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Order of events: Phagocytosis
- 1. Chemotaxis
- 2. Adherence
- 3. Ingestion
- 4. Digestion
- 5. Formation of residual body
- 6. Discharge of waste material
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Examples of 2 main phagocytes
- Monocytes (macrophages)
- Neutrophils
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Phagocytosis: Ingestion
- By formation vesicle (by pseudopods of phagocyte) and
- after ingestion called phagosome
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Phagocytosis: digestion
Phagocyte fuses with lysosome (have digestion enzymes) --> Phagolysosome bacteria is digested
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Residual body
Phagolysosome containing undigested components of pathogen
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Non specific defense
Same immune response any type of pathogen
Quick response time, no memory of previous exposure
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First Line of Defense
- Skin
- Mucous membranes
- Secretions
- Normal Microbiota
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Protective Factors of Skin
- 1. Sebum/oil (lysozyme) rich in fatty acid --> acidic pH on skin
- 2. Keratinized epidermis keeps skin dry
- 3. Closely packed cells
- 4. Periodic shredding of skin cells
- 5. Sweat- high salt concentration
- 6. Lysozyme present in sweat (damages peptidoglycan) hurt GM positive bacteria
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Protective factors of conjunctiva of eye
- Tears (rich in salt and lysozyme)
- Tears flush out eyes
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Protective factors of respiratory tract
Mucous: Ciliary living (ciliary escalator)
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Protective factors of GI tract
- Acidic pH (gastric juice)
- Movement of food (peristalsis) through GI tract
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Genitourinary tract
- Urine- flushes the urinary tract
- Vaginal pH and normal floura is acidic (prevents pathogen growth)
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gastroferritin
reduces iron for pathogen to use
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microbial antagonism
Competition among microbes (observed b/w normal microbiota and pathogens)
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Normal microbiota protect host by
- Occupying niches that pathogens might occupy
- producing acids
- producing bacteriocins
- changing oxygen availability
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Second Line of Defense
- Complement System
- Inflammation
- Phagocytosis
- Fever
- Antimicrobial compounds
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Antimicrobial compounds
- Interferon
- Transferrin
- Antimicrobial peptides
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Blood
- Plasma (fluid)
- Formed elements RBC (Erythrocytes)
- WBC (Leukocytes defense)
- Platelets (Thrombocyts) blood clotting
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3 Types of white blood cells
- Granulocytes
- Agranulocytes
- Lymphocytes
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3 Types of Granulocytes
- Neutrophils
- Basophils
- Eosinophils
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Basophils
- Granulocytes
- Produce histamine
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Eosinophils
- Granulocyte
- Allergic reaction, destroy helminths
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Agranulocytes (monocytes) Macrophages
Large nucleus, mature into macrophages, phagocytosis
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2 categories of agranulocytes (macrophages)
- Wandering- Can leave blood vessel and reach infection)
- Fixed- Non motile, localized to specific tissue
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Examples of Fixed agranulocytes
- Microglia cells (nervous tissue)
- Kupffer cells (liver)
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Lymphocytes
- Natural Killer cells
- T cells
- B cells
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Helper T Cells
Secrete cyotkine (chem messenger) and activates other cells (B cells, T cytotxic cells) Cytotoxic T Cells (destroy infected cells)
tumor specific response
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High during viral infections
Lympohtocytes
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Eosinophils
High during allergies/ helminth infection
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HIgh w/ bacterial infection
Neutrophils
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Plasma
Has blood clotting factor
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Serum
- Not clotting factors present (rich in antibodies)
- Used to diagnose an infection by detecting presence of specific antibodies
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Primary lympoid organs
- Production and maturation of blood cells
- Red Bone Marrow (production of all RBCs)
- Thymus gland (T lymphocytes mature here)
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Secondary lymphatic organs
- Lymph nodes (maturation, storage of WBCs)
- Spleen
- Tonsils
- Pever's patch (small intestine)
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Complement System
Consists of a group of proteins called complement components (C1-C9, P, B, D). One component then triggers another. Present in inactive form in blood serum (no pathogen present)
When activated, splits into two subcomponents
All pathways activate C3 component
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Classical Pathway of complement activation
- Mediated by antibodies against protein or polysaccharide angiten
- (2 sites- antigen binding site; part of cell surface against which antibodies are produced)
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Alternative pathway for complement activation
Mediated by factor B, P (properdin), D, able to recognize LPS (lipopolysaccharide) angitens
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Lectin Pathway of complement activation
Carbohydrate binding proteins that bind to carbohydrate antigen of a pathogen
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Three results of complement system
- Opsonization
- Inflammation
- Cytolysis
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Opsonization
- Coat the pathogen, helps phagocyte recognize and ingest pathogen easily
- C3b- oposonin, coating protein bind to antigens of pathogen
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Inflammation (and chemotaxis)
By release of histamine from some cells (mast cells, ect.)
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Cytolysis
Formation of MAC in plasma membrane of bacteria
Destroys the pathogen (forms holes in pathogens membrane) C5b+C6+C7+C8+C9 all bind together and form an attacking complex which forms holes in invading pathogens cytoplasm membrane
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C3a activates
C5--> C5a and C5 b
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C5a and C3a act as
Chemotatic factors (attracts phagocytes) also initiates inflammation
Mast cells have receptors for C3a, C5a, which activate mast cells to release histamine (vasodilator)
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Inflammation
Localized, nonspecific immune response, 2nd defense
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Purpose of Inflammation
- Prevent spread of pathogen
- Destroy pathogen
- Tissue repair
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Signs and symptoms of inflammation
Pain, localized heat, redness, swelling
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Sequence of events of inflammation
- 1. Tissue Damage
- 2. Release of acute phase proteins (histamine, prostaglandins, leukotrienes)
- 3. Vasodilation: Increase in diameter of blood vessel, supplies WBC's , more O2, clotting factors
- 4. Phagocytic migration (Chemotaxis) (ex- C3a, C5a, complement componenet, leukotrienes)
- 5. Phatgocytic margination: attachment of phagocyte to inner lining of blood vessels (endothelium)
- 6. Phagocytic emigration (diapedesis)- phagocytes are released (squeezed out) between gaps of endothelial cells increased vascular permeability
- 7. Phagocytosis
- 8. Tissue Repair (more nutrients and O2)
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Examples of vasodilators
Histamine, Protaglandins
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Protaglandin
Increases vascular permeability
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Fever
A systemic immune response (not localized)
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Purpose of fever
Enhances immune response; helps inhibit growth of bacteria (denatures enzymes)
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Interferons
Proteins produced in response to viral infection
- Host-cell-specific (species specific) but not virus specific
- Have to be of human orgin to create disease in humans
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Types of interferons
- Alpha and Beta- Inhibit viral infection
- Gmmas- activate macrophages and neutrophils (cytokines)
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Mechanism of alpha and beta interferons
- Produced by a
- viruses infected cells
Infected cell secretes infereron that bind to receptor on neighboring, uninfected cell.
- Uninfected cell is stimulated to produce anti-viral
- protines (AVP’s)
- AVP’s degrade viral RNA and inhibit
- protein synthesis
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Transferrin
Iron binding proteins in teh blood, reduces availability of free iron for pathogen
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Antimicrobial peptides
- example: Defensins, 40 amino acids long
- Broad spectrum of activity; inhibit metabolism, forms holes in membrane of pathogen
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