non-specific barriers include the physical defences, such as skin that contains
epidermis, which has keratin and some water, so microorganisms are able to
grow. The sebaceous gland of the dermis release water-proofing oils that keep
the hair follicles clear of bacteria. Secondly, by cleaning up any cuts and
covering them, the microorganisms are prevented from entering.
mechanical defences are mucus cells and cilia cells found in the inside layer
cells of the trachea and airways. The nasal cells clean the air moving into the
nasal. Microorganisms get stuck in the mucus (given out by goblet cells, on the
lining of the air passage and are removed from the lungs by cilia). The cilium
is always moving the mucus and traps the microorganism, so it leaves the lung
area and goes to the mouth to be swallowed.
chemical defences such as tears, nasal excretions, urine, mucus, saliva, ear
wax and sweat which have an enzyme (lysosome) that stops microorganisms
Biological defences are harmless bacteria habituating in the skin and mucous
membranes that stop the expansion of many pathogen-like microbes. The harmless
bacteria protect us by challenging the pathogenic bacteria for nutrients.
lines of defence are phagocytes, fever, Leukocytes killing the outside cells,
inflammation and Non-specific chemical defences.
such as white blood cells ingest bacteria and unfamiliar microorganisms found
in the blood and tissues.
happens due to damage of body tissues by trauma, burns, cuts and infection. The
role of inflammation is to remove the cause of infection or prevent the growth
killing by Leukocytes take place by Natural killer Lymphocytes and Eosinophil that
kill outside the cell.
chemical defences help carry out phagocytosis, attack pathogens or enhance features
of nonspecific resistance.
Fever is an abnormal increase of internal body temperature and is impermanent
in the body’s thermoregulatory set-point at 1-2 °C.
specific barriers are used in the final line of defence against pathogens which
includes the lymphocytes that give out antibodies towards the specific antigen pieces.
Each individual cell releases a specific antibody; the body also has a variety
of B cells that detect specific antigen Helper T cells, which upholds the B
cell roles, so many antibodies are released when needed.
Non- Specific Defences
(catalyse) the breakdown of molecules in the cell walls due to reactions with
water. This stops the bacteria from infecting the living cells of the skin,
respiratory and digestive tract. The lactate in sweat slows down bacterial
growth. The Hydrochloric acid in gastric juice kills most microorganisms in the
stomach. The vagina has safe bacteria that change carbohydrate to lactate,
which kills the pathogen’s bacteria.
or cut is a way for microbes and foreign materials to come in the body. A blood
clot will quickly cover the wound however inflammation is the inflammatory
response and causes the killing of microbes that got in. The injured white
blood cells and mast cells located in the connective tissue below the skin and
around the blood vessels release chemical Histamine. Histamine allows the arterioles
in the area to expand, so more blood flow will reach the capillaries at the infection.
Histamines also increase the porousness of the capillary and cells in the
capillary walls causing the vessels to leak. This leak carries plasma fluid,
white blood cells and antibiotics from the blood to enter the tissue, therefore
swelling happens. Plasma proteins attack the bacteria. Then neutrophils,
macrophages and phagocytes ingest invaders and debris.
are white blood cells and can be neutrophils and macrophages. The many
phagocytic cells accumulate at the site to swallow many bacteria. Then the site has many dead cells of neutrophils
to form pus. The pus can break into the skin, or will get broken down and enter
the surrounding tissue.
killing by Leukocytes take place by Natural killer Lymphocytes that release
toxins onto the surface of virally infected cells and tumours. Eosinophil is
another Leukocyte that wage war on the parasitic worms by attaching to the
surface and releasing toxins that weaken or destroy the worm. Higher eosinophil levels are a sign of worm
happens by the immune system releasing certain chemicals in response to
infection or inflammation. In a state of fever interlukin-1 causes a person to
be drowsy, lowering the body’s need for energy. And that energy can be focused
on defending the body and tissue repair. Fever intensifies phagocytic and
B and T cells are lymphocytes, a type of white blood
cells used by the body to kill and
remember antigens. B cells are formed and grow in the bone marrow. They take
part in the antibody mediated response. T cells are formed in the bone marrow
and grow in the thymus. They take part in the cell mediated response.
T-lymphocytes first enter the thymus (lymph gland in
the neck) where they are activated. And in the thymus, they learn to
differentiate self from non-self (foreign). The T-cells that can successfully
identify the non- self-antigen molecules grow and leave the thymus. Else
T-cells would attack the body’s own cells and tissues.
The mature T cells enter the bloodstream and the
When these T cells come across a foreign or abnormal cell, they are immediately
stimulated and scan for more abnormal cells. There are a variety of T-lymphocytes.
mediated immunity takes place as the Macrophages ingest the pathogens and
breaks down the protein molecules. The antigen part of these proteins is on the
outside of the macrophage (epitopes). As soon as the antigen presents itself to
the immune system, the macrophage becomes an antigen-presenting cell (APC).
