Chronic inflammation can last for months or years and is driven by macrophages and lymphocytes. It can be caused by persistent infections, autoimmune reactions, and foreign bodies. Activated macrophages and T cells secrete cytokines and growth factors that lead to tissue damage and fibrosis over time. Macrophages and T cells also interact and stimulate each other, prolonging the inflammatory response. Granulomas are clusters of macrophages that form in response to chronic inflammation and surround foreign materials to isolate them.

2. Fig: Tissue response to an injury

3. Chronic inflammation

4. asbestos, silicon
cholesterol and other lipids

6. Fig: A. Chronic inflammation in the lung, showing all three characteristic histologic features: (1) collection of chronic
inflammatory cells (*), (2) destruction of parenchyma (normal alveoli are replaced by spaces lined by cuboidal
epithelium, arrowheads), and (3) replacement by connective tissue (fibrosis, arrows).
B. In contrast, in acute inflammation of the lung (acute bronchopneumonia), neutrophils fill the alveolar spaces and blood
vessels are congested.

8. Fig. Monocyte

9. Fig: Origin of macrophage

11. 1 day
several months or years
48 hours

13. IL-4 and IL-13,

14. Fig: Classical and alternative macrophage activation. Different stimuli activate monocytes/macrophages to develop into
functionally distinct populations. Classically activated macrophages are induced by microbial products and
cytokines, particularly IFN-γ. They phagocytose and destroy microbes and dead tissues and can potentiate
inflammatory reactions. Alternatively activated macrophages are induced by other cytokines and are important in
tissue repair and the resolution of inflammation.

15. cytokines
eicosanoids

16. Fig:The roles of activated macrophages in
chronic inflammation. Macrophages are
activated by nonimmunologic stimuli
such as bacterial endotoxin or by
cytokines from immune-activated T
cells, particularly interferon-γ (IFN-γ).
The products made by activated
macrophages that cause tissue injury
and fibrosis are indicated. AA,
Arachidonic acid; PDGF, platelet-
derived growth factor; FGF, fibroblast
growth factor; TGF-β, transforming
growth factor β.

17. Fig: Accumulation of macrophages in chronic inflammation

18. Lymphocyte: Morphology and function.

19. T lymphocytes

22. Fig: Macrophage-lymphocyte interactions in chronic inflammation. Activated T cells produce cytokines that recruit
macrophages (TNF, IL-17, chemokines) and others that activate macrophages (IFN-γ). Activated macrophages in
turn stimulate T cells by presenting antigens and via cytokines such as IL-12.

23. Plasma cell: Morphology and function.

26. Fig: Fibroblast: Morphology and function.

32.  Based on morphology:
1. Diffuse granulomatous reaction: Lepromatous
leprosy
2. Tuberculoid granulomatous reaction: Three
varients-
i. Non-caseating tuberculoid reaction
ii. Caseating tuberculoid reaction
iii.Suppurative tuberculoid reaction

37. 4 COMPONENTS
FIBROBLASTS
LYMPHOCYTES
HISTIOCYTES
“GIANT” CELLS

38. Fig: Typical tuberculous granuloma showing an area of central necrosis surrounded by multiple
Langhans-type giant cells, epithelioid cells, and lymphocytes.

39. Fig: Granuloma

40. Fig: Granulomatous inflammation. A. Section of lung from a patient with sarcoidosis reveals numerous discrete
granulomas. B. A higher-power photomicrograph of a single granuloma in a lymph node from the same patient
depicts a multinucleated giant cell amid numerous pale epithelioid cells. A thin rim of fibrosis separates the
granuloma from the lymphoid cells of the node.

41. Fig: A Langhans giant cell shows nuclei arranged on the periphery of an abundant cytoplasm.

42. Fig: A foreign body giant cell has numerous nuclei randomly arranged in
the cytoplasm.

43. Fig: Granulomas of sarcoidosis in a lymph node. They consist mainly of packed macrophages (epithelioid cells)with a
few lymphocytes. Note the presence of a giant cell (red arrow) in the central granuloma and the absence of central
necrosis. Capillaries are also absent, as in all granulomas.

44. 3.
a. Histoplasmosis
b. Blastomycosis
c. coccidiomycosis
4.
a.Schistosomiasis
b.Trichiniasis
c.Filariasis

52. Features Acute inflammation Chronic inflammation
Onset Rapid onset Insidious/delayed onset
Duration of course Short (Days) Long (Weeks to Months)
Specificity Non-specific Specific as it involves Acquired Immunity
Cardinal signs Pain (Dolor),Heat (Calor)
Redness (Rubor),Swelling (Tumor)
Loss of Function (Functio Leasa)
Absent in any of cardinal signs
Causative agents Physical and Chemical damages
Pathogen invasion
Tissue necrosis
Immune response
Presistent infection
Presence of foreign bodies
Autoimmunity
Fundamental Cells
Neutrophils
Macrophages
Monocytes/macrophages, lymphocytes, plasma cells,
fibroblasts, eosinophils, mast cells, neutrophils
Primary Mediators Vasoactive amines (Serotonin, Histamine)
Eicosanoids (Prostaglandins, Thromboxane)
Interferon Gamma , IL12, TNF , Growth Factor, ROS, NO
Fluid Exudation and Edema Present Absent
Tissue injury and fibrosis Usually mild and self limiting Often severe and progressive
Angiogenesis Absent Present
Systemic Manifestation High grade fever
Other 5 cardinal signs
Low grade fever, Loss of weight
Loss of appetite
Peripheral Blood Changes Neutrophil Leukocytosis (bacterial infection), Lymphocytosis
(viral infection)
Often absent
Increase in the level of Antibodies

54. THANK YOU