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Pathogenic Microbiology > Lecture 3 > Flashcards

Lecture 3 Flashcards

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Biology 101 flashcards
1
Q

What are integrins?

A

dimeric integral proteins on the surface of the host cell. Hetero dimers; one alpha and beta chain.
inactive state on the surface of the host cell; You can have binding of the integrin on the surface of the cells that causes a change of beta integrin which can initiate change on the inside of the cell rendering it active

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2
Q

What are the components of the ECM?

A

collagen, fibronectin, laminin, proteoglycan

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3
Q

How is collagen formed?

A

3 left handed helices wound up next to each other and create a fibril which associate with one another to produce collagen fibers

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4
Q

How are Proteoglycans formed?

A

Sugars bound to protein moieties.

  1. You have a central molecule in the middle made up of hyaluronic acid sugar molecules that attach to each other forming a middle piece,
  2. and then proteins are attached to the central PolyGram hyaluronic acid called core proteins.
  3. Sugars are attached to the core proteins, and can be either chondroitin or keratin sulfate
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5
Q

What is laminin?

A

Laminin is a based component of protein lamina that provides structural features important for the ECM, and is also involved in interactions and signaling aspects as well.
made up of 3 chains of proteins come together to form a cross-shape with long arms chains to interact with the surface of the host, or interact through collagen

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6
Q

What is Granuloma?

A

aggregates of macrophages and t-cells that are fuse together by tnf-alpha
Can be beneficial for the bacteria by providing a protective environment for bacteria in which they are immune to other cells

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7
Q

Pathogen-Induced Upregulation of Adhesion Molecules

A

A. You can have a receptor on the host cell that bacteria binds to which gives signal to the cell for bacteria to make more of the receptor on the host cell for more bacteria to attach on and cause infection
B. bacteria goes in and causes up-regulation of specific receptors on the surface of the cell that can signal t-cells to active them

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8
Q

What is Non-specific Adhesion?

A

Weakly adhering bacteria - easily removed by physical shear forces or washing

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9
Q

What are M protiens?

A

Streptococcus pyogenes (M proteins) are virulence factors that facilitate attachment to various host cells

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10
Q

What are the types of adhesions?

A

Pili / fimbriae
Non-pilus surface proteins
Polysaccharides

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11
Q

What is the structure of fimbriae?

A 
Structural subunit of proteins that come together to facilitate attachment
At the tip, you have adhering molecules that interacts with the surface of the host 
Protruding thing (from outer membrane of gram negative, or cell wall from gram positive bacteria) is to provide safe distance for the bacteria to occur on the surface of the host cell
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12
Q

What are the consequences of adhesion?

A

A. Organism colonizes surface – e.g. normal flora
B. Pathogen colonizes surface and secretes toxins
C. Colonize surface and form a biofilm

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13
Q

What is biofilm?

A

a community of microorganisms, associated with a surface, and encased in an extracellular polymeric matrix.

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14
Q

What is the difference between single and complex biofilm?

A

Simple Biofilms: comprises a single species
Complex Biofilms: Comprise multiple species
Some species produce polysaccharides, ‘trapping’ others

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15
Q

What are the steps in biofilm formation?

A

1) Free-floating bacteria become attached to a surface.
2) They associate and begin to produce slimy extracellular polymeric substances (EPS) and to colonize the surface.
3) EPS production allows the emerging biofilm to grow and develop into a complex, three-dimensional structure that is influenced by a variety of environmental factors.
5) Biofilms can also propagate through detachment of small or large clumps of cells, or by a type of
“seeding dispersal” that releases individual cells. Either type of detachment allows bacteria to attach to a surface or to a biofilm downstream of the original community.

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16
Q

What is Quorum sensing?

A

the signaling for biofilm formation to control gene expression for a variety of things

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17
Q

What processes does quorum sensing control?

A

biofilm formation
virulence gene expression
competence

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18
Q

What is (Acyl hormone lactones) AHL quorum sensing?

A

Mediate quorum sensing in Gram-negative bacteria through exclusive intracellular communication.
These are of several types depending on their length of acyl side chain.
Able to diffuse through membrane.
synthesized by an autoinducer synthase LuxI and recognized by an autoinducer receptor/DNA binding transcriptional activator protein Lux

19
Q

What are autoinducer peptides?

A

These are small peptides, regulate gene expression in Gram-positive bacteria such as Bacillus subtilis, and Staphylococcus aureuas etc.
Recognized by membrane bound histidine kinase as receptor.
Regulates competence and sporulating gene expressions.

20
Q

What is A1-2?

A

Involve in interspecies communication among bacteria.

Present in both Gram (+) and Gram (-) bacteria.

21
Q

What is the process of A1-2?

A
  1. Induces expression of stationary phase genes

2. Inhibition of initiation of DNA replication

22
Q

Why is it difficult for bacteria to enter cell junctions?

A

Epithelial cells are bipolar and very tightly packed next to each other creating cell junction
Site of bacterial attachment is on the basal side which is facing the lumen and not the outside part of the cells. cell junctions makes it hard for the bacteria to get through, and if it does it doesn’t have access to the receptor that it needs to bind

23
Q

What is the intestinal epithelial model system?

A

Mechanical damage or local inflammation as a result of infection in the epithelial cells, gives signal to granulocytes (EX: neutrophils) to go through the epithelial cells, and they essentially open up layer between cell junctions, and bacteria can squeeze in and interact with receptors on the lumen side to get into and come out through the lumen

24
Q

What are DRms?