This alerts T and B lymphocyte cells that specific pathogens have entered the
body. Then the binding sites on top of
the T-lymphocytes identify the non-self-antigens that the macrophages show on
their surface and fit into them. The T-lymphocytes then activate and increase
quickly. They produce many clones of identical cells to identify the antigen as
foreign. The clones are sub divided into 4 cells types: helper T-cells,
cytotoxic T-cells (killer T-cells), memory cells and suppressor cells. The
T-cells are involved in the humoral and Cell medicated humanity. The function
of the T-cells in the humoral response is to release chemicals (Cytokines) that
activate B cells and give out antibodies. The function of the T-cells in the
cell medicated response is to activate cytotoxic T cells. The cytotoxic T-cells
cover the infected or cancerous cells. This causes the release of proteins
(perforin) that forms holes in infected cell’s membrane, which leads to the
destruction of the infected cell. The memory T-cells only multiply quickly if a
second invasion of a foreign antigens happens, which gives a larger army of
T-lymphocytes, so there is a faster attack on the antigen causing infection. The
suppressor T cell decreases the speed of response from T-cytotoxic cells and
helper T-cells, which also decreases the speed and brings the immune response
to a halt. This also helps the immune system from exaggerating when detecting a
Antibody mediated response needs the manufacture of B-Lymphocytes which is
stimulated by the helper T-cells. The B lymphocytes attack and kill the antigen
on the outside layer of microorganisms and foreign cells by giving out
antibodies that flow in the blood, lymph and tissue fluid. The antibody will either
stick to the antigen to perform agglutination, trigger phagocytosis by
neutrophil, become an antitoxin for the precipitation of soluble bacteria
toxins or keep pathogen-like bacteria away from cell membranes. The B cells
separate by mitosis for the release of three clone cells. The first clone cell
is B effector cells whose role is to differentiate and produce plasma cells
that quickly give out antibodies into the blood and lymph, as each antibody
must be specific to the pathogenic antigen. The second clone cell is B memory
cells that live longer than plasma cells and stay in the body for many
months/years in the body. Their role is to recall a specific antigen and
respond fast to an infection. Thirdly, the dividing B cells whose role is to release
more B-lymphocyte cells. This is known as clonal selection. When the B cells are
first chosen by an antigen, the antibody-producing cells production happens
from 10-17 days.
reason the coach driver didn’t catch that virus or get the symptoms was because
he had that same bacterium infection before. And the first time the pathogen
invaded his body, the immune system responded by triggering the release of
T-lymphocytes and B-lymphocytes for the immune response. Then the memory cells
that were formed gave long-term immunity as they were always active. So when
that same pathogen arrived the memory B and T cells reacted faster to their
The body’s first
line of defence, the innate immune system is not efficient at killing pathogens
as it takes “four to seven days” (The innate and adaptive immune systems,
August 2016) for the specific adaptive immune response to activate. The
adaptive immune response is effective as it does take more time to exactly target
the pathogen. However, the innate immune system is efficient at remembering and
acting against specific antigens. If there is contact again with an antigen,
the defence response is more efficient then the innate defence. The adaptive
immune response is not efficient as after first contact with the pathogen it
takes the immune system many days to respond, whereas at the second infection
the immune system is much more efficient at preventing symptoms.
The adaptive innate
system is more efficient than the innate immune system as its antigen specific
and only reacts with the microorganism that caused its response. The adaptive
immune system also has an immunologic memory which can be effective as by
remembering the antigens on a particular pathogen, the B and T-lymphocytes are
able to react more rapidly. However, the immunologic response is not effective as
it may recognise a person’s transplanted tissue as foreign which then leads to
its attack by the recipient’s immune system.
humoral response is inefficient as the B effector cells differentiate to
produce plasma cells that have a short life; however they produce an effective number
of antibodies as much as 2000 antibodies per plasma cell. This process clonal
selection is also inefficient as it takes 10-17 days to produce enough
anti-body producing cells when spotting an antigen. In comparison to the
secondary immune response which is more efficient due to the memory B and
T-lymphocytes that can spot an antigen quicker, within “2-7 days” (Microbiology
Notes, 2018). The secondary immune response is also more effective than the humoral
response as there is a greater production of antibodies into the blood, which
leads to a greater defence of the immune system.
lines of defence as skin is ineffective as it can be easily damaged or wounded which
also makes it an ideal penetration for microorganisms when a wound is not
properly covered. Thirdly, mechanical defences as mucus secretion by goblet
cells can also be ineffective as research shows overproduction may lead to
breathing problems and instead raise chances of infection. The chemical
defences are efficient as lysosome lies through many different substances as tears,
nasal secretions, urine, mucus, saliva, ear wax and sweat. Biological defences
such as populations of harmless bacteria can be ineffective as they can be easily
destroyed by wide-spectrum antibiotics which also destroy this body’s defence.
second lines of defence as phagocytes are involved in non-specific responses.
They are inefficient at killing infections as they can’t multiply rapidly,
neutralise or completely destroy a pathogen like specific defences. Secondly,
inflammation is an ineffective response as it can be easily reduced by
anti-inflammatory drugs, for instance “Ibuprofen” (Memory cells and long-term
immunity, 2017). Thirdly, research shows fever to be effective as it increases
the body’s temperature by a couple of degrees which also increases the responses
from phagocytes and antibodies, which means better immune response to
infection. However, fevers are also inefficient as they can last anywhere
between “3 days to 2 weeks” (Memory cells and long-term immunity, 2017).