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biology - microbiology > Structure - LPS > Flashcards

Structure - LPS Flashcards

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AP® Biology flashcards
1
Q

Lipopolysaccharides

A

A constituent of gram-negative bacteria membrane, providing integrity.

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2
Q

What are the three poritons of LPS?

A

Lipid A
Core Oligosaccharide
O Antigen

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3
Q

What is the function of Lipid A?

A

Anchors LPS to the membrane
Acts as an Endotoxin

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4
Q

What is the structure of Lipid A?

A

Two glucosamine residues linked by beta 1-6 glycosidic bonds with variable acyl chains.

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5
Q

What is an example of Lipid A alteration?

A

Phosphorylation of glucosamine alters charge/solubility.

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6
Q

How does Lipid A act as an endotoxin?

A

TLR4 pathway being a macrophage/DC expressed receptor

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7
Q

What does Lipid A interaction with TLR4 result in?

A

Signalling cascades and TF activation like NF-kb resulting in cytokine stimulation of inflammation.

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8
Q

What is an example of acyl chain variability?

A

Long chain C18 or C20 fa increases hydrophobicity and decreases solubility thus more prone to aggregation.

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9
Q

Why do longer Acyl chains have lower affinity for TLR?

A

Less stability between Lipid A and TLR4

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10
Q

What is the function of the Core Oligosaccharide?

A

Structural integrity LPS and a recognition site.

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11
Q

What is the structure of the Core Oligosaccharide?

A

Anchors Lipid A by 3-deoxy-D-manno-octulosonic acid with three structural regions( inner and outer core and terminal reigon)

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12
Q

Structure of CO inner core?

A

Heptose residue, 2-3 Kdo residues and N-Acetylcglucosamine

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13
Q

Structure of CO outer core

A

Terminated by galactose, glucose or NAG, bound by the terminal region

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14
Q

What is the function of the O-antigen Polysaccharide?An

A

Antigenic component
Host immune defense
Virulence Factor

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15
Q

What is the structure of the O Antigen?

A

Several dozen sugar residues

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16
Q

How does the O-antigen assist host infilitration?

A

Prevent recognition and binding of LPS like TLR

17
Q

Virulence Factor

A

Bacteria associated molecules required for bacteria to cause disease whilst infection eukaryotic host.

18
Q

What makes LPS amphiphatic?

A

Hydrophobic Lipid A and hydrophilic O-antigen and CO

19
Q

What determines LPS effects on membrane packing?

A

Length and saturation of the acyl chains.

20
Q

What happens when Lipid A binds TLR4?

A

Dimerisation bringing it into contact with cytoplasmic domains of two TLR, inducing downstream signalling pathways.

21
Q

Anaphylatic Shock

A

This is an acute allergic reaction with airway and circulatory problems.

22
Q

What is the most diverse component of LPS?

A

O Antigen.

23
Q

What is the primary function of the LPS?

A

Establishes a permeabilit barrier, protecting cell from entry of toxic molecules.

24
Q

Pathogenicity

A

The property of causing disease.

25
Q

What makes LPS a strong barrier?

A

Its amphiphatic nature, and its ability to pack densely together.

26
Q

What type of FA are Lipd A acyl portions?

A

Saturated FA.

27
Q

How is condensing of LPS complicated?

A

Repulsion of the negatively charged phosphate groups.

28
Q

How do LPS counter the negative repulsion of the phosphate groups?

A

Divalent cations like Mg which intercalate between LPS, forming interactions that enhance packing and promote barrier function.

29
Q

What makes LPS an endotoxin?

A

Its prevalence on surface of bacteria, thus host immune systems respond dramatically to it.

30
Q

What is an example of Lipid A structural diversity in relation to stimulation of TLR4?

A

Hexacylated, biphosphorylated Lipid A produced by E.Coli and Salmonella are highly immunogenic, whilst others are less so.

31
Q

Immunogenic

A

Substances that can produce an immune response.

32
Q

What are the ways GNB increase Lipid A diversity?

A

Covalent modifciations leading to changes in FA length, number of phosphates and carbohydrate moieties.

33
Q

How might bacteria evade host immune response, with respect to Lipid A?

A

Production of less immunogenic Lipid A.

34
Q

How does Yersinia Pestis modulate Lipid A response to TLR4?

A

Modulates acylation of LA at mammalian body temp, producing less immunogenic Lipid A.

35
Q

How does temperature regulate Yersinia Pestis acylation?

A

At 37 degrees, Lipid A is tetraacylated, with weaker stimulation, but at lower temperatures, its hexacylated with increased stimulation.

36
Q

What is the PagL gene?

A

A modifcation gene encoding Lipid A 3-0-deacylase in the outer mmebrane, modulation lipid A signalling.

37
Q

Kdo moieties

A

3-Deoxy-D-Manno-2-octulosonic acid, a key cell wall component.

biology - microbiology (19 decks)

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