week 18 p2 Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

Why are some bacteria good

A

Commensal bacteria colonise- Commensal bacteria act on the host’s immune system to induce promote responses
that prevent colonization and invasion by pathogens.

Microenvironmental can contribute to a healthy epithelia interface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does bad bacteria form

A

• Disrupting the commensal bacterial flora creates an opportunity for pathogenic bacteria

• Pathogenic  exploits epithelial dysfunction  and weaken innate immunity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Example of bacteria linked to diseases

A

• E.coli = urinary infection

S.aurus= epithelial infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why can bacterial pathogen can overcome epithelial barrier

A

Through IgE portray which changes the surface of the cell

Causing it to be more resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the bacterial cell wall

A

• Gram positive
• Gran negative
• Mycobacteria
Spinchodate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the mechanism of immunopathogenesis

A

• 1.single toxin or epithelial attachment
• 2.Invassion
3.local invasions and toxify

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the protective mechanism without lymphocytes

A
  • Increased vascular permeability
    • Chemotaxis
    • Activation of phagocytosis

Activation of endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the function of antibody of antibody and complect functions

A
  • Attachment: antibodies to fimbriae, lipoteichoic acids, and some capsules
    • prevents mediated damage to GN and AB block transport mechanism and receptors
    • Avoidance of phagocytosis: AB neutralises immunodepletes and AB to M proteins and promote opsonisation
    • Damage the host: promote toxic and invasive: AB neutralize spreading and AB to promote neutralisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does bacteria escape from antibody(Neisseria gonorrhoeae)

A

• AB blocks killing function of damaging antibodies

Supress the production of antibodies that can damage the organism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does bacterial escape occurs from complement attack

A

• Complement (no activation)
• Lyric complex
• Degraded by enzyme
Secreted decoy proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is CD4+ cell mediated immune mechanism

A
  • T cell binds to CD4 in two ways
    • First way is through th1 and causing isotype switching

Second , th1 causes macrophage activation promoting intracellular killing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is CD4+ cell mediated immune mechanism

A
  • T cell binds to CD4 in two ways
    • First way is through th1 and causing isotype switching
    • Second , th1 causes macrophage activation promoting intracellular killing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is CD8+ T cell activate

A

• CD8 is activated through uptake of apoptotic blebs, infection induced apoptosis and phagosome maturation

CTL: is activated through macrophage activation, macrophage activation

First CD8 happens and then CTL is activated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the structure of LPS

A
• Lipopolysaccharide  ands  porin
	• Outer membrane
	• Periplasm
	• Plasma membrane
Membrane protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is sepsis syndrome to invasive syndrome

A
  • LPS recognitions is done by innate immune system
    • Sepsis results happen from activation of LPS responsive cells in the blood
    • Inflammation leads to endothelial cell activation and organ dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the pyogenic exotoxins

A
  • Bacteria are superantigen

* And activate T cells expressing unique V beta TCRs

17
Q

What is the diverse modes of superantigen

A
  • All superantigen bind to both MHC class II and TCR but in different ways
    • 1.TCR bound to peptide MHC in the abscess of superantigen
    • 2.superantigen acting as a changing TCR to peptide MHC complex
    • 3.act as a bridge
    • 4.acting as a shift by displacing TCR from peptide, with TCR bound to MHC beta chain
18
Q

Why is Listeria monocytes is the most well studies pathogen

A

Bacteria’s replication in the liver in and spleen occur in 5 days

After 14 days mice are immune

19
Q

What re the ways to control TB

A

HIV infection, malnutrition and immune definicy

And/or compromised or warn immunity

20
Q

What is the mechanism to develop vaccine for TB

A

Effector CD4 and CD8 T cells are stimulated, which mature into Tm cells

Both effector and Tm cells participate in efficacious

protection and/or T cell exhaustion.

Treg cells interfere with protective immunity via unknown

mechanisms that perhaps involve IL-10 and/or TGF-β.

Better understanding of antigen processing

in tuberculosis, homing of T cells to the infected lung, and the role of Treg and Tm cells in sustaining

or curtailing protective immunity, respectively, will facilitate future vaccine design against
tuberculosis.

21
Q

How can parasites escape mechanism

A

Resistance to complement

Intracellular parasites avoid being killed by
oxygen metabolites and lysosomal enzymes

Parasites can also hide from immune attack
22
Q

How does Malaria infected RBCs expressing PfEMP-1

A
  • Plasmodium falciparum erythrocyte membrane protein 1
    • Uses syncytiotrophblast causes placental a malaria
    • Endothelial by chondroitin sulphate A
    • Uses endothelial cell through CD36 causes cerebral m malaria
    • Ruses resetting of blood cells by CR1 to cause serve malaria
    • Uses pathosis by DC by CD36 fr modulated immunity