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Acute inflammation
Árpád Szállási
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Inflammare (Latin), to set on fire
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Terminology: tissue+itis (Greek, „pertaining to”)ασθένεια γαστήρ + „itis” (the disease of the stomach”)
tongue glossitis
oral mucose stomatitis
cornea keratitis
lung if infectious: pneumonia (πνευμονία); if not, pneumonitis
stomach gastritis
small intestine enteritis
coecum typhlitis
rectum proctitis
testis orchitis
vagine colpitis
fallopian tube salpingitis
belly bottom omphalitis
breast mastitis
adipose tissue panniculitis
brain encephalitis
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The objectives of the lecture
1. The inflammatory cascade: understand the
chain of vascular and cellular events in the
natural history of acute inflammation
2. Understand the roles of humoral factors
(chemical mediators) during acute inflammation
3. Know the three possible outcomes of acute
inflammation
4. Describe the morphologic patterns of acute
inflammation
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Inflammation can be protective
(essential for survival), but can
also be harmful
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„A cascade of events by which our body
fights things that can harm us, such as
infections, injuries and toxins, in attempt to
protect and heal itself.”
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Prototypical inflammatory
reaction
• The host recognizes the noxious agent, that
• Attracts leukocytes and humoral factors from the
circulation
• The activated leukocytes act in concert with the humoral
factors to kill/eliminate the noxious agent
• The response remains controlled and ends the same
way
• The injured tissue heals itself
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The five cardinal signs of acute inflammation
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Aulus Cornelius Celsus
De morborum: „Inflammation is a
disease.”
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Galenus added „functio laesa” (loss of function) as the 5th
cardinal sign of inflammation
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John Hunter (1728-1793)
„Inflammation is not a disease but a non-
specific response that has a salutary
effect on its host.”
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Julius Cohnheim (1839-1884),
microscopic description of inflammation
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Ilya Mechnikov (1845-1916) describes
phagocytosis in 1882
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Nobel prize, 2020, HCV
Harvey J. Alter (NIH), Michael Houghton (U. Alberta) and Charles M. Rice
(Rockefeller U)
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Sir Thomas Lewis (1881-1945), chemical
substances mediate the vascular changes of
inflammation
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Denerved paw
(saphenous nerve
cut)
Intact paw
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Hőgyes Endre (1847-1906)
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Ifj. Jancsó Miklós and Gábor Aranka
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Inflammation is a universal and ancient form of host defence
Not a disease per se!; rather it is a protective, non-specific response tovarious noxious agents
Inflammation is not equal with infection!
Inflammation may be of two types, acute (this lecture) and chronic (thetopic of next lecture)
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The objectives of the lecture
1. The inflammatory cascade: understand the
chain of vascular and cellular events in the
natural history of acute inflammation
2. Understand the roles of humoral factors
(chemical mediators) during acute inflammation
3. Know the three possible outcomes of acute
inflammation
4. Describe the morphologic patterns of acute
inflammation
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Stimuli that can evoke acute
inflammation
• Infections
• Tissue necrosis (e.g. ischemia, trauma,
thermal or chemical injury)
• Foreign body
• Hypersensitivity reaction
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Innate immunity (~ acute inflammation): evolutionary ancient defense
strategy that recognizes „non-self”
Adaptive immunity: highly adaptable system that creates immunological
„memory” (it becomes a problem when „maladaptive”!)
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Robert A. Good (1922-2003) discovers
adaptive immunity
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In 1965, Max Cooper and Robert Good published a landmark study in Nature that led to the birth of the B cell field. Working with chickens, they showed that cells that develop in the bursa of Fabricius ('B cells') are responsible for antibody production, whereas those cells that develop in the thymus ('T cells') are necessary for delayed-type hypersensitivity responses.
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1st step: to recognize the danger: Pattern Recognition Receptors (PRRs)
Cellular receptors for microbes PRRs recognize PAMPs (pathogen-associated molecular pattens)
Sensors of cell damage PRRs recognize DAMPs (damage-associated molecular patterns), that is,
molecules released from damaged cells; uric acid (a product of DNA breakdown), ATP (released from
damaged mitochondria), reduced intracellular K + concentrations (reflecting loss of ions because of
plasma membrane injury), DNA (when it is released into the cytoplasm and not sequestered in nuclei, as it
should be normally), and many others.
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Necroptosis = a „fail-safe”
mechanism to eliminate infected
cells when virus blocks apoptosis
Pyroptosis = host cell death
triggered by intracellular
pathogens
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Toll-like receptors
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„das ist toll!” (this is great!)
Christiane Nüsslein-Volhard (1942), Nobel prize 1995
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The cascade of acute inflammation
• Vasodilation
• Increased vascular permeability/leakage of exudate
• Leukocytes:
● margination, rolling, and adhesion
● diapedesis (transmigration)
● chemotaxis
● PMN activation
● phagocytosis (recognition, engulfment, killing)
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Vascular events of inflammationThe purpose of the inflammatory vascular reaction is to deliver the humoral and
cellular factors to the site of defence reaction
Changes in vascular flow and caliber- Arteriolar dilation,
Changes in vascular permeability
Dilatation
Endothelial gaps
Direct endothelial injury
Leukocyte injury
Transcytosis (endo/exo)
LEAKAGE of a proteineaceous fluid EXUDATE and not
TRANSUDATE!!!!!
