(19) Antibacterial Immunity Flashcards
1
Q
- Are there a few bacteria cells where NK can come into play?
(unrelated) 2. What FE2 binding protein do bacteria make to compete with the host proteins?
A
- yes
- siderophores
2
Q
What are some imporant differences between eukaryotic and prokaryotic cells?
A
- ribosomes
- few sterols and cholesterols in prokaryotes
- bacteria replicate very quickly
- most bacteria small enough to be phagocytosed
3
Q
- Is there any correlation between shape/size/gram stain and pathogenesis?
- are there any gram-negative cocci of veterinary importance?
A
- no
- no
4
Q
- which type has thicker peptidoglycan?
- what layer of gram - has the LPS?
A
- gram +
- outer bilayer (the pro-inflammatory compoenent of gram -)
5
Q
- Peptidoglycan is a polysaccharide backbone composed of alternating residues of what and what?
- cross-linked via what?
- Teichoic acids are found in what? are what? can these be antigenic?
A
- N-acetylglucosamine and N-acetylmuramic acid
- peptide bridges
- gram +; repeating cross-linked simple sugars; yes
6
Q
- LPS (lipolysaccraride) found in what?
- aka what?
- highly what?
- what part of molecule is highly active?
A
- gram -
- endotoxin
- inflammatory
- lipid A
7
Q
- What are the 3 basic processes or components which prevent colonization by pathogenic bacteria?
A
- surface barriers, innate immunity, and adaptive immunity
8
Q
just read this
A
9
Q
- why no lyme disease in southwest
A
- powerful lizards kill bacteria in infected ticks
10
Q
- What are the most important cells in the innate defense against bacteria?
- mostly consist of what?
- Ingestion of the microorganisms cause what to fuse with what?
A
- phagocytes
- macrophages and neutrophils
- lyosomes with phagosome
11
Q
read pages 9 and 10 in this lecture (I think he just skipped them though)
A
12
Q
- the binding and phagocytosis of bacteria is greatly enchanced by what?
- The macrophages and neutophils have what that recognize opsonins?
- The receptors also signal the peptides to do what?
- What are the major opsonins (3 of them)?
A
- opsonization
- receptors
- activated the respiratory burst
- antibodies, complement C3b, lectin binding proteins (MBL, acute phase proteins)
13
Q
- Do phagocytes bear receptors that many bacterial structures, particularly CD14, CR3, (CD18/CD11c), Fc, and TLR that are specific for LPS?
- Are macrophages activated following encounter with bacteria?
A
- yes
- yes
14
Q
- Anti-microbial activites of phagolysomes are catergorized as what and what?
A
- oxidative and non-oxidative
15
Q
What are ROP made from?
A
NADPH oxidase
16
Q
(Bacteria)
- Do they try to avoid destruction?
- What are some ways they try to accomplish this?
- What are two enzymes they express too counter ROP?
A
- yes
- Have a thick capsule, prevent lysosome-phagosome fusion; escape into cytoplasm; resistance to lysosomal enzymes
- superoxide dismutase and catalase
17
Q
(Neutrophil Extracellular Traps)
- What occurs when neutrophils have released enough ROP?
- Is it just them dying?
- what does it accomplish?
- NETs are fibers made of what?
- I guess they also ensnare and kill what?
- What else do they release?
- CAlled the what cell death pathway?
- Does it have pro-inflammatory effects?
A
- regurgitate their DNA
- no, it is a programmed event
- it makes cell environment more viscous (due to presence of DNA), therefore makes it harder for bacteria to move around
- DNA and histones
- bacteria, fungi, and parasites
- antimicrobial peptides
- ETosis
- yes
18
Q
(Acute Phase Response Proteins)
- produced by what in response to what?
- Many are pattern recognition factors that bind to structures found on what?
- Acute phase proteins include what?
- What two things do they do?
