of the inflammation. Because they are long-lived, indigestible material may remain inside macrophages in vesicles for long periods. As described previously, macrophages are important secretory cells releasing inflammatory paracrines, growth factors, and a variety of other proteins.
Macrophages are avid phagocytes, and, even if they can't digest all the material phagocytized, they will continue to engulf more. Here is a light micrograph of macrophages distended with lipid from broken down myelin at the site of necrotic tissue due to a blocked blood vessel in the brain. Observe the large amount of nearly clear cytoplasm.
Lymphocytes entering the inflammed tissue can serve several roles. Most notable, perhaps, are the T cells that activate macrophages. This is important for dealing with difficult pathogens. But this issue will arise most frequently in the context of autoimmune diseases, in which activated macrophages often are a major factor causing the damage. B cells making antibodies also can be present in inflammed tissue, adding antibodies locally to those that enter from the blood.
This light micrograph is of brain tissue in multiple sclerosis. Observe the lymphocytes emerging from the venule. (How can you tell they are lymphocytes?)
This light micrograph shows thyroiditis in Hashimotos disease, in which chronic inflammation destroys the thyroid gland. Note the lymphocytes.
In certain cases of chronic inflammation, macrophages collect in layers surrounding the problematical material. Sometimes the macrophages will fuse, forming giant cells. The structure so formed, with layers of macrophages surrounding a central core, is called a granuloma. Granulomas are a characteristic feature of a tuberculosis, in which macrophages can't destroy the phagocytized bacteria, apparently because the bacteria somehow prevent lysosomes from fusing with the phagocytic vesicles. What happens in chronic granulomatous disease?.
The figure to the right shows an early granuloma, triggered by tuberculosis bacteria, in which the interior of the granuloma has not yet become necrotic.
QUESTION: Macrophages are characteristically found in chronic inflammation. Name a second cell of this type.
QUESTION: Name two disorders characterized by granulomas.
QUESTION: Scroll up through the figures on this page, briefly describing what you see and why.