Interstitial Myocarditis
Damage to the myocardial stroma most commonly results from infectious or toxic agents. Two main forms of the disease are distinguished: predominantly exudative and predominantly productive.
In the productive form, histological sections (stained with hematoxylin and eosin) clearly demonstrate an inflammatory infiltrate within the myocardial interstitium. This infiltrate is composed primarily of lymphohistiocytic and monocytic cells. A distinct variant is Fiedler's myocarditis—a severe form of the disease with an allergic pathogenesis.
Tubulointerstitial Nephritis
Inflammation of the renal interstitium develops secondary to impaired urine outflow (with the development of acute pyelonephritis), various infections, intoxications, or prolonged drug therapy (e.g., phenacetin). Renal stroma exhibits marked edema and infiltration by lymphocytes and plasma cells. 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 interstitium alongside the development of fibrosis (predominantly perivascular and periductal). Against the background of tubular degeneration and necrosis, epithelial regeneration is triggered.
Interstitial Inflammation of the Liver
In the liver, the process can also occur in acute or chronic forms, primarily involving stromal elements.
- Acute inflammation: changes are localized in the portal tracts, where a serous mononuclear infiltrate forms, sometimes admixed with polymorphonuclear leukocytes. Hepatocellular degeneration is observed in the parenchyma. Progression may lead to transformation into chronic hepatitis.
- Chronic hepatitis: lymphomacrophagic infiltration of the stroma is typical. The process is accompanied by the destruction of parenchymal elements and inevitably leads to portal tract sclerosis.
Interstitial Pneumonia and Fibrosing Alveolitis
Interstitial pneumonia is most commonly caused by viruses, rickettsiae, or mycoplasmas. During the acute phase, edema of the interstitial tissue develops along with its infiltration by hematogenous cells. The productive component of the inflammation is represented by damaged type II pneumocytes, alveolar macrophages, septal cells, and endothelial cells.
Chronic interstitial pneumonia is known as fibrosing alveolitis. It is often idiopathic, but occasionally triggered by toxic substances or drugs. The pathogenesis includes four sequential stages:
- Damage to cellular and extracellular structures of the interalveolar septa.
- Proliferation of endothelial cells and type II pneumocytes.
- Infiltration of the interstitium by hematogenous inflammatory and immunocompetent cells.
- Accumulation of fibroblasts.
The regular outcome of fibrosing alveolitis is the development of septal-alveolar sclerosis.