Kapitel 1 (Tobias) - Inflammatory Response Flashcards
Vad är negavtiva effekter vid förlängad och ukontrollerad inflammation?
1) Smärta
2) Immunosuppression
3) Organ dysfunktion
4) Död
Akronym: DOSI
Vad är de klassiska makroskopiska symtom på inflammation?
1) Rubor (Rödma)
2) Dolor (Smärta)
3) Calor (Värma)
4) Tumor (Svullnad)
5) Functio Laesa (Förlust av funktion)
Vad är faserna av det akuta vaskulära respons i inflammation?
1) Vasodilation (Snabb vasoconstriction initiellt)
2) (Ökad) Permeabilitet
3) Stasis
4) Leukocyt extravation
Vilka vasoaktiva substanser stimulerar den snabba vasokonstriktion som kommer innan vasodilationen i akut inflammation?
Hur/var ifrån frigörs de?
Kringliggande vävnad: catecholaminer, serotonin, bradykinin, och prostaglandins
Sympatiska nervsystem: Norepinephrine
Vilka substanser stimulerar vasodilation i akut inflammation?
Nitric oxide, histamine, leukotriener, prostaglandiner och komplement faktorer
What are the 4 stages the leukocyte undergoes leading to extravation (after hemostasis has occured)?
Vad är de 4 faser som leukocyterna går igenom som ledar till extravation (efter hemostasen)?
1) Rolling
2) Integrin aktivation
3) Stabil adhesion
4) Extravasion
Acronym: RISE
Vad är E selektin och vad är funktionen?
Receptor på kärl endothelceller.
Binder till korresponderande ligander på leukocyter (och thrombocyter).
Vad kallar man processen där leukocyten går ut från kärlet?
Var händer det?
Diapedes.
Genom interendotheiala junctions i postkapillära venuler
Vad är den första leukocyt som ingår i inflammationen typiskt?
Efter hur lång tid har de peak population?
Neutrophiler
Efter24-48 timmer
Nämn 2 typer av makrofager
- Tissue-resident Macrophages
- Monocyte-derived Macrophages
Vad är funktionen av tissue-resident macrophager?
- Tidigt detektion av inflammatoriska stimuli och är en stor tidig producents av proinflammatoriska cytokiner.
Vad triggar monocyter till att extravasera iut i vävnaden?
- Chemotaxiner
(including cytokines, fibronectin, elastin, complement factors (C3a, C5a), thrombin, and growth factors (e.g., platelet-derived growth factor [PDGF], transforming growth factor-beta [TGF-β]))
Macrophage polarization refers to the ability of macrophages to assume two distinct functional phenotypes - which phenotypes are these?
M1 and M2
Vad aktiveras M1 makrofager av och vad är deras funktion?
Activated by:
- Infectious agents
- Proinflammatory cytokines
Function:
- Debridement by phagocytosis of foreign material, pathogens, and damaged cells.
- Production of proinflammatory cytokines (IL-1β, IL-6, and TNF-α) and prostaglandins, enhancing the inflammatory response
- Secretion enzymes like collagenases and elastases to dissolve the extracellular matrix, facilitating phagocytosis and remodeling,
- (antigen presenting cells that interact with lymphocytes.) (Adaptive immunesystem)
What is M2 macrophages classically activated by and what are their function?
Activated by:
- Anti-inflammatory cytokines
Function:
- Aid in wound repair and healing
- Secretion of growth factors like PDGF or TGF-β, which stimulate fibroblasts to produce collagen, further dampening the inflammatory response
- Secretion enzymes like collagenases and elastases to dissolve the extracellular matrix, facilitating phagocytosis and remodeling,
- (antigen presenting cells that interact with lymphocytes.) (Adaptive immunesystem)
What are the life-spans of Tissue derived Macrophages and circulating Monocytes - respectively?
Tissue-resident Macrophages:
- Months to years
Circulating Monocyte:
- Day(s)
What are the cellular components of acute inflammation?
- Neutrophils
- Macrophages and monocytes
- Lymphocytes
- Mast Cells
- Endothelial cells
- (Antigen presenting cells like dendritic cells to cells of mesenchymal origin like fibroblasts and myocytes, the impact of these other cell types must be considered.)
Where do we find Mast Cells?
Mast cells are ubiquitously distributed in all organs
What do Mast cells degranulate in response to?
- Physical trauma
- Complement factors
- Microbial products
- Neuropeptides
What do Mast cells release?
And what are their overall function?
- Histamine (Primary soruce in acute inflammation)
- Pro-inflammatory mediators like:
- serotonin
- leukotrienes
- prostaglandin metabolites
- heparin
- cytokines
Overall function:
- Enhancing local inflammatory response
List as many inflammatory stimuli as possible
- Trauma
- infection, foreign material
- caustic chemicals
- allergens
- autoimmune disease
What are lipopolysaccharide, lipoteichoic acid, peptidoglycan, and microbial oligonucleotides examples of?
PAMPS
Pathogen-associated molecular patterns
What is the difference between DAMPS and PAMPS (Where are they produced - what do they signal?
PAMPS:
- Microbial molecules
- Recoqnized as “foreign” to the host
DAMPS:
- Endogenous molecule released with cellular damage (ex. fibrinogen, high-mobility group B1, Heat Shock Proteins, etc.)
- Alert the body to cellular damage initiated by infectious or noninfectious agents
How do PAMPS and DAMPS signal the immune system?
- By interacting with cell surface receptors.
What are: toll-like receptors, scavenger receptors, mannose receptors, C-type lectin-like domain–containing receptors, peptidoglycan recognition receptors, and nucleotide-binding site–leucine-rich repeat receptors - examples of?
What are their function?
- PRR´s (Pattern Recognition Receptors)
- Bind DAMPs and PAMPs -> Inflammation
Where do we find PRR´s?
- Expressed on the cell surface
- Within the intracellular compartment
- Soluble forms may be found in bodily fluids
