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IMIN 200 > Bacterial Structure > Flashcards

Bacterial Structure Flashcards

1
Q

What does peptidoglycan consist of?

A

A repeating disaccharide of NAG and NAM

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2
Q

What is NAG?

A

A monosaccharide derivative of glucose
An amide between glucosamine and acetic acid

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3
Q

What is NAM?

A

A monosaccharide derivative of NAM (ether of lactic acid and NAM)

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4
Q

What are NAG and NAM cross-linked with?

A

Oligopeptides at the lactic acid residue of NAM

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5
Q

How do cross-linking peptides differ between Gram-negative and Gram-positive bacteria?

A

MAIN DIFFERENCE: Gram-positive links tetrapeptides with a pentaglycine crosslink and Gram-negative tetrapeptides link directly to other tetrapeptides

Gram-positive = 9-13 aa long
Gram-negative = 8 aa long

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6
Q

What is unique about D isomers and why do bacteria use them in their PG?

A

They are uncommon in nature and are used by bacteria to avoid protease digestion

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7
Q

Why does gonorrhea have some resistance to antibiotics?

A

Because they have highly cross-linked PG layers

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8
Q

What is the LPS a major component of and what does it do?

A

The outer membrane of Gram-negative bacteria
It is important for the structural integrity of the bacteria and protects the membrane from chemical attack

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9
Q

What does the LPS do to the charge of the cell membrane and why does it do that?

A

It increases the negative charge
Helps stabilize the overall membrane structure

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10
Q

What does LPS associate with and why?

A

Divalent cations (Mg++) to neutralize charge repulsion

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11
Q

What are the 3 molecular domains of LPS?

A

Lipid A
The core
The O-antigen

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12
Q

What is the structure of Lipid A and what does it allow?

A

Phosphorylated glucosamine disaccharide with associated fatty acids
The fatty acids allow bilayer formation and it is antigenic

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13
Q

What is the core made up of and what does it attach to?

A

The core is made up of mostly sugars (can contain amino acids) and it attaches directly to lipid A
Diverse

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14
Q

What is the O-antigen attached to and what does it determine?

A

It is attached to the core oligosaccharide and due to it being highly diverse, it often determines strain type

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15
Q

What are the implications of O-antigen being presented on the cell surface?

A

It is antigenic and therefore the bacteria are always changing it

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16
Q

What are long O-antigens associated with?

A

Virulence

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17
Q

What does smooth O-antigens make?

A

A gel and it appears smooth

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18
Q

What are rough O-antigens associated with?

A

Non-pathogens

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19
Q

What part of lipid A anchors the LPS into the bacterial membrane? Where is the rest of the LPS?

A

The hydrophobic fatty acid chains anchor LPS into the cell membrane
The rest of the LPS projects from the cell surface

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20
Q

What is the lipid A domain responsible for?

A

The toxicity of Gram-negative bacteria

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21
Q

When bacterial cells are lysed, what does the release of lipid A into circulation cause?

A

Fever
Diarrhea
Endotoxic shock (sepsis)

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22
Q

What types of bacterial PAMPs can PRRs detect?

A

PG
Lipid A
Teichoic acid (links layers of Gram-positive PG)
Capsules

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23
Q

What do TLRs do and where are they expressed?

A

They recognize PAMPs
They are expressed in all cells of the innate immune system and can be found on the cell surface or inside endosomes

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24
Q

Where are endosomes located?

A

In between the plasma membrane and Golgi

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25
Q

What does TLR6 recognize?

A

PG in Gram-positive
Lipoteichoic acid in Gram-positive
Lipoproteins of Gram-negative

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26
Q

What does TLR4 recognize?

A

LPS in Gram-negative + LPS with co-receptor MD2

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27
Q

What does TLR3 recognize and where is it found?

A

Detects intracellular and phagocytized pathogens
Found in endosomes

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28
Q

What are NODs and what do they detect?

A

Nucleotide-binding domain, Leucine-rich repeat-containing receptors
They detect intracellular PAMPs

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29
Q

Why is there often an overlap between TLRs and NODs?

A

They can detect the same pathogen

30
Q

Where is H. pylori found, what is unique about it, and what does it cause?

A

It infects the gut lining
It is acid tolerant
It can cause acute gastritis and chronic inflammation

31
Q

How does H. pylori survive in the gut?

A

It secretes a base to neutralize the acid and liquifies mucous
Its flagellar bundle and spirochaete shape allows it to penetrate the mucous layer

32
Q

Which NODs recognize H. pylori?

A

NOD-1 and NOD-2

33
Q

What does NOD-2 recognize?

A

PG from both Gram-positive and Gram-negative

34
Q

What does NOD-1 recognize?

A

A modified dipeptide commonly found in Gram-negative (mDAP)

35
Q

What is the cause of listeriosis and who is most susceptible?

