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Inflammation Grad > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Pro inflammatory cytokines

A

TNF, IL1 IL6, most Chemokines (CCL2 CCL3)

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2
Q

Anti inflammatory cytokines

A

IL4, IL10, IL13, TGF-B

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3
Q

Antiviral cytokines

A

IFN-a, IFN-b

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4
Q

B-cell activating cytokines

A

IL4, IL5, IL6, IL21

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5
Q

T-cell activating cytokines

A

IFN-y, IL2, IL4, IL12

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6
Q

Macrophages activating cytokines

A

IFN-y

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7
Q

Eosinophil and mast cell activating cytokines

A

IL3, IL4, IL5, IL13

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8
Q

Order of leukocyte infiltration in response to inflammation

A

Neutrophil spike (pro-inflammatory cytokines released), Macrophage spike (anti-inflammatory cytokines relased), lymphocytes come in (adaptive T cells/B cells too), and then resolution

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9
Q

Plasma vs serum

A

Plasma has clotting factors as well, Serum lacks clotting factors. None have RBC or WBC

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10
Q

Lymphocyte characteristics

A

Large circular nucleus, little else

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11
Q

Monocyte characteristics

A

dumb-bell-shaped nucleus, little else

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12
Q

Macrophages

A

Derived from monocytes and larger cells

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13
Q

Neutrophils

A

Large granules and polarized

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14
Q

Eosinophils

A

Crystallized granules staining with eosin in H&E stain

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15
Q

Basophils

A

Dense granules staining cytoplasmic blue in H&E stain

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16
Q

Symptoms of inflammation

A

redness, swelling, heat, pain, LOF

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17
Q

Steps of WBCs entering site of inflammation

A

1) tethering/rolling. Selectins bind to epithelial cells. 2) integrin activation. Endothelial cells have vesicles filled with chemokines/cytokines and release them, which activates integrin on WBCs. Integrins slow roll drastically. 3) Stable adhesion, integrins anchor WBC and they search for ways to pass endothelial to enter basement membrane. 4) Diapedesis. Can either be paracellular (between) or transcellular (through)

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18
Q

IL1 interacts with receptor, what happens?

A

IL1R is a type1 cytokine receptor that activates NF-kB and MAPK

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19
Q

IL1 antagonist

A

IL1ra. drug analog: Anakinra

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20
Q

IL6, IL2, IL3 interacts with receptor, what happens?

A

Type 1 Tyrosine Kinase receptor and activates JAK-STAT signaling. 1) receptor dimerization. 2) Dimerization activates JAK phosphorylation of cytokine receptor. 3) Recruits STATs phosphrylated by JAK. 4) Phosphorylated STATs dimerize and translocate to nucleus to activate genes

21
Q

JAK-STAT inhibitors

A

Ruxolitinib, Tofacitinib. Both treat rheumatoid arthritis and psoriasis

22
Q

TNFa interacts with receptor, what happens?

A

TNFa interacts with TNFa-R induces both gene transcription AND apoptosis, depending on downstream complexes because the TNFa-R has a “death domain” that allows for TRADD to bind (leads to apoptosis) or TRAF (gene transcription)

23
Q

Clinical actions of TNFa

A

low levels: local inflammation, leukocyte activation, endothelial activation
moderate levels: systemic inflammation - fever, liver inflammation, leukocyte proliferation
high levels: septic shock

24
Q

Negative regulators of TNFa

A

AU-Rich elements in the 3’UTR of oncogenes (including TNFa) allows destruction of TNFa. KO of ARE have chronic inflammation

25
Q

Complement system activation

A

inactive proteins are cleaved by proteases to generate active components to promote inflammation and opsonize pathogens to promote clearance/ C1/C3/C5 become C3a, 4a, C5a

26
Q

C3a, C4a, C5a roles

A

Complement system proteins that have anaphylatoxin activity to degranularize mast cells and increase vascular permeability and smooth muscle contraction and increase leukocyte recruitment.