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Neutrophils (PMN granulocyte)
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Adhesion molecules affecting rolling and adhesion
1.Selectins (E,P and L) from endothelial cells (E and P) or leukocytes (L)-rolling
2.Integrins from many cells (ICAM, VCAM)-adhesion
Transmigration: mediated by CD31
CHEMOTAXIS PMNs going to the site of the injury after transmigration (chemokines)
EXTRAVASATION of PMNs
• MARGINATION
• (PMN’s go toward wall)
• ROLLING (tumbling and
HEAPING)
• ADHESION
• TRANSMIGRATION
(DIAPEDESIS)
Chemoattractants: N-formylmethionine, C5a, leukotrienes
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Weibel-Palade body stores CD62P in
edothelium
CD31
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IL-8
IL-8
MARGINATION
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ADHESION
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TRANSMIGRATION
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TNF inhibitors as a new generation of
antiinflammatory drugs
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For rheumatoid arthritis, psoriasis, etc
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LEUKOCYTE
„ACTIVATION”
• „triggered” by the offending stimuli for PMNs to:
─ 1) Produce eicosanoids (arachidonic acid
derivatives)
• Prostaglandin (and thromboxanes)
• Leukotrienes
• Lipoxins
─ 2) Undergo DEGRANULATION
─ 3) Secrete CYTOKINES
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An additional mechanism of killing microbes is the extracellular traps-NETosis
PHAGOCYTOSIS
• RECOGNITION
• ENGULFMENT
• KILLING
(DEGRADATION/
DIGESTION) (oxigen dependent and
independent mechanisms)
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Oculocutaneous albinism
White tiger (a big cat with
Chediak-Higashi!)
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Oculocutaneous albinism:
melanin is produced but not
packed into melanosomes
Albino: no melanin production
due to Tyrosinase deficiency
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Defective NADPH oxidase
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Neutrophil Extracellular
Trap
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The objectives of the lecture
1. The inflammatory cascade: understand the
chain of vascular and cellular events in the
natural history of acute inflammation
2. Understand the roles of humoral factors
(chemical mediators) during acute
inflammation
3. Know the three possible outcomes of acute
inflammation
4. Describe the morphologic patterns of acute
inflammation
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Humoral elements „Mediators”
• Vasoactive amins: histamine, serotonine (vasodilatation, permeability, pain)
• Vasoactive peptids: bradykinin
• Complement system (MAC, vasodilatation, permeability, chemotaxis, opsonisation)
• Clotting, fibrinolitic cascade
• Immunglobulins
• Arahidonic acid derivatives
• Cyclooxigenase prostaglandins
• Lipoxigenase leukotriéns
• Cytokins TNF, IL-6, IL-1
• Exogenous mediators: fMLP, endotoxin, superantigens
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CHEMICAL
MEDIATORS
„general”
•From plasma or cells
•Have triggering stimuli
•Usually have specific targets
•Can cause a cascade
•Are short lived
CLASSIC MEDIATORS –Histamine, -Serotonine-Complement, -Kinins, -Clotting factors
-Eicosanoids, -Nitric oxide , -etc
HISTAMINE
• Mast Cells,
basophils
• POWERFUL
Vasodilator
• Vasoactive
„amine”
• IgE on mast cell
SEROTONIN
• (5HT, 5-Hydroxy-
Tryptamine)
• Platelets and
EnteroChromaffin Cells
• Also vasodilatation, but
more indirect
• Evokes N.O. synthetase
(a ligase) from arginine
COMPLEMENT SYSTEM• >20
components,
in circulating
plasma
• Multiple sites
of action, but
LYSIS is the
underlying
theme
KININ SYSTEM• BRADYKININ is KEY
component, 9 aa’s
• ALSO from circulating plasma
• ACTIONS
− Increased permeability
− Smooth muscle
contraction, NON
vascular
− PAIN
CLOTTING
FACTORS• Also from circulating plasma
• Coagulation, i.e., production of
fibrin
• Fibrinolysis
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Paroxysmal Noctural Hemoglobinuria
(PNH)
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EICOSANOIDS(ARACHIDONIC ACID
DERIVATIVES)
• Part of cell membranes
• 1) Prostaglandins (incl.
Thromboxanes)
• 2) Leukotrienes
• 3) Lipoxins (new)
MULTIPLE ACTIONS AT MANY LEVELS
PROSTAGLANDINS(THROMBOXANES
INCLUDED)
• Pain
• Fever
• Clotting
LEUKOTRIENES
• Chemotaxis
• Vasoconstriction
• Increased Permeability
LIPOXINS
• INHIBIT chemotaxis
• Vasodilatation
• Counteract actions of
leukotrienes
PLATELET-ACTIVATING FACTOR
(PAF)
• Phospholipid
• From MANY cells,
like eicosanoids
• ACTIVATE
PLATELETS,
powerfully
• VASOCONSTRICTION
• …………….
