Download The Body`s Response to Infection

The Body’s
Response to
Infection
Topic 6.3
Specification- topic 6
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10 Describe the major routes pathogens may take when entering
the body and explain the role of barriers in protecting the body
from infection, including the roles of skin, stomach acid, gut and
skin flora.
12 Describe the non-specific responses of the body to infection,
including inflammation, lysozyme action, interferon and
phagocytosis.
13 Explain the roles of antigens and antibodies in the body’s
immune response including the involvement of plasma cells,
macrophages and antigen-presenting cells.
14 Distinguish between the roles of B cells (including B memory and
B effector cells) and T cells (T helper, T killer and T memory cells) in
the body’s immune response.
15 Explain how individuals may develop immunity (natural, artificial,
active, passive).
Key terms 
What is the immune response?
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What is a pathogen?
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An organism or something which causes disease
What is an antigen?
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responses of an organism when infected by a
pathogen
a molecule the body recognises as foreign: this is
what activates an immune response
What are the 2 types of immune response?
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non-specific and specific
Planning an attack- mission
impossible !
 Where
could our team of intrepid
pathogen enter «THE BODY»?
 What are the weak points?
Physical barriers and chemical
defences which prevent entry into
our body
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Keratin (protein) of the skin and mucus and cilia in the
mucous membranes, physical barrier
Lysozyme in tears, saliva, mucous break down bacterial
cell walls causing them to burst. Q 6.27
Hydrochloric acid in the stomach kills most bacteria which
enter with food
Skin and gut flora are harmless bacteria suited to the
environment (in gut or on skin in spite of the salty sweat,
urea and fatty acids – low pH) which can compete for food
and space better than harmful bacteria. The harmless
bacterial are better adapted to the conditions. In the gut
they may help with digestion and secrete chemicals which
harm the pathogens.
Lysozyme- more detail
 Enzyme
found in tears, saliva and nasal
secretions
 Breaks down bacterial cell walls
 Lysozyme hydrolyses peptidoglycan
 Hydrolysis:
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Breakdown with the addition of water
 Examples
of hydrolysis reactions:
 Polypeptide  amino acid
 starch  maltose  glucose
Now the Pathogens are
inside !!!!
Infection!!!!!
The invasion and multiplication of microorganisms
within the cells and tissues of the body having
evaded the barriers.
Damage to tissue causes
Inflammation
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1.
2.
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From Latin ‘inflammo’= to set on fire
For each of the steps below explain the
significance (purpose)
Histamine is released by damaged tissues causes:
Capillary arterioles to dilate
Capillaries become more permeable
Increased blood supply= redness and heat
More tissue fluid formed= oedema
More white blood cells are present in the tissue,
these fight off any microbes
White blood cells
 Where
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Also found in tissues, not just blood
 Three
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are they found?
types of white cells:
lymphocytes, neutrophils and
monocytes(macrophages)
 What
are phagocytes? Which of the above
are phagocytes?
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Cells which ingest foreign organisms or
chemicals by endocytosis
Neutrophils and monocytes
Neutrophils
 70%
of white cells
 Made in bone marrow
 Live a few days
 Non-specific
 Are attracted by chemicals from
damaged cells: chemotaxis
 Often self destruct during destruction of
invaders: can only ingest 5-20 bacteria

https://www.youtube.com/watch?v=uNG-jZxvhcg
Monocytes
/macrophages
 About
5% of white cells
 Move into tissues soon after production
and become macrophages (big eaters)
 Some move into infected tissues but some
are found permanently in certain tissues:
lungs, brain, lymph nodes
 Longer lived than neutrophils, can ingest
up to 100 bacteria
Phagocytosis
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Activity 6.7 Phagocytosis: Watch animation and draw a
flow diagram with annotated diagrams
Pathogen engulfed by phagocytes
Enclosed within a vacuole
Lysosome fuses with vacuole
Hydrolytic enzymes are released into vacuole= bacteria
destroyed
Radicals also released into vacuole= damage bacterial
DNA and proteins
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Free radicals: are highly reactive due to having unpaired
electrons in the outer shell, important in many processes but are
known to cause cell damage
Phagocytes then present antigens from bacteria to other
immune cells. They do this by placing the antigens in their
cell surface membrane - sticking out.
Phagocytosis
Activity 6.7b, Lymphatic System
1.
2.
3.
4.
5.
6.
Tissue fluid
Blood in under pressure and the high hydostatic
pressure forces some of the plasma out of the thin,
permeable capillary walls. Small molecules can
also cross the capillary wall. Some water re-enters
the capillary due to osmosis at the venule end of
the capillaries.
