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non-specific primary & secondary defences in animals 4.1.1, inactive…
non-specific primary & secondary defences in animals 4.1.1
primary defences
skin
main primary defence
outer layer = epidermis
most skin cells are called keratinocytes - produced at base of epidermis
as they migrate away they dry out & the cytoplasm is replaced with keratin
takes 30 days for new skin cells to be fully keratinised
skin cells are dead by the time they reach the surface - dead layer acts as protective barrier - eventually they fall away
blood clotting
mucous membranes
exchange surfaces are thinner making them less protected from pathogens - they are protected by mucous membranes
airways
epithelial cells contain layer of goblet cells secreting mucous trapping pathogens
cilia waft the mucous & pathogens up & away from the
its swallowed & the pathogens enzymes are denatured in the stomach acid
found in the gut, genital area, anus, ears, nose, & airways
coughing, sneezing, vomiting
designed to respond to irritation that may be cause by microbes or toxins which they release
inflammation
result from infection
area is swollen, red, painful & feels hor
mast cells detect the presence of microbes & releases histamine - a cell signalling chemical
effects of histamine
vasodilation - brings more blood to affected site (inc wbc)
capillary walls are more permeable to wbc - wbc can enter tissue fluid
more tissue fluid id formed leading to swelling (odema) - excess tissue fluid enters drainage system called lymphatic system
many lymphocytes are stored in the lymphatic system - & some pathogens may now come into contact with them - triggers a specific immune response
other primary defences
ear canal lined with wax which traps pathogens
female reproductive system protected by mucous & acidic conditions
eyes protected by antibodies & enzymes in tear fluid
Lysozyme action – lysozyme is an enzyme found in secretions such as tears and mucus which kills bacterial cells by damaging their cell wall
secondary defences
used once the pathogen have entered the body
pathogens are recognised by chemical markers on their out membrane called antigens
our own cells have antigens that are recognised as 'self cells' & aren't attacked
sometimes things go wrong & we attack our own cells (autoimmune diseases)
Opsonins
a type of antibody
are protein molecules & attach to the surface of a pathogen
some are more specific than others but generally non-specific
they 'label' pathogens - enables phagocytes to identify & engulf them more easily
phagocyte has opsonin binding sites
phagocytes - neutrophils
a neutrophil is a common phagocyte & wbc
about neutrophils
have a multi-lobed nuclei - to squeeze out into tissue fluid
made in bone marrow
have granular cytoplasm cause all of the lysosomes in their cytoplasm
have receptors to bind to opsonins
well designed cytoskeleton to allow it change shape
many mitochondria for releasing energy for engulfing
lots of ribosomes to synthesise lysozyme
phagocytosis
neutrophil binds to the opsonin attached to the antigen of the pathogen
the pathogen is engulfed by endocytosis forming a phagosome
lysosome fuse to the phagosome & release lytic enzymes into it
after digestion the harmless products can be absorbed into the cell - things that can't be digested are expelled by exocytosis
macrophages
larger wbc made in bone marrow
begin life & travel in blood as monocytes
they settle in lymph nodes & body tissues & mature into macrophages - they now wait to engulf a pathogen
they don't digest & destroy pathogens entirely - the antigens from the surface of the pathogen are saved & moved to a special protein complex on the surface of the cell
the macrophage is now an antigen presenting cell
antigen presenting cells
with the antigens now being 'advertised' on the surface of the cell - it alerts other cells (e.g. lymphocytes) in the immune system
they start to move around the body
the antigens are part of a complex on the outside of the cell cause if only the antigens were present your immune system might attack the antigen presenting ell - by incorporating them into a complex it avoids this
inactive thrombokinase in blood
(<-- factors activate it) active thromnokinase (an enzyme)
(<-- both must be present) active thrombin (an enzyme)
insoluble fibrin (protein) forms fibres which trap platelets & red blood cells
damage to blood vessel wall & platelets (when exposed to O2) releases clotting factors
(precursor) - prothrombin in blood (inactive)
Ca^2+
soluble fibrinogen in plasma