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Summary BBS2001 Threats and Defense mechanisms
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A condensed summary of the course "threats and defense mechanisms BBS2001" that contains all the necessary information for the exam.
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BBS2001 Threats and Defence MechanismsCase 1: The first aid troops
What is the function of the different cell types from the graph in the case?
Neutrophils: Neutrophils are white blood cells. They
provide the first line of defense when there is an
invader. They engulf and destroy bacteria and other
pathogens through a process called phagocytosis. They
recognize the invaders by receptors which are present
on the surface of the neutrophil.
Eosinophils: Eosinophils help fighting infections, by
releasing highly toxic proteins and free radicals. This
causes the inflammatory response in the body goes up,
because of the production of chemical mediators
(prostaglandins/cytokines)
-Mainly located within the connective tissue.
Basophils: Also known as granulocytes, which store and release several enzymes which help
fighting infections. They also use phagocytosis (like neutrophils). They release enzyme
histamine, which dilates the blood vessel around the infections site. Also, they release
heparin, which prevents blood clotting at the infection site. (more present when you have an
allergic reaction)
Monocytes: They recognize the invader and become a dendritic cell or macrophage.
Dendritic cells ask other immune cells for help, by releasing cytokines. They collect antigens.
Macrophages defend your body from invader at the front line. They surround the invader
and kill them with toxic enzymes (like eosinophils). The macrophage is also involved in
cleaning up dead cells from your blood stream.
Platelets/ thrombocytes: Forms a clot at a wound and stops or prevent bleeding.
Erythrocytes: are red blood cells which are made within the bone marrow (like all other
blood cells). They transport oxygen from lungs to the body and waste products (CO2) from
the body to the lungs. (originate from the yolk sac → later in bone marrow)
Lymphocytes: small lymphocytes stem from the common lymphoid progenitor, and will
differentiate in a T-lymphocyte, B-lymphocyte or will become a plasma cell after
differentiating from a small lymphocyte into a B-cell and then into a Plasma cell. T-cells
respond directly through attacking and killing the infected cells (damaging the membrane
etc.) B-cells make antibodies which are proteins that target invaders. Some of the B-cells will
develop in memory cells (which can remember the invaders after the first time). B-cells can
also develop in plasma cells which can make the right antibodies.
NK-cells: NK cells are best known for killing virally infected cells, and detecting and
controlling early signs of cancer. As well as protecting against disease, specialized NK cells are
also found in the placenta and may play an important role in pregnancy. Besides cytotoxic
activity, NK cells activation is accompanied by secretion of pro-inflammatory cytokines.
Hence, NK cells have the potential to act both in driving inflammation and in restricting
adaptive immune responses that may otherwise lead to excessive inflammation or even
autoimmunity.
, - Leukocytes: Basophils, eosinophils and neutrophils are called granulocytes because
they contain cytoplasmic inclusions that give them a granular appearance.
Agranulocytes are the lymphocytes and the monocytes.
The signs of acute inflammations
• Pain: The inflamed area is likely to be painful, especially during and after touching.
Chemicals that stimulate nerve endings are released, making the area more sensitive.
• Redness: This occurs because the capillaries in the area are filled with more blood than
usual.
• Immobility: There may be some loss of function in the region of the inflammation.
Impaired function.
• Swelling: This is caused by a buildup of fluid.
• Heat: More blood flows to the affected area, and this makes it feel warm to the touch.
Acute inflammation
Inflammation is a tissue reaction that delivers
mediators of host defense—circulating cells and
proteins— to sites of infection and tissue damage. The
process of inflammation consists of recruitment of
cells and leakage of plasma proteins through blood
vessels and activation of these cells and proteins in the
extravascular tissues. The initial release of histamine,
TNF, prostaglandins, and other mediators by mast cells
and macrophages causes an increase in local blood
flow and exudation of plasma proteins. These
contribute to redness, warmth, and swelling, which
are characteristic features of inflammation. This is
often followed by a local accumulation in the tissue of
phagocytes, mainly neutrophils and blood monocyte-derived macrophages, in response to
cytokines, discussed below. Activated phagocytes engulf microbes and necrotic material and
destroy these potentially harmful substances. Cytokines and other mediators are produced
by macrophages, dendritic cells, mast cells, and other cells in tissues in response to microbial
products and damaged host cells. Some of these mediators (e.g., histamine, prostaglandins)
increase the permeability of blood vessels, leading to the entry of plasma proteins (e.g.,
complement proteins) into the tissues, and others (IL-1, TNF) increase expression of
endothelial adhesion molecules and chemokines that promote the movement of leukocytes
from the blood into the tissues, where the leukocytes destroy microbes, clear damaged
cells, and promote more inflammation and repair.
