Path Mechanisms II 1: PMNs and Inflammatory Disease Flashcards

1
Q

What are PMNs designed to do?

A

Chemotaxis
Phagocytosis
Bacterial Killing

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2
Q

What is LAD Deficiency?

A

Diminished Neutrophil rolling and recurrent bacterial infections….severe periodontitis in children

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3
Q

What PMN and monocyte cell receptors are missing in LAD patients?

A

Mac1

LFA1

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4
Q

What is Chediak-Higashi Syndrome

A

Chemotaxis defect with increased oxygen consumption and increased H202 production. Sever periodontitis and ulceration due to recurrent pyogenic S. aureus infections

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5
Q

What is Neutropenia Agranulocytosis Myelosuppression?

A

Diminished number of phagocytes which leads to severe, life threatening infections and severe PD

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6
Q

What is Hyper-IgE or Job’s Syndrome

A

Chemotaxis defect due to cytokine dysfunction.

Leads to PD with oral ulcerations

Higly elevated IgE

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7
Q

What Th produced inflammatory PMN responses?

A

Th17

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8
Q

Why is IL-17 such a problem for PD?

A

Its primary function is the call PMNs out of the blood. When the PMNs can’t get out, more and more IL-17 is secreted by Th Cells.

Problem is that IL-17 also promoted bone resorption

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9
Q

What enzymes do PMNs produce that can destroy host tissues?

A

MMP-8

Acid hydrolases

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10
Q

Why do PMNs produce oxygen radicals that can leak out and destroy host tissue?

A

For use in their lysosomes

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11
Q

What do PMNs also synthesize that are also pro-inflammatory response?

A

Platelet activating factor
Thromboxane
Leukotrienes

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12
Q

What is PMN hyperactivity?

A

When PMNs are overloaded by bacteria that they are trying to kill. Their enzymes, inf factors, and o2 rads build up and become toxic.

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13
Q

PMNs are the first responders, what comes next in the immune response?

A

Monocytes and Activated Macrophages

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14
Q

What do Monocytes and activated Macrophages release when they encounter endotoxin?

A

TNF

IL-1

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15
Q

What do TNF and IL-1 do

A

They further inflammation related tissue damage

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16
Q

What cells produce MMPs

A

PMNs
Fibroblasts
Macrophages

17
Q

What does the drug resolvyx target?

A

IL-17

IL-23

18
Q

What are lipoxins, resolvins, and protectins?

A

They are mediators produced by PMNs that actually stop the inflammatory response

19
Q

What can low dose aspirin induce?

A

lipoxin production

20
Q

How can neutrophils help to resolve inflammation?

A

by changing phenotype and producing resolving factors

21
Q

What fat molecules are protectins, resolvins, and lipoxins produced from?

22
Q

What does RvE1 do?

A

Restores bone loss due to P.gingivalis in mice

23
Q

What is RvE1?

A

A resolvin

24
Q

What pro-inflammatory mediator can be turned into RvE1

A

Leukotrienes

25
What do Th1 Cells do?
Increase macrophage production
26
What do Th2 Cells do?
Increase antibody production
27
How do Th1 and B Cells lead to PD destruction?
Can release inflammatory cytokines that call for more Macrophages
28
How do T Cells lead to PD damage?
Produce cytokines that lead to osteoclast activity
29
How do Th-17 Cells lead to PD damage
Secrete cytokines that enhance inflammatory response and promote autoimmunity
30
What chemical signal allows Th1 Cells to recruit macrophages?
INF gamma
31
What other signal can T-cells and B-Cells produce that directly affects bone resorption?
RANK-L
32
What cells are the primary source of RANK-L in PD patients?
T and B Cells
33
What are the 3 disease modifiers?
Diabetes Genotype Smoking