Inflammation
Inflammation is a fundamental biological response to pathogens, injury, and toxins. It is a core program of The Immune System and is essential for defense, repair, and homeostasis.
The Five Cardinal Signs
| Latin | Meaning | Physiologic Basis |
|---|---|---|
| Rubor | Redness | Arteriolar vasodilation and increased blood flow (histamine, NO) |
| Calor | Heat | Hyperemia and elevated local metabolism |
| Tumor | Swelling | Vascular permeability → exudate in interstitium (bradykinin, leukotrienes) |
| Dolor | Pain | Nociceptor sensitization by prostaglandins, bradykinin, cytokines |
| Functio laesa | Loss of function | Tissue damage, edema, protective guarding |
Classically described by Celsus and expanded by Virchow in the 19th century.
Acute vs Chronic Inflammation
| Acute | Features |
|---|---|
| Onset | Minutes–hours |
| Cells | Neutrophils → monocytes/macrophages |
| Mediators | Histamine, prostaglandins, leukotrienes, complement, cytokines (IL‑1, TNF) |
| Outcomes | Resolution, suppuration (pus), abscess, or progression to chronic |
| Chronic | Features |
|---|---|
| Onset | Weeks–months |
| Cells | Macrophages, lymphocytes, plasma cells; fibroblasts |
| Mediators | IFN‑γ, IL‑12, TNF, growth factors (TGF‑β) driving fibrosis |
| Outcomes | Tissue destruction, fibrosis, granulomas (if persistent stimuli) |
Cellular Players & Mediators
| Component | Role in Inflammation |
|---|---|
| Endothelium | Vasodilation/permeability; adhesion molecules (selectins, ICAM/VCAM) for leukocyte rolling/firm adhesion |
| Neutrophils | Early responders; phagocytosis; degranulation; NETs |
| Macrophages | Cytokines (IL‑1, TNF), phagocytosis; switch to resolution (IL‑10) or fibrosis (TGF‑β) |
| Mast cells | Histamine release; immediate hypersensitivity |
| Complement | Opsonization (C3b), chemotaxis (C5a), MAC lysis |
| Eicosanoids | Prostaglandins (pain/fever), leukotrienes (permeability/bronchospasm), lipoxins (resolution) |
| Cytokines | IL‑1/TNF (fever, acute‑phase); IL‑6 (CRP/serum amyloid A); chemokines (cell recruitment) |
Resolution & Repair
| Program | Key Elements |
|---|---|
| Active resolution | Class switch to pro‑resolving mediators (lipoxins, resolvins); efferocytosis of neutrophils by macrophages |
| Tissue repair | Angiogenesis, fibroblast activation, collagen deposition; remodeling by MMPs |
| Failure to resolve | Chronicity, fibrosis, organ dysfunction |
Morphologic Patterns
| Pattern | Examples/Notes |
|---|---|
| Serous | Blister fluid; viral pleuritis |
| Fibrinous | Fibrin‑rich exudate lining serosa (uremia, post‑MI pericarditis) |
| Purulent (suppurative) | Abscesses with pus (neutrophils + debris), e.g., Staph infections |
| Pattern | Examples/Notes |
|---|---|
| Ulcer | Loss of epithelium and inflamed base (peptic ulcer) |
| Granulomatous | Macrophage aggregates (epithelioid cells, giant cells) in TB, sarcoid, some foreign bodies |
| Fibrosing | Chronic cytokine drive → collagen deposition and scarring |
Clinical Markers & Evaluation
| Marker/Tool | Use |
|---|---|
| CRP, ESR | Systemic inflammatory activity |
| Leukocyte count / differential | Bacterial vs viral patterns; eosinophilia in allergy/parasites |
| Procalcitonin | Bacterial sepsis guidance |
| Imaging (US/CT/MRI) | Abscess detection, effusion, synovitis |
| Biopsy / cytology | Define pattern (granulomatous vs suppurative), rule out malignancy |
Management Principles
| Scenario | First Principles |
|---|---|
| Infection‑driven | Source control + targeted antimicrobials; avoid unnecessary steroids |
| Sterile inflammatory | NSAIDs, corticosteroids, disease‑modifiers or biologics per diagnosis |
| Resolution support | Address triggers; optimize sleep, nutrition, metabolic health |
Therapy is diagnosis‑specific. This page is educational only.