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Summary 7 Caput lectures
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Summary of the seventh lecture clinical immunology which were caput lectures about the concepts of inflammation and the off switch of immune cells
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Clinical Immunology Evelien FloorHC7 Caput lectures
The concept of inflammation I
Definitions
• Inflammation
o A protective tissue response to injury or destruction of tissues, which serves to
destroy, dilute, or wall of both the injurious agent and the injured tissues. The
response is associated with mobilization of inflammatory cells.
o Inflammation results in redness, swelling, pain, warmth and loss of function
• Infection
o Invasion and multiplication of microorganisms in body tissues, especially that causing
local cellular injury due to competitive metabolism, toxins, intracellular replication, or
antigen-antibody response
• Bacterial colonization
o Colonization occurs when microorganism live on or in a host organism but do not
invade tissues or cause direct damage
• Systemic inflammation
o Systemic inflammation is an often-used term in the literature but is poorly defined. It
generally refers to the process that inflammatory processes can be measure in the
peripheral blood. These processes then can affect distant tissues not affected by the
primary inflammatory response.
• Relation between infection and inflammation
o Infection can be present during inflammation, but inflammation does not always mean
there is an infection.
Innate immune system
Four levels of an innate immune response in chronological order:
1. Protection by barriers
2. Identification and elimination of pathogens (PRRs for DAMPs and PAMPs)
3. Mobilization of effector cells (inflammation)
4. Production of cytokines (communication with the adaptive immune response)
Pattern recognition receptors recognize conserved molecular patterns on microbes called microbe-
associated molecular patterns (MAMPs) which are not present on the host. MAMPs are often essential
for microbe survival.
Chemoattractants allow immune cells to find the wound, in case there is no wound no inflammatory
cells are present in the tissue. Neutrophils can enter damaged tissue and chase bacteria to
phagocytose them (small targets). Eosinophils can kill nematodes extracellularly (large targets), when
this fails granulomas are formed around the nematode.
There are three main mechanism involved in killing by neutrophils:
1. Oxidant release by the NADPH oxidase complex (phagocytosis)
o Production of superoxide (O2-) and H2O2.
2. Degranulation
3. NETosis
o DNA NETs trap bacteria, cytotoxic proteins are present on those NETs
All processes are part of a potent but sufficient immune response for killing of microorganisms and
cancer cells. It results in limited tissue damage and return to homeostasis. However, there also can be
a hyperactive immune response causing collateral damage to the tissues. This is then called chronic
inflammatory disease: SLE, RA, eczema, psoriasis, asthma, MS.
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, Clinical Immunology Evelien Floor
Kinetics of inflammation
After injury there first is a pro-inflammatory phase with pro-inflammatory cytokines (TNF-a, IL-1).
When the injury is controlled after 5-8 hours, the pro-inflammatory cytokine levels decrease, and the
anti-inflammatory cytokine (IL-10) levels increase. Again, if there is too much injury the whole system
is not well coordinated.
Neutrophils form a very homogenous population in the peripheral blood. In case of an acute
inflammation new populations are found in the peripheral blood. Those cells are associated with other
functionalities. During inflammation, the phenotype of the cells in the peripheral blood change
because more cells are coming from the bone marrow. Therefore, a completely other picture is seen
in people who are diseased compared to people who are healthy.
In conclusion, there should be a balance between pro- and anti-inflammatory mechanisms. In case to
much pro-inflammation is present this will result in infection and tissue damage. In case to much anti-
inflammation is present this will result in chronic inflammatory diseases such as autoimmune diseases
and allergy.
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