Inflammation - causes, symptoms, diagnosis, treatment, pathology
Summary
TLDRInflammation is the body's complex response to harmful stimuli like pathogens, toxins, or trauma, aiming to restore balance. It involves heat, pain, redness, and swelling, leading to temporary loss of function. Key players include macrophages, mast cells, and leukocytes, which release cytokines and other mediators to attract immune cells and initiate tissue repair. The innate immune response, activated by pattern recognition receptors, is rapid but non-specific. If mild, tissue regenerates; severe damage results in fibrous scarring.
Takeaways
- 🔍 Inflammation is characterized by four key signs: calor (heat), dolor (pain), rubor (redness), and tumor (swelling), which can lead to a fifth sign, functional lysa (temporary loss of function).
- 🌡 Inflammation is triggered by stimuli such as pathogens, toxins, or trauma, and is a response to restore balance and repair tissue damage.
- 🦠 Both external (like allergens and irritants) and internal (like DAMPs) factors can initiate inflammation, with microbial factors including virulence factors and PAMPs.
- 🛡 The immune system recognizes foreign substances through Pattern Recognition Receptors (PRRs), which activate leukocytes and initiate the inflammatory response.
- ⏰ The innate immune response is non-specific, rapid (occurring within minutes to hours), and lacks memory, distinguishing it from adaptive immunity.
- 🔬 There are two main types of leukocytes: granulocytes (like neutrophils and eosinophils) and agranulocytes (like lymphocytes and monocytes), which play crucial roles in inflammation.
- 🚨 Mast cells and macrophages are early responders in inflammation, releasing inflammatory mediators and increasing vascular permeability to allow immune cells to reach the site of injury.
- 🔄 Neutrophils are the first leukocytes to be recruited and they phagocytose pathogens, often leading to their own destruction in a process called neutrophil extracellular traps (NETs).
- 🩸 The complement system, activated by antibodies or pathogen molecules, aids in attracting leukocytes and optimizing pathogen phagocytosis, and can directly kill pathogens.
- 🛠️ Tissue repair involves macrophages clearing dead cells, angiogenesis for new blood vessel formation, and fibroblasts synthesizing collagen, leading to either tissue regeneration or scarring.
- 🔚 Inflammation concludes with tissue repair and resolution, aiming to restore tissue integrity or, in cases of severe damage, leaving a fibrous scar.
Q & A
What are the four classical signs of inflammation?
-The four classical signs of inflammation are calor (heat), dolor (pain), rubor (redness), and tumor (swelling).
What is the fifth sign sometimes associated with inflammation?
-The fifth sign sometimes associated with inflammation is functional lysa, which refers to a temporary loss of function due to pain or swelling.
What are the common causes of inflammation?
-Inflammation can be caused by pathogens, toxins, and trauma. For example, intense workouts can lead to muscle soreness due to inflammation.
What are the two main types of external factors that can trigger inflammation?
-The two main types of external factors that can trigger inflammation are non-microbial factors, such as allergens, irritants, and toxic compounds, and microbial factors.
What are the microbial factors that trigger inflammation?
-The microbial factors that trigger inflammation include virulence factors and pathogen-associated molecular patterns (PAMPs), which are small molecules shared across different pathogens.
What are Damage-Associated Molecular Patterns (DAMPs) and how do they relate to inflammation?
-DAMPs are intracellular proteins released when a cell's plasma membrane is injured or when a cell dies, signaling serious cell damage and triggering inflammation.
How do Pattern Recognition Receptors (PRRs) contribute to the inflammatory response?
-PRRs are cell surface receptors on leukocytes that recognize PAMPs and DAMPs, activating cells and sparking the inflammatory response.
What are the two main types of leukocytes involved in inflammation?
-The two main types of leukocytes involved in inflammation are granulocytes, which include neutrophils, eosinophils, basophils, and mast cells, and agranulocytes, which include lymphocytes and monocytes.
How do neutrophils contribute to the acute inflammatory process?
-Neutrophils are the first leukocytes recruited during the acute inflammatory process. They phagocytose pathogens and damaged cells, and then commit suicide to destroy the pathogens they've taken in.
What is the role of the complement system in inflammation?
-The complement system is a family of soluble proteins that get activated in the presence of antibodies or pathogen molecules. They help attract leukocytes, optimize phagocytosis, and directly kill pathogens by forming channels in their membranes.
How does the inflammatory response typically end?
-The inflammatory response typically ends with tissue repair, involving macrophages clearing dead cells, angiogenesis for new blood vessel formation, and fibroblasts synthesizing collagen for wound healing.
