Lecture 15: Chronic Inflammation final

Question 1

Tuberculosis

13

Answer 1

Prototype of granulomatous disease
Closely related slow growing mycobacteria

M. tuberculosis, M. africanum (Human TB)
M. bovis (domestic & wild animals – zoonotic)

M. microti, M. caprae, M. pinnipedii

attenuated M. bovis BCG vaccine

Question 2

Describe the pathogenesis of Terburculosis

15

Answer 2

Bacteria enters the body –usually via inhalation (ingestion, skin penetration).
Phagocytosis by mØ (alveolar mØ) may travel to regional LN.
Bacillus is destroyed (usually ~95%),
OR is inhibited by the mØ (suspended animation),
OR it multiplies and eventually destroys the alveolar mØ.

Bacilli multiply, lyse host cells, infect other mØ and may disseminate.
With time, mØ and bacilli accumulate in the lesion (alveoli, lymph nodes)  tubercle formation.
There is concurrent Ag presentation by infected mØ to Helper T-cells

Question 3

Describe the acquired immune response

20-21

Answer 3

Acquired Immune Response
Ag presentation by mØ to THo, is associated with IL-12 production by the mØ and activation of the THo TH1,
mØ also produce TNF to recruit monocytes
TH1 –> IFN-g to activate the mØ
AND –> IL-2 to activate other T cells
Activated mØ attempt to kill the IC mycobacteria via NO, NO2 & HNO3.

Acquired Immune Response
IL-2 activated CD8 T cells kill infected mØ
–> caseous necrosis (may allow disease spread)
Mycobacteria- decrease survival in the ECS (=acidic, low O2),
Activated mØ (IFN-g from CD4 or CD8 T cells) may phagocytose the released mycobacteria and destroy

Question 4

What is the mechanism that mycobacteria use to evade the host response?
24

Answer 4

Mechanisms Mycobacteria use to evade host response:
Cell envelope components (lipids)
Mycobacterial metabolic pathways (urease)
Modulation of acquired immune response (IL-10, IFN-g, TNF-a) eg LAM

Question 5

There is many histology picture in this one you might need to know about

Answer 5

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