Lymphocytes and macrophages, they destroy
microbes
Through the right lymphatic duct and thoracic
duct, which enter into the subclavian vein.
Due to the production of more white blood cells to
destroy the pathogen and fight the infection.
Septic shock/blood poisoning- pathogens spread
around the body via blood.
Antimicrobial proteinsInterferon What
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Protein produced by virus infected cells
 What
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does it do?
Protein diffuses to nearby cells
Prevents viral protein synthesis and therefore
formation of new viral particles AND prevents
viruses from attaching to the host cell and therefore
prevents the entry of DNA/RNA into host cell
 How
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is it?
can it be produced as a drug?
Can be produced by using GM bacteria
 Why
is it not widely used?
Fever- explained
 Discuss
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in pairs: what do you think?
Why do we get a fever when we have an infection?
What is the significance of this fever?
Caused by pyrogens, chemicals released by
some white blood cells
 Raises the thermostat- the temperature our body is
set to remain at a higher temperature than 37
degrees Centigrade
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Inhibits growth of some microbes
Speeds up reactions, may speed up repair of tissues
Can facilitate phagocytosis
https://www.youtube.com/watch?v=GIJK3dwCWCw
Checkpoint 6.4
 Complete
the flow diagram about the
sequence of events that occur in the nonspecific response at the site of a cut
Specific Immune System
https://www.youtube.com/watch?v=CkTKZTCxrtc
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In what way if the specific immune system specific?
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How is this possible? Explain using your knowledge of the
tertiary structure of proteins.
Review: What is an antigen.
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1.
2.
Lymphocytes have receptors that bind to specific non-self
antigens on pathogens.
Usually a protein molecule expressed on cell surface membrane
or virus exterior. Our immune system recognises it as foreign
when it comes from another organism.
Two main types of cells involved in the specific immune
system? Describe the function of each one.
B cells – secrete antibodies: memory cells and plasma
cells
T cells – aid B cell division(T helper cells), and destroy
virus- infected cells (T killer): memory cells, helper cells
and killer cells
 Antibody:
Class of protein called
immunoglobulin
Antibodies
 What
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is the function of an antibody?
Bind to non-self antigens and label the cell
for destruction by phagocytes
See figure 6.38
 Each
B cell produces one type of
antibody and has receptors on its surface
including trans-membrane versions of the
antibody
Activation of T helper cells
 Initiated
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by professional antigen presenting cells.
Ie. Macrophages and B lymphocytes
 Function?
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Present «non-self» antigens on the surface of their
cells
Bind to complementary CD4 receptors on T helper
cells to activate them
 Significance?
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T helper cells can activate specific B cells (the ones
which produce antibodies complementary to the
antigen) by clonal selection
Activation of T Killer cells
 Infected
cells present «non-self» antigens
on the surface of their cells
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Bind to complementary CD8 receptors on T
killer cells to activate them
 Significance?
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T killer cells kill any cells infected with viruses
containing this specific antigen
Primary and secondary
immune response
 Primary:
occurs after first exposure to an
antigen
 Secondary: If infected by same antigen
again
 Response is much faster, involves the
memory cells
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http://highered.mcgrawhill.com/sites/0072507470/student_view0/chapter22/animation__the_immune_response.html
Activity 6.8d
1.
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What happens during the primary immune response?
Macrophages engulf and present antigen of pathogen
which activates T-helper cells and produce memory
cells
T-helper cells bind with B-cells specific for the antigen,
release cytokines which stimulate B-cell division to
produce plasma cells which will produce antibodies
specific to antigen – labelling them for easier
destruction by macrophages.
T-helper cells also release cytokines that stimulate T-killer
cells to divide and destroy infected body cells.
B and T-cell memory cells are made for a secondary
exposure to same antigen.
Activity 6.8d
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How long did it take for the antibody number to reach a
maximum after the first exposure to antigen A?
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Why does the antibody number remain higher than the
original value?
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Some of the antibodies remain in the blood
How long did it take for the antibody number to reach
a maximum after the second exposure to antigen A?
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2 weeks
Less than 2 weeks
Describe the differences between the responses to the
two antigens after exposure to both.
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Antibody production occurs sooner (happens immediately
– not really a big difference in graph), faster (Second
exposure line is steeper) and more antibody is produced
(peak is higher).
Activity 6.8d
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Explain these differences.
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Why are people often unaware of infections during the
secondary immune response?
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Secondary immune response involves memory cells that
detect the antigen faster and can respond to it faster
meaning that antibody production occurs sooner, faster
and more antibody is produced.
Pathogen is destroyed before body has any symptoms of
the disease
Define ‘immune’.