Outlines
🔴 Inflammation: Causes and Initial Response
Inflammation is characterized by four key signs: calor (heat), dolor (pain), rubor (redness), and tumor (swelling). These signs can lead to a fifth sign, functional lysa (temporary loss of function). Inflammation is triggered by stimuli such as pathogens, toxins, or trauma. The immune system recognizes foreign substances like pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs), which activate pattern recognition receptors (PRRs) on leukocytes. The inflammatory response, a part of the innate immune system, is non-specific, rapid, and lacks memory. Leukocytes like macrophages and mast cells respond to tissue damage by releasing inflammatory mediators, which increase vascular permeability and attract immune cells to the site of injury.
🔵 Leukocyte Recruitment and Inflammatory Resolution
Neutrophils are the first leukocytes recruited during acute inflammation, where they phagocytose pathogens and damaged cells. The complement system, activated by antibodies or pathogen molecules, aids in leukocyte attraction and pathogen optimization for phagocytosis. Dendritic cells activate the adaptive immune system by presenting pathogen fragments to T lymphocytes. In response to injury, platelets and clotting factors form a clot to stop bleeding and prevent pathogen entry. Tissue repair involves macrophages clearing dead cells, angiogenesis forming new blood vessels, and fibroblasts synthesizing collagen. The inflammatory response concludes with tissue regeneration or scar formation, depending on the extent of damage.
Mindmap
Keywords
💡Inflammation
💡Calor
💡Dolor
💡Rubor
💡Tumor
💡Functional Lysa
💡Pathogens
💡PAMPs
💡DAMPs
💡Leukocytes
💡Complement System
Highlights
Inflammation is characterized by four key signs: heat (calor), pain (dolor), redness (rubor), and swelling (tumor).
A fifth sign, functional lysa, can occur due to pain or swelling, leading to temporary loss of function.
Inflammation can be triggered by stimuli such as pathogens, toxins, or trauma, including muscle soreness after intense exercise.
The goal of inflammation is to restore balance by eliminating the cause of tissue injury and initiating tissue repair.
Inflammation can be caused by external factors like allergens, irritants, and microbial factors like virulence factors and PAMPs (Pathogen-Associated Molecular Patterns).
DAMPs (Damage-Associated Molecular Patterns) are released when cells are damaged, signaling serious cell injury and triggering inflammation.
PRRs (Pattern Recognition Receptors) on leukocytes recognize PAMPs and DAMPs, activating an inflammatory response.
There are two main types of leukocytes: granulocytes (neutrophils, eosinophils, basophils, mast cells) and agranulocytes (lymphocytes, monocytes).
Macrophages and mast cells in tissues respond to PAMPs or DAMPs, initiating the inflammatory process.
Inflammatory mediators released by mast cells affect endothelial cells, increasing vascular permeability and allowing fluids to leave circulation.
Neutrophils are the first leukocytes recruited during acute inflammation and play a key role in phagocytosing pathogens.
The complement system, activated by antibodies or pathogen molecules, aids in attracting leukocytes and optimizing phagocytosis.
Dendritic cells phagocytose pathogens and present antigens to T lymphocytes, activating the adaptive immune system.
In response to cuts or scrapes, platelets and clotting factors form a clot to stop bleeding and prevent pathogen entry.
Tissue repair involves macrophages clearing dead cells, angiogenesis forming new blood vessels, and fibroblasts synthesizing collagen.
Inflammation concludes with tissue regeneration or scar formation, depending on the severity of the damage.
Inflammation is a complex response to harmful stimuli, involving blood vessels and immune cells to restore tissue integrity or leave a fibrous scar.
