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