7226037
Non-Specific Immunity
- Initial response to foreign bodies
- innate
- responds non-specifically to
any non-self bodies
- rapid
- innate
- Physical Barriers
- Skin
- relatively thick,
impermeable layer of
epidermal cells
(overlaying a rich
vascular dermal layer).
- epidermal cells
are produced at
the base of the
epidermis as
basal cells and
proliferate,
moving
outward.
- become flattened and die.
- dead cells contain keratin - forms a waterproof
protective layer that reduces moisture loss and
protects underlying tissues from microorganisms.
- tight junctions join
epidermal cells which
impede water loss
and microbial
penetration
- tight junctions join
epidermal cells which
impede water loss
and microbial
penetration
- dead cells contain keratin - forms a waterproof
protective layer that reduces moisture loss and
protects underlying tissues from microorganisms.
- become flattened and die.
- epidermal cells
are produced at
the base of the
epidermis as
basal cells and
proliferate,
moving
outward.
- Secrete sebum and sweat
- low pH acidic
secretions impair
bacterial growth
- low pH acidic
secretions impair
bacterial growth
- relatively thick,
impermeable layer of
epidermal cells
(overlaying a rich
vascular dermal layer).
- Lungs
- bacteria
trapped by
stick mucous
in the lining of
the bronchi
and
bronchioles
- bacteria
trapped by
stick mucous
in the lining of
the bronchi
and
bronchioles
- Gut
- bacteria destroyed by
acid secretions of the
stomach
- 'chemical barriers'
- 'chemical barriers'
- bacteria destroyed by
acid secretions of the
stomach
- Skin
- Cytokines
- interferons
- released
from cells
infected
by
viruses.
- bind to uninvaded cells, causing the
production of inactive enzymes
capable of break down viral mRNA,
inhibiting protein synthesis.
- when viruses enter
activated cells,
viral-blocking enzymes
are activated.
- virus is unable to multiply in
newly invaded cells.
- virus is unable to multiply in
newly invaded cells.
- when viruses enter
activated cells,
viral-blocking enzymes
are activated.
- bind to uninvaded cells, causing the
production of inactive enzymes
capable of break down viral mRNA,
inhibiting protein synthesis.
- stimulate
other
immune
responses
- released
from cells
infected
by
viruses.
- interleukins
- secreted by
macrophages
and lympocytes
- regulate interactions
between various parts
of the immune system
- secreted by
macrophages
and lympocytes
- special proteins
secreted by various
cells of the immune
system when
pathogens enter the
tissues
- interferons
- Inflammation
- characterised by
redness, swelling or
pain
- pathogens invading
tissues trigger an
inflammatory response
- damaged cells release
histamine, serotonin
and other substances,
which dilate blood
vessels in the infected
area.
- increased blood flow brings
monocytes and neutrophils +
plasma protein gamma
gobulins (antibodies)
- increased blood flow brings
monocytes and neutrophils +
plasma protein gamma
gobulins (antibodies)
- capillary wall
permeability
increases leading
to tissue oedema
- damaged cells release
histamine, serotonin
and other substances,
which dilate blood
vessels in the infected
area.
- sometimes the
entire body is
involved
producing fever, or
pyrexia
- thought to be caused by
the neutrophils and
macrophages releasing
endogenous pyrogens
(including prostaglandins)
- pyrogens travel to
the hypothalamus,
turning the
thermostat up,
increasing the
body's
temperature.
- directly affects bacterial metabolism
- optimum temp for
bacteria is ~ 37
degrees i.e. normal
body temp
- optimum temp for
bacteria is ~ 37
degrees i.e. normal
body temp
- higher temperatures for
prolonged periods can
cause problems.
denaturation of body
proteins (esp. enzymes
needed for biochemical
reactions in body cells)
- mild fevers cause
the spleen and
liver to remove
additional iron
from blood. most
disease causing
bacteria require
iron to reproduce
- fever decreases rate
of bacterial replication
and increases body's
metabolism
(facilitating healing
and accelerating
cellular defence
mechanisms i.e.
phagocytosis)
- fever decreases rate
of bacterial replication
and increases body's
metabolism
(facilitating healing
and accelerating
cellular defence
mechanisms i.e.
phagocytosis)
- directly affects bacterial metabolism
- pyrogens travel to
the hypothalamus,
turning the
thermostat up,
increasing the
body's
temperature.
- thought to be caused by
the neutrophils and
macrophages releasing
endogenous pyrogens
(including prostaglandins)
- characterised by
redness, swelling or
pain
- Phagocytosis
- major
function of
inflammation
is increased
phagocytosis.
- main
phagocytotic
leucocytes are
monocytes
and
neutrophils
- monocytes leave circulation
and transform into
macrophages in tissues. can
phagocytose ~100 bacteria
before dying
- macrophages are widely
distributed in the tissues but are
particularly numerous in the gut
wall and lungs.
- as part of the
inflammatory
process, they
release
interleukin-1.
- macrophages are widely
distributed in the tissues but are
particularly numerous in the gut
wall and lungs.
- smaller
neutrophils
phagocytose
~20 bacteria
before dying.
Pus is largely
formed of
dead
neutrophils
- monocytes leave circulation
and transform into
macrophages in tissues. can
phagocytose ~100 bacteria
before dying
- limited because if there is a
high number of pathogenic
microorganisms in the body,
the normal blood flow rate is
insufficient in bringing
enough macrophages and
neutrophils to the site of
infection.
- some bacteria (tuberculosis
bacilli) can resist
phagocytosis - protective cell
walls/ proteins on the
surface.
- major
function of
inflammation
is increased
phagocytosis.
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