Inflammation Mediators Flashcards

(41 cards)

1
Q

Toll-Like Receptors

A

Activated by PAMPs; upregulated NF-kB leading to activation of immune response genes to multiple immune mediators (also seen on lymphocytes for both acute and chronic)

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2
Q

PGI2, PGD2, PGE2

A

Vasodilation and increased vascular permeability; PGE2 also mediates pain and fever

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3
Q

LTB4

A

Attracts and activates neutrophils

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4
Q

LTC4, LTD4, LTE4

A

Vasoconstriction, broncospasm, and increased vascular permeability (by contracting smooth muscle)

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5
Q

Mast Cells

A

Activated by tissue trauma, C3a, C5a or cross-linking of cell surface IgE by antigen; release of histamine granules (vasodilation and increased vascular permeability)

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6
Q

What are Rubor (redness) and Calor (warmth) due to?

A

Due to vasodilation, resulting in increased blood flow; mediated by histamine, bradykinin, and prostaglandin

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7
Q

What is Tumor (swelling) due to?

A

Leakage of fluid from post-capillary venules into interstitial space (exudate); mediated by histamine (endothelial cell contraction) and tissue damage (endothelial cell disruption)

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8
Q

What is Dolor (pain) mediated by?

A

Bradykinin and PGE2 that sensitive free nerve endings

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9
Q

What is Fever mediated by?

A

Pyrogens (such as LPS) from bacteria that cause macrophages to release IL-1 and TNF, increases COX in perivascular cells of the hypothalamus

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10
Q

What mediator raises set point temperature?

A

PGE2

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11
Q

What causes margination?

A

Vasodilation, slowing down flow in POST-CAP VENULE; allowing cells to marginate from center to periphery

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12
Q

What releases and mediates P-selectin?

A

Released from: Weibel-Palade bodies

Mediated by: histamine

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13
Q

What induces E-selectin?

A

TNF & IL-1

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14
Q

How does rolling occur?

A

Selectins bind to Sialyl-Lewis X found on leukocytes

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15
Q

Where and how are I-CAM and V-CAM regulated?

A

Upregulated on endothelium by TNF and IL-1

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16
Q

What do I-CAM and V-CAM interact with, what does it cause, and how does it happen?

A

I-CAM and V-CAM interact with Integrins on leukocytes; via C5a and LTB4 causing firm adheshion

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17
Q

What is LAD due to, and what type of disease is it? (x-linked, autosomal dominant, autosomal recessive)

A

Autosomal recessive defect of Integrins (CD 18)

18
Q

How does LAD present?

A

First is delayed separation of umbilical cord, will see increased circulation of neutrophils, and recurrent bacterial infections that lack bus

19
Q

What are neutrophils attracted by?

A

IL-8, C5a, LTB4

20
Q

What do IgG and C3b do?

A

Phagocytosis; consumption of pathogens or necrotic tissue

21
Q

What is Chediak-Higashi due to, and what type of disease is it? (x-linked, autosomal dominant, autosomal recessive)

A

Autosomal recessive defect in protein trafficking leading to impaired phagolysosome formation

22
Q

How does Chediak-Higashi present?

A

Increased risk for pyogenic infections, neutropenia, giant granules in leukocytes, albinism, peripheral neuropathy

23
Q

Fill in the enzymes on top of the arrows:

O2 —> O2* —> H2O2 —> HOCl (bleach)

A
  1. NADPH oxidase (oxidative burst)
  2. Superoxide dismutase
  3. Myeloperoxidase
24
Q

What is CGD due to, and what type of disease is it?

A

NADPH Oxidase deficiency leading to poor O2-dependent killing; x-linked recessive

25
How does CGD present?
Infection and granuloma formation by catalase positive organisms such as Staph Aureus, Nocardia, etc.
26
Results of nitroblue tetrazolium test in CGD?
Positive; means it's colorless, if it turns blue, that would be the NORMAL.
27
What is MPO deficiency due to and how does it present?
Myeloperoxidase enzyme missing; most patients are asymptomatic but at increased risk for Candida infections
28
What do macrophages secrete for resolution and healing?
IL-10 & TGF-beta (anti-inflammator)
29
What do macrophages secrete to continue an acute infection?
IL-8 (attracts neutrophils)
30
What do macrophages secrete to form an abscess?
FGF & cytokines (fibrosis around inflammation)
31
What are MHC-Class II linked to, and what type of antigen?
CD4+ T Cells; Extracellular
32
What are MHC-Class I linked to, and what type of antigen?
CD8+ T Cells; Intracellular
33
What does the Th1 subset of CD4+ T Cells secrete?
IL-2 (T-cell growth factor and CD8 activator), and IFN-gamma (activates macrophage)
34
What does the Th2 subset of CD4+ T Cells secrete?
IL-4 (class switch IgG and IgE), IL-5 (eosinophil chemotaxis, and mature B-cell class switch to IgA), and IL-10 (inhibits Th1)
35
How do CD8+ Cytotoxic T Cells kill?
Perforins and granzymes to induce apoptosis
36
What is the characteristic cell of granuloma formation?
Epitheliod histiocytes (macrophages with abundant pink cytoplasm)
37
What are the steps of a granuloma formation?
1. Macrophages process and present antigen via MHC Class II-CD4+ Helper T Cells 2. Interaction leads to macrophage secretion of IL-12 causing Helper T to form Th1 3. Th1 cells secrete IFN-gamma which differentiates macrophages into epithelioid histiocytes
38
Where would you see a non-caseating granulatoma?
Reaction to foreign material, sarcoidosis, beryllium exposure, Chron's, Cat Scratch
39
Where would you see a caseating granuloma?
Tuberculosis and Fungi
40
What causes Bruton's and what do you expect to find?
Deficiency of IgG so opsinization through C3b only; recurrent infections from things such as Haemophilus, Strep, Hepatitis. Will have lymphoid hypoplasia (tonsils & adenoids) SIGNIFICANT DROP IN ALL Ig LEVELS!
41
What does the interaction of CD31 and PCAM-1 cause?
Diapedesis.