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CYTOKINES/CHEMOKINES
• CYTOKINES are PROTEINS produced by MANY
cells, but usually LYMPHOCYTES and
MACROPHAGES, numerous roles in acute and
chronic inflammation
-TNFa, IL-1 by
macrophages
• CHEMOKINES are small proteins which are
attractants for PMNs (>40)
NITRIC OXIDE
• Potent vasodilator
• Produced from the action of
nitric oxide synthetase from
arginine
LYSOMAL CONSTITUENTS
• PRIMARY• Also called
AZUROPHILIC,
or NON-specific
• Myeloperoxidase
• Lysozyme (Bact.)
• Acid Hydrolases
• SECONDARY• Also called SPECIFIC
• Lactoferrin
• Lysozyme
• Alkaline Phosphatase
• Collagenase
FREE RADICALS
• O2 –(SUPEROXIDE)
• H2O2 –(PEROXIDE)
• OH- –(HYDROXYL
RADICAL)• VERY VERY DESTRUCTIVE
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The objectives of the lecture
1. The inflammatory cascade: understand the
chain of vascular and cellular events in the
natural history of acute inflammation
2. Understand the roles of humoral factors
(chemical mediators) during acute inflammation
3. Know the three possible outcomes of acute
inflammation
4. Describe the morphologic patterns of acute
inflammation
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OUTCOMES OF ACUTE INFLAMMATION
• 1) 100% (COMPLETE) RESOLUTION
• 2) SCAR
• 3) CHRONIC INFLAMMATION (next lecture!)
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The objectives of the lecture
1. The inflammatory cascade: understand the
chain of vascular and cellular events in the
natural history of acute inflammation
2. Understand the roles of humoral factors
(chemical mediators) during acute inflammation
3. Know the three possible outcomes of acute
inflammation
4. Describe the morphologic patterns of acute
inflammation
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Classification of acute inflammation based on the
exudate
Serous Common cold, pleuritis exs., burns, catarrhal inflammation of mucous
membranes
Fibrinous Serous membranes: Pleuritis/pericarditis sicca, Peritonitis fibrinosa
Mucous memebranes: Diphtery, typhoid fever, dysentery
Purulent folliculitis, furuncule, carbuncule
Abscess: circumscibed pus in parenchymal organs
Empyema: circumscribed pus in preformed body cavity
Phlegmone: inflammation spreading in tissue spaces
Haemorrhagic plague, smallpox, anthrax, flue
Gangraenous - failure of inflammation
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Classification of acute inflammation based on the exudate
Serous („watery”)
Examples for this type of
inflammation!!!!!!!
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Diphteria
Fibrinous
- fibrin is the endpoint of coagulation,
and had a characteristic appearence
both grossly and macroscopically
- Severe injury with excessive
deposition of fibrin in serosus cavities
- The fibrinous exudate may be
degraded by FIBRINOLYIS and
removed by macrophages resulting in
RESOLUTION
- Incomplete removal of fibrin resulting
in organization and scarring with
FIBROUS ADHESIONS of pleural or
pericardial surfaces
Tonsillitis follicularis
Pericarditis fibrinosa
PSEUDOMEMBRANE results when the upper
portion of a mucosal surface undergoes
necrosis, freeing fibrinogen from vessels that
then clots along the surface
- diphtheria (in the upper airway) or antibiotic-induced
pseudomembranous colitis (in the lower gut).
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Dressler syndrome(described by William Dressler in 1956)
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Furuncle
CarbuncleFolliculitis
Purulent
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(Empyema thoracis)
Abscess: circumscibed pus in parenchymal organs, in organs
with non-preformed cavity
Empyema: circumscribed pus in preformed body cavity
Phlegmone: inflammation spreading in tissue spaces
Empyema thoracis
Meningitis purulenta
Empyema v.felleae
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Sepsis puerperalis (childbed fever)
Ignác Semmelweis (1818-1865)
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Semmelweis Museum of Medical History
(his birthplace)
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Haemorrhagic inflammation
Variola vera
Urocystitis acuta
Skin anthrax
Influenza Virus Infections (lungs)
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Anthrax as biological weapon
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1979, Swerdlows (USSR), military research
facility accidentally releases anthrax
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Anthrax as tool for terrorists
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Smallpox: 12,000 years of
terror!
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Variola vera (smallpox), eliminated in 1977
last outbreak was in Yugoslavia (1972)
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COVID-19 (SARS-CoV-2)
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Necrotizing inflammation
The combination of necrosis, inflammation and bacterial
putrefaction is called gangrene.
Cholecystitis acuta gangrenosa
Appendicitis acuta gangrenosaPneumonia gangrenosa
Gangrene
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Ulcerative
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INFLAMMATION
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