Body Defence Mechanisms
Non specific defence mechanisms Specific defence mechanisms
general protection against all types of - 3rd line of defence
foreign substances, X distinguish one - Antigens
infectious agent from another - Lymphocytes (B cells, T cells)
- 1st line of defence
- Physical barriers (skin, blood clot,
inner wall of respiratory tract)
- Chemical barriers (tears, sebum,
gastric juice, vaginal secretion)
- 2nd line of defence (enter body
already)
- Phagocytosis (WBCs,
antimicrobial proteins)
- Inflammatory responses 紅腫痛
熱 (redness, swelling, pain,
hotness)
Inborn, always active Acquired when immune system stimulated
by antigens
Immediate protection (within hours) Slow protection (in days)
No memory of type of pathogens Immunological memory produced by
memory cells
Non adaptive (x improved protection) Adaptive (protective improves in
subsequent invasions by same antigen)
Non specific defence mechanisms
Physical barriers
Skin Blood clot Inner wall of respiratory tract
Cover ~whole body 1. Damaged blood vessel - Closely packed
- Dead outermost attract blood platelets cells (barrier):
epidermal cells (tough, 2. Soluble fibrinogen prevent pathogen
impermeable barrier): @plasma > net of entry
prevent pathogen entry insoluble fibrin - Mucus @mucus
- Constantly shed, (trapping blood secreting cells: trap
replaced by new cells platelets, RBCs, WBCs) pathogens in inhaled
underneath: remove 3. Blood clot dries up > air
, pathogens on skin scab - Cilia @ciliated
surface epithelial cells beat:
- Prevent further bleeding sweep mucus with
- Seals wound: prevent trapped pathogens
pathogen entry towards the pharynx
- Protect underneath > coughed up /
injured tissue while new swallowed into
skin grows stomach (pathogens
killed by HCl)
Chemical barriers
Tears (tear glands), Sebum Gastric juice Vaginal secretion
saliva (sebaceous glands) (gastric glands)
(salivary glands)
Lysozyme: break Antiseptic: kill HCl: kill most Acidic: discourage
down bacterial cell pathogens @skin pathogens bacterial growth
wall > kill certain
bacteria
Phagocytosis
by phagocyte: a kind of WBC @blood, organs lungs liver spleen lymph nodes
1. Phagocytes move toward pathogen
2. Engulf pathogen by phagocytosis
3. Pathogens digested by enzymes inside phagocytes
4. Phagocytes release waste materials from digestion by exocytosis
Inflammatory response
Damaged body cells and certain WBCs release substances that stimulate mast cells to
release histamine
1. Arterioles dilate
a. Increase blood flow to infected area
i. higher metabolic activity
ii. Blood carries heat, increased skin temp at wound
b. Infected area become: red and hot
2. Permeability of capillary walls increase
a. More plasma, phagocytes squeeze out to infected area:
i. More tissue fluid formed, accumulated locally
1. Infected area become: swollen
ii. More tissue fluid press against nerve ending, exert pressure,
stimulating pain receptors
1. Infected area become painful
Non specific defence mechanisms Specific defence mechanisms
general protection against all types of - 3rd line of defence
foreign substances, X distinguish one - Antigens
infectious agent from another - Lymphocytes (B cells, T cells)
- 1st line of defence
- Physical barriers (skin, blood clot,
inner wall of respiratory tract)
- Chemical barriers (tears, sebum,
gastric juice, vaginal secretion)
- 2nd line of defence (enter body
already)
- Phagocytosis (WBCs,
antimicrobial proteins)
- Inflammatory responses 紅腫痛
熱 (redness, swelling, pain,
hotness)
Inborn, always active Acquired when immune system stimulated
by antigens
Immediate protection (within hours) Slow protection (in days)
No memory of type of pathogens Immunological memory produced by
memory cells
Non adaptive (x improved protection) Adaptive (protective improves in
subsequent invasions by same antigen)
Non specific defence mechanisms
Physical barriers
Skin Blood clot Inner wall of respiratory tract
Cover ~whole body 1. Damaged blood vessel - Closely packed
- Dead outermost attract blood platelets cells (barrier):
epidermal cells (tough, 2. Soluble fibrinogen prevent pathogen
impermeable barrier): @plasma > net of entry
prevent pathogen entry insoluble fibrin - Mucus @mucus
- Constantly shed, (trapping blood secreting cells: trap
replaced by new cells platelets, RBCs, WBCs) pathogens in inhaled
underneath: remove 3. Blood clot dries up > air
, pathogens on skin scab - Cilia @ciliated
surface epithelial cells beat:
- Prevent further bleeding sweep mucus with
- Seals wound: prevent trapped pathogens
pathogen entry towards the pharynx
- Protect underneath > coughed up /
injured tissue while new swallowed into
skin grows stomach (pathogens
killed by HCl)
Chemical barriers
Tears (tear glands), Sebum Gastric juice Vaginal secretion
saliva (sebaceous glands) (gastric glands)
(salivary glands)
Lysozyme: break Antiseptic: kill HCl: kill most Acidic: discourage
down bacterial cell pathogens @skin pathogens bacterial growth
wall > kill certain
bacteria
Phagocytosis
by phagocyte: a kind of WBC @blood, organs lungs liver spleen lymph nodes
1. Phagocytes move toward pathogen
2. Engulf pathogen by phagocytosis
3. Pathogens digested by enzymes inside phagocytes
4. Phagocytes release waste materials from digestion by exocytosis
Inflammatory response
Damaged body cells and certain WBCs release substances that stimulate mast cells to
release histamine
1. Arterioles dilate
a. Increase blood flow to infected area
i. higher metabolic activity
ii. Blood carries heat, increased skin temp at wound
b. Infected area become: red and hot
2. Permeability of capillary walls increase
a. More plasma, phagocytes squeeze out to infected area:
i. More tissue fluid formed, accumulated locally
1. Infected area become: swollen
ii. More tissue fluid press against nerve ending, exert pressure,
stimulating pain receptors
1. Infected area become painful
