Interstitial inflammation

Interstitial myocarditis

Damage to the heart muscle stroma most often occurs as a result of infectious or toxic exposure. There are two main forms of the disease: predominantly exudative and predominantly productive.

In the productive form, an inflammatory infiltrate is clearly visualized in the interstitial tissue of the myocardium on micropreparations (stained with hematoxylin and eosin). Its basis consists of lymphohistiocytic and monocytic cells. Fiedler's myocarditis (Abramov-Fiedler myocarditis) stands apart as a severe form of the disease of an allergic nature.

Tubulointerstitial nephritis

Inflammation of the renal interstitial tissue develops against the background of impaired urine outflow (with the development of acute pyelonephritis), various infections, intoxications, or prolonged medication use (e.g., phenacetin). Marked edema and infiltration by lymphocytes and plasma cells are observed in the renal stroma. A characteristic morphological feature is the frequent presence of eosinophils.

• Acute course: macrophages appear in the cellular composition of the infiltrate. Dystrophic and necrotic changes predominate in the renal tubules.
• Chronic course: lymphoid infiltration increases in the interstitial tissue, and fibrosis develops (predominantly perivascular and periductal). Against the background of dystrophy and necrosis, epithelial regeneration is triggered in the tubules.

Interstitial inflammation of the liver

In the liver, the process can also occur in an acute or chronic form, affecting predominantly stromal elements.

• Acute inflammation: changes are localized in the portal tracts. A serous mononuclear infiltrate forms there, sometimes mixed with polymorphonuclear leukocytes. Hepatocyte dystrophy is observed in the parenchyma. An outcome with transformation into chronic hepatitis is possible.
• Chronic hepatitis: lymphomacrophagic infiltration of the stroma is typical. The process is accompanied by the destruction of parenchymal elements and inevitably leads to sclerosis of the portal tracts.

Interstitial pneumonia and fibrosing alveolitis

Interstitial pneumonia is most often caused by viruses, rickettsia, or mycoplasmas. In the acute period, edema of the interstitial tissue and its infiltration by cells of hematogenous origin occur. The productive component of inflammation is represented by damaged type II pneumocytes, alveolar macrophages, septal cells, and endotheliocytes.

The chronic form is known as fibrosing alveolitis. It is often idiopathic in nature, but is sometimes provoked by toxic substances or drugs. The pathogenesis includes four consecutive stages:

1. Damage to the cellular and extracellular structures of the interalveolar septa.
2. Proliferation of endotheliocytes and type II pneumocytes.
3. Infiltration of the interstitium by hematogenous inflammatory and immunocompetent cells.
4. Accumulation of fibroblasts.

The regular outcome of fibrosing alveolitis is the development of septoalveolar sclerosis.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Morphological differences between the exudative and productive forms of interstitial myocarditis
• Pathogenesis of Fiedler's allergic myocarditis (Abramov-Fiedler myocarditis)
• Mechanisms of renal tubular damage upon administration of phenacetin-containing drugs
• Cellular interactions during the transformation of acute interstitial hepatitis into chronic
• The role of type II pneumocytes and alveolar macrophages in the development of septoalveolar sclerosis

Other topics in the "Inflammation" section

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