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Already have antibodies and or memory cells present in
body for that specific antigen/pathogen.
Avoiding attack to one’s own
immune system
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Some membrane proteins on our cells label us
as self.
B and T cell mature in bone marrow and
thymus -any lymphocytes for self membrane
proteins are destroyed by apoptosis
Sometimes cells may change so that they
appear foreign to body
Auto immune diseases
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Insulin dependent diabetes
Rheumatoid arthritis
Multiple sclerosis
Becoming actively immune
 Active
natural immunity – you are
exposed to the pathogen and this causes
an specific immune response.
 You now have B and T memory cells to
this antigen
 Active
Artificial immunity – you are
vaccinated with an antigen and this
causes an immune response.
 You now have B and T memory cells to
this antigen
Passive immunity
 Passive
natural – you received antibodies
across the placenta and in breast milk
when you were a foetus and newborn.
 You were able to fight any antigen you
came in contact with at the time but this
immunity only lasts for a few months
 You had no immune response, therefore
no memory cells made.
Passive artificial immunity
 You
are given an injection of antibodies if
you know you have been exposed to a
pathogen but have not previously been
vaccinated against it.
 The disease is known to be very fast
acting and deadly.
 eg tetanus, rabies
 This fights the pathogen immediately but
does not give you long lasting immunity.
 Q 6.38
Vaccinations
 Attenuated
pathogen eg. measles, BCG,
polio
 Killed pathogen eg. whooping cough
bacteria
 Harmless form of toxin eg, tetanus
 Antigen bearing fragment eg hepatitis B,
meningitis C
Challenges for vaccinations
 Poor
immune response eg. due to
malnutrition
 Antigenic changes
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Due to mutations eg. flu
Due to different stages in a life cycle eg.
malaria
 Antigenic
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concealment
In cells
In intestine eg. cholera
 Boosters
required for some vaccinations
Herd immunity
• When enough people are
immunised the pathogen is
less likely to be transferred.
• Therefore there is less
disease in the community.
• Anyone who cannot have
a vaccination for medical
reasons is also protected.
• Eg. for measles 95% of the
population needs to be
immunised for herd
immunity.
Successful vaccination
programme – smallpox
https://www.youtube.com/watch?v=jJwGNPRmyTI
 Edward
Jenner noted that cowpox
sufferers never developed smallpox
 In 1796 he inoculated a healthy boy with
cowpox then injected him later with
smallpox
 The boy do not develop smallpox
 Smallpox vaccination was developed
and made compulsory in UK in 1853
Successful vaccination
programme - smallpox
 WHO
aimed to eradicate smallpox
 The disease was devastating and deadly
 The vaccination was safe, effective and
easy to administer
 The pathogen was stable and did not
mutate
 Sufferers were easy to spot and isolate
 Last case was in Somalia in 1977
A stalled vaccination
programme - measles
Deadly and debilitating in
developing countries – leading
cause of blindness, 2.6 million
deaths per year prior to
vaccination.
Targeted by WHO for
eradication.
Effective, safe vaccine.
95% vaccination needed for
herd immunity.
A stalled vaccination
programme - measles
However the uptake of the vaccine in
developed countries has declined
significantly.
Measles seen as a “minor” illness.
Vaccination fraudulently linked to
several diseases eg. autism, bowel
disease.
Serious outbreaks of measles in central
Europe eg 2008 Switzerland
Vaccinations for TB?
 Were
you vaccinated against TB?
 Vaccine introduced to UK in 1950s
 Vaccine gave immunity to 80% of TB
strains
 Initially very effective
 TB cases declined
 Vaccine not given to all children in UK
now.
 Why?
Vaccination for TB
 TB
now limited to very specific groups
 - London or major cities
 Born abroad in certain countries
 Regular visitors (or close family
members)to certain countries
 No longer as effective
Vaccine for HIV?
 Not
yet
Would you vaccinate your
children?
 Side
effects?
Specification- topic 6
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10 Describe the major routes pathogens may take when entering
the body and explain the role of barriers in protecting the body
from infection, including the roles of skin, stomach acid, gut and
skin flora.
12 Describe the non-specific responses of the body to infection,
including inflammation, lysozyme action, interferon and
phagocytosis.
13 Explain the roles of antigens and antibodies in the body’s
immune response including the involvement of plasma cells,
macrophages and antigen-presenting cells.
14 Distinguish between the roles of B cells (including B memory and
B effector cells) and T cells (T helper, T killer and T memory cells) in
the body’s immune response.
15 Explain how individuals may develop immunity (natural, artificial,
active, passive).