Basics on inflammation

1. Chronic inflammation
NURS 218

2. ACUTE INFLAMMATION,
CHRONIC INFLAMMATION,
OR FIBROUS SCARRING?
Acute
insult
Acute
inflammation
Damage
slight?
Y
es
Resolution
possible
No
Chronic
insult
Chronic
inflammation
Repair
and
SCARRING

3. CHRONIC INFLAMMATION
• May ‘take over’ from acute inflammation
• if damage is too severe to be resolved within a few days.
• May arise directly in some circumstances
• e.g. some autoimmune conditions, some chronic
infections
• i.e. chronic low-level irritation
• May develop alongside acute inflammation
• in more severe persistent irritation
• What is chronic inflammation?
• Characterised by the microscopic appearances.
• Most important characteristic is the type of cell present.

4. Macrophages

5. Macrophages
• Derived from blood monocytes. Various levels of
‘activation’.
• Functions:
• Phagocytosis and destruction of debris & bacteria
• Processing and presentation of antigen to immune
system.
• Control of other cells by cytokine release
• Synthesis; not only cytokines, but also complement
components, blood clotting factors, proteases, ....

6. Lymphocytes

7. Lymphocytes
• Sometimes called ‘chronic inflammatory cells’
(but note they are a normal component of some tissues)
• Functions:
• Complex, mainly immunological.
• B lymphocytes differentiate to produce antibodies.
• T lymphocytes involved in control & some cytotoxic functions.

8. Other cells involved in chronic inflammation
• Plasma cells:
• Differentiated antibody-producing B lymphocytes. Implies considerable
chronicity.
• Eosinophils:
• Allergic reactions, protozoal infestations, some tumours.
• Fibroblasts / Myofibroblasts:
• Recruited by macrophages; make collagen.

9. Eosinophils
Plasma cells

10. ‘Giant’ Cells
• Multinucleate cells made by fusion of macrophages.
Several types.
• Morphology of most chronic inflammatory reactions is
non-specific, BUT proportions of each cell type may
vary in different conditions.
• For example:
• Rheumatoid arthritis: Mainly plasma cells.
• Chronic gastritis: Mainly lymphocytes.
• Leishmaniasis (a protozoal infection): Mainly macrophages.
• Giant cell type may be a help to diagnosis.

11. Langhans type giant cell - Tuberculosis

12. Foreign body type giant cells

13. EFFECTS OF CHRONIC INFLAMMATION
• Fibrosis
• e.g. gall bladder (chronic cholecystitis), chronic ulcers..
• Impaired function
• e.g. chronic inflammatory bowel disease
• Rarely, increased; e.g. mucus secretion, thyrotoxicosis
• Atrophy
• e.g. gastric mucosa, adrenal glands
• Stimulation of immune response
• Macrophage - lymphocyte interactions

14. GRANULOMATOUS INFLAMMATION
• = chronic inflammation with granulomas!
What is a granuloma?
a mass of granulation tissue,
typically produced in response to
infection, inflammation, or the
presence of a foreign substance.

16. Main causes of granulomatous
inflammation:
• Mildly irritant ‘foreign’ material
• Mycobacteria: Tuberculosis, leprosy
• Syphilis
• Other rare infections e.g. some fungi
• Unknown causes: Sarcoid, Wegener’s
granulomatosis (widespread vasculitis), Crohn’s
disease
• Persistent, low-grade antigenic stimulation
• Hypersensitivity

17. Crohn’s disease of terminal ileum

18. Systemic effects of inflammation
1. Fever-It is coordinated by the hypothalamus & by cytokines (IL -1, IL-
6, TNF-α) released from macrophages and other cells
2. Leukocytosis- neutrophilia (bacterial), lymphocytosis (viral,
mycobacteria), eosinophilia (parasitic, asthma)
3. Leucopenia- esp in debilitating conditions, some viral infections etc
4. Endocrine & metabolic responses-The liver secrets acute phase
proteins such as: C-reactive proteins, Serum Amyloid A, Complement
and coagulation proteins
- Glucocorticoids (increased)
- Vasopressin (ADH) (decreased)

19. Systemic effects of inflammation
5. Autonomic responses include;
-Redirection of blood flow from the cutaneous to the deep vascular
bed.
- Pulse rate and blood pressure (increased)
- Sweating (decreased)
6. Behavioral responses- Rigor, chills, anorexia, somnolence, and
malaise
• 7. Weight loss is thought to be due to the action of IL-1 and TNF-α
which increase catabolism in skeletal muscle, adipose tissue and the
liver with resultant negative nitrogen balance.