All lecture notes for BIOL123 Infection and Immunity
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BIOL123: Infection And Immunity
Instelling
Lancaster University (LU)
25 pages covering all 12 lectures. Includes highlighted definitions. Provides specific examples required in the module.
(I achieved a score of 19.7/75.6%/first in this module)
L1 – Global Impact of Infection diseases
Infectious agent: viruses, bacteria, fungi + parasites
Acute infections = viruses, bacteria + fungi -> symptoms develop rapidly
Chronic infections = parasites -> symptoms have slow progression
Parasites = protists + helminths
Symbiosis: an interaction between 2 different organisms living in close physical association
Types of symbiosis:
Parasitism:1 organism benefits, the other is harmed
Commensalism: 1 organism benefits, the other is neither harmed nor benefits
Mutualism: both organisms benefit
Stages of infectious disease:
1. Incubation period = time between infection + first symptoms
, 2. Prodromal period = short period of mild symptoms
3. Illness = most evident symptoms
4. Convalescence = body returns to normal, immune system fully responded
Resolution = no longer experiencing symptoms
Subclinical disease: host does not reach clinal threshold + clears disease before having a full set of
symptoms
Clinical threshold: full symptoms, disease contracted
Critical threshold: can no longer survive
Disease Progression:
1. Invasion – host transmission + entry
2. Multiplication – some multiply in body
3. Spread – from initial infection site to other areas in body
4. Pathogenesis – causation + development of clinical disease
Disease progression influenced by: number of pathogenic organisms, virulence, host reaction
Disease severity influenced by: infecting dose, age, sex, genetics…
Global burden of disease:
incidence: number of new cases in a population in a time period
Prevalence: total number of infected individuals at a point in time
Mortality: total deaths per year
Economics + Disability:
HIC – major diseases – cancer, Heart disease
LIC – infectious diseases – AIDS, tuberculosis
• Mortality does not give full picture of full burden of disease
• Morbidity: state of ill health -> lower quality of life
DALY = Disability Adjusted Life Year: measure of years lost due to premature mortality + morbidity
DALY = YLL + YLD YLL = Years of life lost YLD = Years lost to disability
DALY Disadvantages: doesn’t consider economic impacts, treatment costs, social stigma around
disease
Innate Immune System: local inflammatory response + systemic acute-phase response
Mechanical Barriers:
Skin – dead cells not infected, low pH in sebaceous gland -> skin dry -> not much nutrients for
pathogen
Tight Junctions – prevent ingested antigens entering bidy
Mucosal surfaces – mucus traps organisms + is shed from body
Innate Immune System Cells:
1. Phagocytes:
Macrophages: engulf + digest pathogens – white, no nucleus, not circular
Neutrophils: internalise bacteria – multinucleated
Dendritic cells: act as APCs – lots of pseudopodia
2. Granulocytes
Basophils: release histamine, heparin + immunoglobin – largest granulocyte + many granules
Neutrophils: release chemicals to kill pathogens + can kill itself to release sticky DNA -> trap
Eosinophils: stimulate mast cells + release granules to kill parasites – bilobed nucleus
Mast cells: release heparin, serotonin + histamine – light green nucleus, dark green
cytoplasm + pink granules
3. Lymphocytes
Natural killer cells: kill infected or cancerous cells – large nucleus
Innate lymphoid cells (ILCs): secrete effector cytokines + regulate functions of other cells
Heparin: anticoagulant -> blood thinner
Histamine: increase blood vessel wall permeability
Serotonin: neurotransmitter
Immunoglobin: antibodies
Inflammation:
Symptoms: Calor, Rubor, Tumor + Dolor
Chemokines = family of cytokines
1. Damaged endothelial cells release IL-8 (Interleukin 8/ CXL8)
2. Macrophages release TNF-α (Tumour necrosis factor)
3. TNF-α + IL-8 recruit Neutrophils
4. Mast cells release histamine -> vasodilation: increase blood vessel permeability
5. TNF-α + IL-6 stimulate Systemic Acute-Phase Response
6. Clotting + complement cascade activation due to pro-inflammatory cytokines TNF- a + IL-6
7. Neutrophils secrete chemokines -> recruits monocytes
8. Phagocytosis by macrophages
9. Macrophages migrate into tissue + release IL-1 (Interleukin 1) + TNF-α
Systemic Acute-Phase Response:
Fever – increase temp -> speed up phagocytosis
Leucocytosis: increase white blood cell production
Acute-phase protein production in liver:
1. C-Reactive Protein (CRP) binds to microbes
2. Activates complement proteins -> aid phagocytosis
• Macrophages secrete IL-6 -> activates complement
• Cells produce IFNs (Type 1 interferons) + IL-8
Complement Summary
Complement system: group of serum (blood) proteins in blood, perform critical defence against
pathogens, especially in extracellular bacteria
= Soluble proteins produced by the liver
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