Chronic Inflammation | Interleukins | Granuloma | Tuberculosis | Macrophages | Pathology Part 3

Chronic inflammation is a delayed response to various factors like autoimmune disorders, cancers, persistent infections, or prolonged acute inflammation. Its basic characteristic involves the presence of macrophages and lymphocytes.

Macrophages phagocytose pathogens or other foreign materials at the inflammation site. Lymphocytes can be T or B types. T cells (specifically CD4+ and CD8+) interact with MHC molecules, and activated CD4+ cells release cytokines, which then prompt B cells and CD8+ cells to release interleukins.

Activated CD4+ cells induce B cells and CD8+ cells to release interleukins, including IL-4, IL-5 (for eosinophil chemotaxis), and IL-10 (which inhibits CD4+ T cells). CD4+ T cells release IL-2 and interferon-gamma (a macrophage activator). CD8+ cells release perforins and granzymes, leading to apoptosis, also known as cytotoxic killing.

In granulomatous inflammation, macrophages ingest material, become enlarged, and fuse to form giant cells, creating a granuloma. Macrophages in this context are also referred to as epithelioid or histiocytes. Granulomas are classified into two types: caseating and non-caseating.

Caseating granulomas have central necrosis and are typical in tuberculosis and certain fungal infections. Non-caseating granulomas lack central necrosis and can occur in response to foreign bodies, sarcoidosis, cat-scratch disease, or Crohn's disease.

For diagnosing tuberculosis, an acid-fast bacterial (AFB) stain is used. For fungal infections, a GMS (Grocott's Methenamine Silver) stain is employed.

The video concludes by reiterating the main points: the importance of macrophages and lymphocytes in chronic inflammation, the role of T and B lymphocytes and interleukins, and the details of granulomatous inflammation, particularly the distinction between caseating and non-caseating types, with special emphasis on tuberculosis.