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Chronic and granulomatous inflammation
Chronic inflammation is prolonged inflammation in which inflammation, tissue destruction and attempted repair proceed together, with mononuclear cells — macrophages, lymphocytes and plasma cells — and a granuloma is a special form of it: an organised collection of epithelioid macrophages, sometimes with giant cells, around an agent that is hard to eliminate.
Why it matters in the exam
The bank asks about macrophage types, granuloma types and their causes. A "classically activated" (M1) macrophage, driven by IFN-γ from Th1 cells and microbial products, kills micro-organisms and promotes inflammation. An "alternatively activated" (M2) macrophage, driven by IL-4 and IL-13, secretes growth factors and TGF-β, promotes repair and fibrosis and acts against inflammation. The Th1 response is based on IFN-γ and activates macrophages; Th2 on IL-4, IL-5 and IL-13 and recruits eosinophils; Th17 on IL-17 and recruits neutrophils.
In a granuloma, IFN-γ turns macrophages into epithelioid cells, and some fuse into multinucleated giant cells: in the Langhans cell the nuclei are arranged like a horseshoe at the periphery, and in the foreign-body giant cell they are scattered. A granuloma with central caseous necrosis characterises tuberculosis, and sometimes fungal infections. Non-necrotising granulomas are seen in sarcoidosis, Crohn disease, berylliosis and foreign-body reactions. Stellate suppurative granulomas in lymph nodes characterise cat-scratch disease (Bartonella).
Multinucleated giant cells do not arise only in granulomas: viruses such as measles, herpes and RSV cause cell fusion (polykaryon). Systemic consequences of chronic inflammation: anaemia of chronic disease mediated by hepcidin, deposition of AA amyloid, and weight loss from TNF. In a biopsy with granulomas, stains for acid-fast bacteria and fungi are mandatory and culture should be considered before diagnosing a non-infectious disease.
Key points
- Chronic inflammation: inflammation, destruction and repair together.
- M1 driven by IFN-γ kills; M2 driven by IL-4 and IL-13 repairs.
- Caseating: tuberculosis; non-necrotising: sarcoidosis, Crohn, foreign body.
- Stellate suppurative: cat-scratch disease.
- Always exclude infection by stains and culture.
Summary table
| Type | Morphological feature | Examples | Stain or test |
|---|---|---|---|
| Caseating granuloma | Cheesy central necrosis | Tuberculosis, some fungal infections | Ziehl-Neelsen, GMS, culture |
| Non-necrotising granuloma | Epithelioid macrophages without necrosis | Sarcoidosis, Crohn, berylliosis | Exclude infection |
| Foreign-body granuloma | Giant cells with scattered nuclei around material | Sutures, talc | Polarised light |
| Stellate suppurative granuloma | Central pus | Cat-scratch disease | Warthin-Starry |
| M2 macrophage | TGF-β and growth factors | Repair and fibrosis | — |
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Sources
- Robbins and Cotran Pathologic Basis of Disease, 10th edition (2021) — Inflammation and repair — chronic inflammation
- Rubin's Pathology: Mechanisms of Human Disease, 8th edition (2020) — Inflammation — granulomatous inflammation
- Abbas AK, Lichtman AH, Pillai S. Cellular and Molecular Immunology, 10th edition (2022) — Macrophage activation and T helper subsets
Sources are given for further reading; the text is written afresh and not copied from them.
Reviewed by the Examqo AI Professor · 2026-11-06. The text may contain errors; when in doubt, check the source.