Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
26 Cards in this Set
- Front
- Back
|
1. What are the four cardinal signs of inflammation?
|
1. Pain (dolor)
2. Redness (rubor) 3. Heat (calor) 4. Swelling (tumor/edema) |
|
|
2. Why does vasodilation occur?
What do resident tissue macrophages do? |
Due to release of kinins and triggering of coagulation
Sense microbial invaders and elaborate cytokines and chemokines to call in and activate other cells of the immune system |
|
|
3. What are cytokines?
What are chemokines? In what function can cytokines act? In what function can chemokines act? |
Low MW proteins that mediate communication between cells of the immune system
*signal transmission requires specific receptors on the target cells Subclass of cytokines that cause immune cells to undergo directed migration toward them Cytokines - paracrine, endocrine, and autocrine manner Chemokines - paracrine manner |
|
|
4. What do chemokines call in to the site of inflammation?
What do cytokines activate? |
PMNs and macrophages
Macrophages and leukocytes |
|
|
5. What are four acute phase response proteins (APRPs) in the blood?
|
1. C-reactive proteins
2. Mannose binding lectin 3. Lipopolysaccharide 4. Serum amyloid |
|
|
6. What does C-reactive protein bind?
What does mannose binding lectin protein bind? What does it trigger? What do lipopolysaccharide (LPS) binding proteins facilitate the binding of? |
Polysaccharides on pneumococci
Mannose motifs on bacteria Triggers complement activation which promotes phagocytosis Facilitates binding of bacterial LPS to macrophages and release of cytokines and chemokines |
|
|
7. What makes PMNs leave the circulation and migrate into the tissues?
How do neutrophils/leukocyte migrate to the site of microbial invasion? |
Inflammatory state induces changes in the endothelium which express adhesion molecules to which the PMNs can bind
1. Rolling 2. Activation 3. Adhesion 4. Extravasation |
|
|
8. What mediates rolling?
What are these? What up-regulates these molecules on the endothelial cells? What does adhesion to selectins do? (two things) |
Selectins
Surface molecules on endothelium and leukocytes Cytokines 1. Slows movement of PMNs (stasis) 2. Binds them loosely to the endothelium allowing them to roll along the endothelial surface |
|
|
9. How do cytokines and chemokines activate leukocytes?
What does this activation do? (two things) |
Alter the conformation of molecules on leukocyte surface
1. Allows cells to adhere more tightly to the endothelium 2. Induces adhesion molecules on endothelial cells |
|
|
10. What do ICAMs do?
|
Enhance the tentative interaction between the PMN and the endothelial cell
**PMNs become more tightly bound to the endothelium **ICAM = interaction of cellular adhesion molecules |
|
|
11. What happens during transendothelial mirgation or extravasation?
How is cell movement induced? |
Attached PMN tranverses the epithelial barrier and enters the tissue space to attack the microbe
By chemokines secreted by monocytes/macrophages |
|
|
12. What are Toll-Like receptors (TLR)?
What characterizes TLRs? (three things) |
Group of receptors known as pattern recognition receptors (PRR)
Recognize pathogen associated molecular patterns (PAMP) 1. Low specificity 2. Broad reactivity 3. Recognize classes of molecules present on microbial but not mammalian cells |
|
|
13. Which TRLs are on the surface of macrophages?
(three receptors) What does it recognize? |
1. TLR2 & TLR6
-gram-positive bacteria -mycobacteria -fungal cell wall products 2. TLR4 -gram negative bacteria (LPS) (bacterial lipopolysaccharide) 3. TLR5 -bacterial flagella (flagellin) |
|
|
14. What TLRs are expressed in endosomal vacuoles?
What does these react with? |
TLR3, 7, 8, & 9
Microbial RNA or DNA or to synthetic ligands |
|
|
15. When the TLRs are engaged what is the result?
Two things.... |
1. Release of massive amount of TNF and other pro-inflammatory cytokines
**lead to septic shock and multiple organ failure 2. Induction of NO **lead to fall in blood pressure and circulatory collapse |
|
|
16. What are NOD-like receptors?
What is the C3b receptor? What are scavenger receptors? |
Nucleotide binding oligomerization domain like receptors
Opsonin (increase phagocytosis) Recognize a variety of target molecules including lipoproteins on pathogens |
|
|
17. What are produced by monocytes and macrophages when they activated?
|
1. TNF
2. IL-1 3. Il-6 4. Il-8 5. Interferon 6. IL-12 |
|
|
18. What is the IL-1?
How does IL-1 act? What does it activate? What does this result in? |
Endogenous pyrogen
Acts via the vagus nerve Activate prostaglandin synthesis in hypothalamus Results in fever **IL-1 also activates endothelial cells |
|
|
19. What does IL-6 do?
What does IL-12 cause the release of? What does this do? |
Induces acute phase proteins in the liver
(C-reactive protein) IFN from natural killer cells Activates macrophages to increase their capacity to make RO intermediates and to initiate synthesis of NO |
|
|
20. What do both TNF and IL-1 induce?
|
Increased expression of adhesion molecules on endothelial cells
Increased production of chemokine IL-8 from macrophages **result is increased adhesion to endothelium |
|
|
21. What is IL-8?
What is the cytokine temporal sequence? |
Chemotactic for neutrophils
1. TNF 2. IL-1 3. IL-12 4. IL-6 **produced in this order over the first 5 hours after exposure to bacterial products |
|
|
22. What happens when microbes trigger TLRs and release too many pro-inflammatory cytokines?
What is the result of a cytokine storm? |
Get cytokine storm
Sepsis syndrome **ultimately can end in multi-organ dysfunction (MOD) and death |
|
|
23. How is sepsis syndrome most commonly mediated?
Why is this significant to dental health? |
Through gram-negative bacteria triggering via TLR4
Many of the bacteria that live in the periodontal tissue are gram-negative and have LPS on their surface Periodontal disease may be in part mediated by inflammation generated by activation of macrophage through TLR4 |
|
|
24. How do pro-inflammatory cytokines mediate the host defense to pathogens?
How is NO made? |
Activated macrophages are induced to make NO and reactive oxygen intermediates
**NO is microbicidal By induction of transcription of inducible nitric oxide synthase (iNOS) |
|
|
25. What is the role of chemokines in inflammation?
What is the role of IL-1 in inflammation? |
1. Attract cells to sites of inflammation
2. Alter integrin conformation to allow their interaction w/ ICAM-1 1. Induces fever 2. Up-regulates ICAM-1 expression on epithelial cells to increase PMN adhesion |
|
|
36. If TLR4 is triggered by LPS would the host be better able to fight a microbe?
|
Yes
TLR4 would amplify the inflammatory response and call neutrophils and more monocytes to the site of the microbial invasion Also cells of the adaptive immune system would arrive |