Transcripts
inflammation classically describes four
key signs
each of which have a latin derivation
calor or heat
dollar or pain rhubarb or redness
and tumor or swelling sometimes these
four signs combine to cause a fifth sign
which is functional lysa or temporary
loss of function due to pain or swelling
alright so inflammation usually starts
with some stimuli like a pathogen
now even though pathogens are a common
cause of infection which can lead to
inflammation
inflammation can be caused by other
things as well like toxins and trauma
for example after an intense workout
your muscles might feel sore
that's due to inflammation trying to
repair your overused muscle fibers
ultimately the goal of inflammation is
to respond to the stimuli and restore
balance
oftentimes that includes eliminating the
cause of tissue injury
clearing out necrotic or dead cells and
starting tissue repair
broadly speaking inflammation can be
triggered by external
and internal factors external factors
can be non-microbial or microbial
non-microbial factors include allergens
irritants
and toxic compounds now the two main
microbial factors that trigger
inflammation are virulence factors in
pathogen-associated molecular patterns
or pamps virulence factors are molecules
that help pathogens colonize tissues and
cause infection
pamps are small molecules with conserved
patterns that are shared across many
different pathogens
including bacterial wall components like
peptidoglycan
lipopolysaccharide or lps and
lipotechchoic acid
and fungal wall components like manin
for intracellular pathogens like viruses
pamps might include the viral rna or dna
our immune system recognizes virulence
factors and pamps as foreign substances
and can trigger an inflammatory response
against them
now in terms of internal factors it
turns out that there's an endogenous
equivalent to pamps
called damage associated molecular
patterns or
damps damps are intracellular proteins
that get released when a cell's plasma
membrane is injured
or when a cell dies so damps are a
signal that there's serious cell damage
and they trigger inflammation now pamps
and damps are recognized by pattern
recognition receptors
or prrs which are cell surface receptors
on various leukocytes that help to
activate those cells and spark the
inflammatory response
which can be thought of as the innate
immune system
key features are that this response is
non-specific
meaning that prrs don't distinguish one
specific pathogen from another
although they can distinguish between
broad categories like viruses from
bacteria
also the response is super fast
occurring within minutes to hours
and finally there's no memory associated
with innate responses
generally speaking there are two main
types of leukocytes
granulocytes which include neutrophils
eosinophils
basophils and mast cells and a
granulocytes
which include lymphocytes and monocytes
which can differentiate into macrophages
or dendritic cells
the inflammatory process usually starts
with either macrophages or mast cells
both of which are found in the tissues
when there's tissue damage these cells
respond to the pamps or damps
mast cells have granules containing
different inflammatory mediators
like histamine serotonin cytokines
and dicosanoids like prostaglandins and
leukotrienes
these inflammatory mediators act on the
endothelial cells surrounding the
capillaries nearby
causing them to separate from each other
in addition macrophages which are the
garbage truck of the body
start to eat up invading pathogens
the release of cytokines causes
capillaries to get larger
and increase vascular permeability
allowing plasma proteins and fluids to
leave the circulation
endothelial cells also help spur on this
process by releasing nitric oxide
which helps vasodilate the capillaries
and makes them more permeable
in addition endothelial cells express
more adhesion proteins to help
leukocytes that are floating by in the
blood to attach and roll along the
vessel wall until they reach the injured
site
in particular neutrophils get attracted
to the site of infection by the
chemokines in microbial products
the neutrophil then starts to squeeze
through the gaps between two endothelial
cells
until it reaches the other side and this
is called extravasation
it's kind of like squeezing between two
fence poles to sneak into an amusement
park
rather than paying admission but that's
not to say you should do that
now next the leukocyte follows the
gradient of inflammatory mediators
to get to the site of inflammation
neutrophils are the first leukocytes
recruited during the acute inflammatory
process
and they're like hungry athletes they
immediately start phagocytosing or
eating pathogens in damaged cells
neutrophils take in a lot of pathogens
quickly kind of like a vacuum
and then commit suicide destroying
themselves and all of the pathogens
they've taken
in now while this is all happening
there's also a family of soluble
proteins called the complement system
the complement proteins most often get
activated in the presence of antibodies
bound to pathogens
or by molecules on the pathogens once
these complement proteins
are active they help attract leukocytes
and help with optimization
meaning that they can bind to microbes
so that leukocytes can more easily
phagocytose them
kind of like sticking a fork in a
meatball so that it doesn't slip away
some of the complement proteins also
kill pathogens by directly forming a
channel in their membrane
literally punching a hole in it
all the while dendritic cells continue
to phagocytose pathogens and present
bits of them to t lymphocytes this
activates the adaptive immune system
which kicks in after a few days if the
stimulus for all of this inflammation
was a cut or a scrape
then platelets and clotting factors from
the plasma reach the area and clot the
wound
this helps stop the bleeding as well as
prevents pathogens from entering the
bloodstream
and provides a framework for tissue
repair
in summary all of these factors
contribute to the heat
pain redness and swelling that's classic
for inflammation
now the inflammatory response ends with
tissue repair
macrophages are recruited to eat up dead
and dying cells
so that when tissue can make room for
new cells this is followed by
angiogenesis
which is the formation of new blood
vessels and that's triggered by growth
factors released by macrophages
these newly formed blood vessels are
temporary meaning that once the wound is
healed
these new vessels regress finally there
are fibroblasts
which come into the area of inflammation
and synthesize collagen to help with
wound healing
overall if there's only mild damage then
the tissue regenerates back to its
normal healthy state
but if there's severe damage then the
damaged cells get replaced by a
non-functional fibrous scar
alright as a quick recap inflammation is
a complex response to harmful stimuli
which could be from a pathogen
but it also could be from trauma or
toxins
the response involves blood vessels
dilating and becoming more permeable
and attracting more immune cells and
fluid into the local tissue
the classical signs of inflammation are
heat pain
redness and swelling and these can lead
to a loss of function
the inflammatory response ends with
wound repair and resolution
either restoring the initial tissue
integrity or leaving a fibrous scar
you
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