A
- liver cells in response to inflammatory signals such as LPS, TNF-a, and IL-6
- bacteria
- serum amyloid A (SAA) in mine, C-reactive protein (CRP), fibrinogen, and mannan-binding lectin (MBL)
- opsonize bacteria and activate complement by binding C1q (MBL also opsonizes and activates complement)
19
Q
(Danger Signals)
- Cells communicate when undergoing cell damage (via K) - the main family that signals cell damage are what?
- Tese start signal chain that activates what? do what two things?
- What cytokines does it activate?
A
- NALPS (are activated only in stressed cells)
- caspases (proteases); regulate apoptosis and process other proteins
- IL-1 and IL-18 (probably just need to know that cyotkines are released)
20
Q
(Does the innate immune system distinguish between various pathogens?)
- The recent discovery of what suggests that the innate immune system can recognize evolutionarily conserved structures and patterns on different types of pathogens?
- This leads to what?
- Can it activate both extracellular and intracellur pathogens?
A
- Toll-like receptors
- Different flavors of cytokines production, thereby influencing inflammation and subsequent adaptive immunity
- yes
21
Q
(Pathogen-associated molecular patterns)
- TLR-2 recognizes what?
- TLR-4?
- TLR-3
- TLR-9?
A
- gram-positive
- gram-negative (LPS)
- double stranded RNA (viruses)
- DNA with unmethylated CpG DNA (bacteria and herpesviruses)
22
Q
- Is discrimination in TLR’s (pamps receptors) perfect? how?
- What kind of discrimination do they exhibit?
A
- yes; selected over evolutionary time
- self-non-self-discrimination
23
Q
- Which toll-like receptors are dimers?
- What happens when they see PAMPS?
- Are TLR in endosomes? why?
A
- TLR-2
- signal transduction to nucleus (which then does signal transduction?)
- yes; so that when the endosome fuses with the phagosome it recognizes the foreign proteins and can therefore eleicit and appropriate response
24
Q
- What are TLR receptor engagements important for (two things)?
- PM or endosome?
TLR 2, 3, 4, and 9
A
- activates the phagolysosome and turns on gene expression in phagocytes
- PM, ENDO, PM, ENDO
25
Q
- What does TLR use to signal to the cell? What does this mostly lead to?
- What is the most important transcirption factor concerning which genes are turned on?
- Which types of genes are turned on?
- What type will TLR-3 turn on? TLR-7?
A
- cascades of kinase reactions; activation of several transcription factors (gene expression)
- NF-kb
- cytokine
- IFN-a, IFN-b and IFN-a (to fight viruses)
26
Q
- Mice given a bunch of LPS -
what happened to control?
what happened when TLR4 knocked out?
TLR2?
A
died (inflammation)
survived (no inflammation - this is the one that recognizes LPS)
died
27
Q
- Are TLRs constantly recruited to phagosomes? to do what? Does this occur constitutively fro most TLRs?
- Will there be increased expression of TLR when there is mastitis for example?
A
- yes; sample their contents; yes
- yes
28
Q
- Are TLRs the other link between innate and adaptive immunity?
- why?
- Can multiple TRS’s respond to the same pathogen?
A
- yes
- they make cytokines which can lead to TH2 activation
- yes, different combos activate different “flavors”
29
Q
- Do fungi have unique sturcutres that are bound by TLRs?
- aren’t they eukaryotic though?
A
- yes
- yes… but they have structures that aren’t found in higher eukaryotes
30
Q
ACTIVATION OF DIFFERENT PATHWAYS LEADS TO DIFFERENT RESPONSES BY PHAGOCYTES
A
31
Q
(NODS)
- What does nod stand for?
- What do they detect and where?
- Do they work with TLRS to give immediate recognition of PAMPS?
- what do they activate (like TLRs)?
A
- nucleotide binding oligomerization domain proteins (NOD)
- PAMPS within the cytoplasm
- yes
- NF-kb