Hemostasis and Thrombosis
General principles of hemostasis, coagulation and thrombosis
• Primary hemostasis – platelet adhesion and aggregation
• Secondary hemostasis – blood coagulation and fibrinolysis
• Thrombosis – as an innate defense mechanism
• Thrombosis - arterial and venous
• Prevention and treatment of thrombosis
,The process of hemostasis
Hemostasis is your body’s natural reaction to an injury that
stops bleeding and repairs the damage. Hemostasis is
divided into 3 different steps: Vasoconstriction / vascular
spasm, primary hemostasis (platelet plug formation) and
secondary hemostasis (coagulation).
Vasoconstriction / vascular spasm
Vasoconstriction is caused by paracrine molecules released
from the damaged endothelium (like serotonin). This is done because it will decrease the
blood flow out of the injured blood vessel.
Primary hemostasis
Blood platelets
A platelet is a very active cell, and has a granular surface. The
platelets are small cell ‘fragments’ without a nucleus. The
platelets are sneered of from megakaryocytes and are taken up in
the blood stream. These platelets can respond to a large variety of
triggers and change its shape (from a sphere to a star shape).
Platelets look a bit like spoges, with open structures called canals.
They also contain granules, which carry coagulation factors and
inflammatory molecules. These platelets form aggregates that can
stop the bleeding.
Primary hemostasis (platelet plug formation)
Platelets are flowing by the injured blood vessel wall and
will be adhered to collagen with the help of integrins. If the
platelets are bound they will release their intracellular
granules like serotonin, ADP and platelet activating factor
(PAF). Platelet activating factor will activate a positive
feedback loop (see image) to attract more platelets to the
damaged blood vessel wall. The platelet activating factor
will also convert platelet membrane phospholipids into
thromboxane Az, which is also a vasoconstrictor.
Thrombopoiesis (production of blood platelets)
Platelet production occurs in the bone marrow (and lung) in
distinct steps:
1. MK development in adult bone marrow
2. Endomitosis to create polyploid nucleus
3. Cytoplasmic maturation
4. Proplatelet formation and release
5. Preplatelet to proplatelet interconversion
6. Platelet release
Platelet producing cells named the megakaryocytes are located
within the bone marrow, but there is also a reservoir of
megakaryocytes found within the lungs. The megakaryocytes
, make protrusions that eventually turn into platelets. The cytoskeleton (microtubule and
actin/myosin) are important for this process.
Platelet signaling
If one platelet gets activated it sends out alarm signals in
the form of autocrine and paracrine signals to other
platelets, meaning that if one platelet gets activated and
there is an alarm situation it sends out signals to other cells.
This signaling always happens by means of activation →
transduction → amplification → feedback.
Platelet adhesion under flow
When tethering occurs, which is the binding of the platelet to
its receptors on the vascular wall the flow of the blood will
push the platelet body towards the wall where translocation
and activation will occur and eventually when the platelet body
is close enough adhesion will occur.
Platelet aggregation
A platelet adhered to the vessel wall then it will turn into an
activated and stable adhered platelet. It then starts to release
factors, these factors attract other platelets, which will adhere
to the initially adhered platelet. Some platelets get
hyperactivated and become pro-coagulant, these platelets are
often times at the outer regions of the mass of adhered
platelets. These hyperactivated platelets support the blood
coagulation reaction and then you get fibrin formation and
stabilization of the clot.
Glanzmann Thrombasthenia: deficiency/defect in aIIbb3, which is responsible for deficient
clot retraction.
Secondary hemostasis
Initiation of blood coagulation (extrinsic pathway)
Tissue damage, if you damage your blood vessel that’s the
moment where you trigger your blood coagulation. The
platelets are triggered, but also your blood coagulation is
triggered. This happens due to the exposure of tissue factor,
which is normally not in your blood circulation, but is exposed
once you have damaged tissue. Tissue factor binds to Factor
VIIa, which is the activated form of Factor VII, but it is
unknown how it gets activated. This complex is called the
Tissue Factor-Factor VIIa complex, which can activate Factor X hereby turning it into Factor
Xa. Then Factor Xa can associate with traces of Factor Va together with phospholipids and
these three form the Prothrombinase complex. Then prothrombiase can turn prothrombin
into thrombin, and thrombin can then convert fibrinogen into fibrin.
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