A

Eating contaminated food
Pregnant women, infants, old people, and the immunocompromised

36
Q

What foods should pregnant women avoid to not get listeria?

A

Soft cheese and raw milk

37
Q

What temperature can Listeria survive at and what type of pathogen is it?

A

0°C-37°C
Opportunistic

38
Q

How does listeria attach to a host and what can it survive?

A

Attaches to the host via D-galactose (sugar on surface)
Can survive phagocytes and manipulate host cytoskeleton

39
Q

What is unique about the peptidoglycan of listeria?

A

50% of NAG is replaced with glucosamine by the PgdA enzyme which is a virulence factor so that the host cannot recognize it

40
Q

What does deacetylation of listeria PG allow the evasion of?

A

NOD-1

41
Q

What are 3 ways that listeria evades NLRs?

A

Deacetylation of NAG by PgdA

Glycosylation of teichoic acid = enhances virulence

Lysine is added to cell walls to increase the positive charge

42
Q

What is the purpose of adapting to enhance positive charges?

A

Normally bacteria are negatively charged
By enhancing positive charges, it allows the avoidance of CAMPs

43
Q

What is Kdo2-lipid A?

A

The most common sugar in core oligosaccharides

44
Q

What are the enzymes to modify Kdo?

A

periplasmic

45
Q

What are modifications of Kdo2-lipid A essential to avoid?

A

AMP
TLR4

46
Q

How does Y. pestis modify Kdo2-lipid A?

A

Glycosylation to PO4-

47
Q

How does H. Pylori modify Kdo2-lipid A?

A

Only has 4 acyl chains
Masking of a negative charge on PO4-

48
Q

How does P. aeruginosa modify Kdo2-lipid A?

A

Glycosylation of PO4- to shield negative charges from AMP

49
Q

How does V. cholerae modify Kdo2-lipid A?

A

Addition of PO4
Addition of acyl chains

50
Q

What are the 3 lipid A evasion strategies that H. pylori uses?

A
  1. dephosphorylation = lose PO4- to remove negative charge which adds resistant to CAMPs
  2. Removal of the negative charge by adding an amine
  3. Fewer HC tails as hexacylated lipid A is very antigenic
51
Q

What does the temperature change from fleas to humans cause in Y. pestis?

A

Causes a change in gene expression which turns on virulent genes

52
Q

What does Y. pestis look like in fleas?

A

Has a hexacylated lipid A but is not antigenic to the flea

53
Q

What does Y. pestis do in humans?

A

An enzyme is activated with the temperature shift that cleaves 2 acyl chains which makes it TLR4 evasive

54
Q

At which temperatures is Y. pestis virulent and non-virulent?

A

Virulent = 37°C
Non-virulent = 25°C

55
Q

What evasion strategies on lipid A does V. cholera use?

A

Addition of a diglycine to lipid A which decreases AMP sensitivity

56
Q

What type of illness is cholera?

A

Water-borne illness that exists in copepod reserviors

57
Q

What are AMPs and what can they kill?

A

Nonspecific components of the immune response, like to punch holes
Can kill Gram-negative and Gram-positive bacteria `

58
Q

What are the subgroups of AMPs?

A

Alpha-helices
Beta-sheets
Mixed alpha/beta
Cyclic
Extended

59
Q

Where might alpha-helix AMPs be found?

A

In the lysosome of macrophages

60
Q

What is Kalata B2?

A

Found in plants and has been shown to have insecticidal, anti-tumor, and antimicrobial functions
CAMPs that detect negative surface charges

61
Q

How do AMPs kill bacteria?

A

By making pores

62
Q

What are defensins?

A

Short peptides with an positive charge and a lot of hydrophobic residues that allows it to adopt amphipathic structures in membrane-mimicking enviornments

63
Q

Where is a high concentration of defensins found and what might they aid in?

A

Breast milk
Colonization of the gut

64
Q

How do Gram-positive bacteria resist defensins?

A

Modification to cell wall teichoic acid to decrease negative charge
Add positively charged membrane proteins to offset negative charge

65
Q

How do Gram-negative bacteria resist defensins?

A

Modification to LPS = more acyl chains = harder for AMP to penetrate
Secrete negatively charged proteins which act as decoys for CAMPS

66
Q

What is the last line of resistance to defensins?

A

Efflux pumps = pump out the AMPs
Proteases = destroy AMP

67
Q

What is molecular mimicry?

A

Structural, functional, or immunological similarities shared between macromolecules found on pathogens and in host tissues

68
Q

What can molecular mimicry induce?

A

Autoimmune responses which attack and destroy body tissues or organs

69
Q

What is Guillain-Barre’s syndrome?

A

An infection with Campylobacter that causes autoimmune disease
temporary

70
Q

How does C. jejuni showcase molecular mimicry?

A

The LPS of C. jejuni has evolved molecular similarity to GH1 gangliosides in human neurons

IMIN 200 (23 decks)

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