27
Q

Exogenous chemoattractants

A

f-MLP (bacterial peptides), Lipids from damaged membranes (LPS)

28
Q

Endogenous chemoattractants

A

Complement proteins (C3a,4a,5a), Platelet activating factor, chemokines, leukotrienes, LPA (lysophosphophatic acid)

29
Q

GPCR desensitization

A

Can happen when chronic agonist binding leads to destruction of receptors. This is known as homologous desensitization (same receptor binding). The same can happen with heterologous desensitization (different GPCR inactivates upstream receptor)

30
Q

Relationship between cytokines and cell movement

A

GPCRs help to move pseudopods. Increase cytokines binding = more protein aggregation towards site of injury. PI3y is absolutely necessary for this movement.

31
Q

Role of PIP3 in polarization

A

PIP3 accumulates on leading edge (from GPCR and PI3Ky activity) and amplified via positive feedback loop, PIP3 and Rho GTPases (Rac). PIP3/Rac(Cdc42) then helps recruit actin polymerization. PIP3 phosphatase and PTEN localizes sides and back to decrease PIP3. Rho activation is at the trailing end and mediates actin/myosin contraction and resolution of adhesion events

32
Q

Role of CCL2

A

increased microvascular permeability, edema and lymph flow

33
Q

Cells of the adaptive immune system

A

T cells, B cell (CD4+, CD8+), NK T cells

34
Q

Cells of the Innate Immunity

A

Dendritic cell, Mast cell, Macrophage, Basiphil, Eosinophil, ?neutrophil, Natural Killer Cell, Complement protein, NK T cell

35
Q

Innate effectors

A

NFkB, IFN, IL-1

36
Q

What types of receptors are in the pattern recognition pathways?

A

Toll-Like receptors (TLR), NLR (nucleotide-like receptors), RLR (Rig-like receptors)- short 20-30bases receptor, cytosolic DNA receptor

37
Q

What pathway does TLRs activate?

A

NFkB

38
Q

What pathway does NLRs activate?

A

Caspase

39
Q

What is a major source of DAMPs

A

mitochondrial factors, HMGB, HSP, Purine

40
Q

Types of phagocytosis

A

Zipper (building around), sinking (invaginating), coiling (going around one sinded)

41
Q

What are the four major chemotactic factors and and how far do they act?

A

FAR Chemokines, complement cascade “by-products,” eicosanoids, Microbial products CLOSE

42
Q

Zipper phagocytosis MOA

A

FcyRI -> activates P13K -> activates Rac / PIP2/3 for actin growth. VERY FAST

43
Q

Sinking Phagocytosis MOA

A

C3R -> RhoA -> F-actin disruption. Slower. Might be beneficial for proper lysosomal fusion, recruitment of other vesicles, preventing the organism from getting into the cell

44
Q

Describe respiratory burst

A

Using NADPH oxidase to transfer electrons into the phagosome to produce superoxides, which are toxic

45
Q

What are NETs released by polymorphonuclear neutrophils and what do they do?

A

NETs, as their acronym suggests, traps bacteria and occur in 1/3 of neutrophils after apoptosis

46
Q

Stages of resolution of inflammation

A

STOP new neutriphil infiltration (eliminating DAMPS/PAMPs and putting out anti-inflammatory mediatirs. SINK, reducing inflammatory receptors and inducing antagonists. KILL induce apoptosis in leukocytes and eliminate debree (Efferocytosis). SKEW reprogram macrophages

47
Q

What is cPLA2

A

an inflammatory protein in the granules of neutrophils, mast cells, macrophages, and platelets and they are released in response to pro inflammatory cytokines. It is the central regulator of arachadonic acid from phospholipids

48
Q

what is COX?

A

COX is an enzyme that is produced in response to inflammation that converts arachidonic acid to prostaglandin. Prostaglandins can be both resolving and inflammatory inducing

49
Q

What are foam cells? What are they derived from?

A

Foam cells are differentiated from macrophages/monocytes and consume lipids/debris

Inflammation Grad (1 decks)

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