A

DRM’S – detergent resistant membranes
Lipid Rafts are typically resistance to non-ionic detergents (DRM’s). Inner leaflet can have interactions with kinase and g-protein receptors

25
Q

What is are the 2 types of single raft models?

A
  1. Receptors associated at steady state with lipid rafts could be activated through ligand binding
  2. Individual receptors with weak raft affinity could oligomerize on ligand binding, and this would lead to an increased residency time in rafts.
26
Q

What is the clustered rafts model?

A

Activated receptors could recruit linking proteins such as cytoskeletal, elements and scaffolds that bind to proteins in other rafts, and this would result in raft coalescence.

27
Q

What are the 2 ways that clustering of lipids rafts happen?

A
  1. Clustering of lipid raft can occur extracellularly, within the membrane, and in the cytosol.
  2. It can also occur through GPI anchored proteins, either as a primary or co-stimulatory response
28
Q

What is TCR?

A

The T-cell receptor or TCR is a heterodimer consisting of an alpha and beta chain.
the Alpha and beta heterodimer associate with CD3 complex and zeta (ζ) homodimer which contain cytoplasmic ITAM motifs (immune receptor tyrosine-based activation motifs).

29
Q

Explain the signaling cascade of TCR/CD3

A
  1. Lipid raft when the t-cell binds the antigen lead to a confirmation change that
  2. causes phosphorylation of the domains of some of the ITAM proteins on the inside of the cell by Src tyrosine kinase which are (activated/phosphorylated through Csk binding to CBP limpid raft protein).
  3. Phosphorylated ITAMs act as a membrane docking site for ZAP-70
  4. ZAP-70 activate other proteins such as LAT (a raft-associated adaptor) through cross linking
  5. LAT can recruit other proteins into the raft and further amplify the signal
30
Q

Why are lipid rafts important?

A

for bacteria invasion and gene expression

31
Q

What are the 5 types of invagination on the surface of the host cell?

A
  1. Invagination dependent on protein called clathrin to form a clathrin coated pits
    - Can intake small molecules
  2. Clathrin–dependent endocytosis: Multiple invaginations are creating cave like structures
  3. Macropinocytosis: big invaginations that takes up cellular fluid
  4. Phagocytosis: the engulfing of microorganisms or other cells and foreign particles by phagocytes
32
Q

What is the role of sorting endosomes?

A

they make the decisions whether to:

  1. destroy or recycled in the cell which can be transferred into an endo or lysosomes,
  2. or into an acid recycling compartment where it can be transferred into some other part of the cell,
  3. or re-routing into some other compartment
  4. Some vesicles pinch off the structure and transport it into the surface of the cell
33
Q

What are phagocytes?

A

usually refers to the white blood cells that engulf and absorb waste material, harmful microorganisms, or other foreign bodies in the bloodstream and tissues
EX: macrophages or monocytes

34
Q

What is the difference between professional and non-professional phagocytes?

A

The main difference between professional and non-professional phagocytes is that professional phagocytes have receptors on their surfaces for detecting harmful objects, such as bacteria, that are not normally found in the body
In contrast to professional phagocytes, non-professional phagocytes principle function is not phagocytosis.

35
Q

What are the types of non-professional phagocytes?

A

lymphocytes, fibroblast, erythrocytes

36
Q

What are the types of professional phagocytes?

A

neutrophils, monocytes, macrophages, sinusoidal, lining cells, langerhan, and mast cells

37
Q

Describe the stages of phagocytosis.

A
  1. You have a microbe hanging out
  2. Complement system of immune system comes and codes bacteria with C3b to recognize and bind to the bacteria,
  3. and another molecule called C5a is produces which is a chemoattractant for macrophages. The cells can recognize and bind these receptors,
  4. and The cell invaginates into the cell via phagosomes which are fused with lysosomes to form phagolysosomes that degrade and kills the bacteria into little pieces that are exited outside of the cell
38
Q

What is required for phagocytosis?

A

Phagocytosis requires actin rearrangements and pseudopod extensions controlled by Rho GTPases

39
Q

What is required for phagosome formation?

A

Phagosome formation often requires high amounts of membrane, which is in excess of plasma membrane capacity (mobilization of membranes of different organelles)

40
Q

What is the difference between induced and active invasion?

A

In induced – both the bacteria and host cells are active participants in the process
Active invasion – host cell is passive and is not doing anything to take the bacteria in, but the bacteria has the activated part and get itself inside of the cell

41
Q

What are the ways that bacteria have evolved to live in various intraceullular niches of host cells?

A

a. Some bacteria are able to live in a low pH acid/hydrolytic environment of the lysosomes
b. Other bacteria evolved ways once inside the vesicle to keep the vesicle at a neutral pH, and therefore no fusion with lysosomes occurs, and therefore they survive
c. Some have evolved ways to lyse the vesicles and go into the cytosol before the cell rids of the vesicle

42
Q

What are M-cells?

A

absorptive cells used for taking parts of the lumen
M-cells have receptors on the surface that some bacteria can attach to, and internalize inside macrophages to be released, or the macrophages can’t destroy them

43
Q

What are GPIs?

A

proteins attached to lipids which can migrate and reside in the lipid raft

44
Q

What are lipid anchored proteins?

A

Proteins linked to cholesterol

Pathogenic Microbiology (12 decks)

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