Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Microbiology > Host Defences > Flashcards

Host Defences Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

“Many factors influence the outcome of an interaction between host and pathogen.

There is a balance between the two, and this is affected by…”

A

HOST- Immune status- Prior exposure, old/young/immunocompromised, vaccination history.

Species- bacteria may have limited host range.

Breed.

Commensal flora- Normal flora present in the GI tract.

PATHOGEN- Balance is affected by virulence, infectivity, host range (broad/narrow), infectious dose, route of infection, antibiotic resistance.

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

HOST DEFENCES

A

NON SPECIFIC (INNATE)

SPECIFIC (ADAPTIVE)

These two lines of defence must interact to work effectively.

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

NON SPECIFIC (INNATE) IMMUNITY

A

Barrier to infection- Skin, mucous membranes.

Innate immune system.

Soluble factors- COMPLEMENT, ACUTE PHASE PROTEINS, IRON BINDING PROTEINS, ANTIMICROBIAL PEPTIDES etc.

PHAGOCYTES are the cells involved.

Fast to respond but low specificity and no memory.

Non specific defences can deal with the majority of microbes and slow pathogens down even if infection does occur.

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

SPECIFIC (ADAPTIVE) IMMUNITY

A

Comprised of components of the adaptive immune system- T cells and B cells.

Soluble factor- ANTIBODY.

Slower to respond than the innate system (lag period on first exposure, not seen on second/repeated exposure), but shows memory and specificity.

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

PHAGOCYTES

A

Part of innate defences.

Very important in defence against bacteria and fungi.

NEUTROPHILS (PMNs) and MACROPHAGES.

As soon as the phagocytic cell makes contact with the bacteria and begins to engulf it, there is a HUGE INCREASE in OXYGEN CONSUMPTION by the phagocyte. This is called OXIDATIVE BURST.

Oxidative burst generates ROIs (Reactive Oxygen Intermediates) which are used to kill bacteria.

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

NEUTROPHILS

A

Only found in inflamed tissue

Not found in healthy tissue

Single mature form

Rapidly form pus

Short lived

Always die after undertaking phagocytosis

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

MACROPHAGES

A

Found in healthy tissues (eg. Kupffer cells)

Variety of mature forms

Slowly form granuloma instead of pus; this requires T cell help.

Long lived (can be exploited by pathogenesis

Can survive after being phagocytosed

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

PHAGOLYSOSOME FUSION

A

The bacteria becomes bound in a phagosome- a membrane bound organelle in the host cells- once it is in the host cell.

This then matures, moving protons (H+) in to the vesicle. These protons are important for action of antimicrobial compounds.

The phagosyme fuses with the enzyme-containing lysosome, forming a phagolysosome.

Once phagolysosome fusion has occured, the bateria will normally be destroyed by oxidative burst and lysosome products.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

OXYGEN DEPENDENT KILLING MECHANISMS

A

Can be peroxidase independent or peroxidase dependent.

Involves oxidative burst.

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

PEROXIDE INDEPENDENT

OXYGEN DEPENDENT KILLING MECHANISMS

A

Oxygen has electrons added by NADPH.

This forms SUPEROXIDE within the phagocyte, which is ANTIBACTERIAL and can be CONVERTED to other antibacterial compounds:

Hydroxyl radical, .OH

Hydrogen peroxide, H2O2

These act on bacterial cells.

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

PEROXIDE DEPENDENT

OXYGEN DEPENDENT KILLING MECHANISMS

A

Peroxide DEPENDENT killing mechanisms are particularly seen in NEUTROPHILS.

The enzyme MYELOPEROXIDASE combines H2O2 in the cell with halides (eg. Cl-)

This creates highly toxic oxidants, such as HYPOCHLOROUS ACID, that act on bacteria.

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

OXYGEN INDEPENDENT KILLING MECHANISMS

A

These mechanisms do not rely on oxygen for formation of antibacterial substances.

The antibacterial substances are instead delivered to the phagosome by the lysosome and granules.

ANTIMICROBIAL PEPTIDES- Small molecules that damage bacterial membranes, disrupting ion uptake systems.

LYSOZYME- An enzyme from lysosomes that hydrolyses peptidoglycan

PROTEASES- Damage proteins on bacterial surfaces eg. Cathepsin G, elastase enzymes.

Some proteases have been shown to be able to hydrolyse bacterial virulence factors.

LACTOFERRIN- An iron binding protein which chelates ion, making it unavailable to bacteria (iron is very important in bacterial infection)

VITAMIN B12 BINDING PROTEIN- Binds vitamin B12, depriving bacteria of it.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

PHAGOCYTOSIS

A

ATTACHMENT of the phagocyte to the pathogen is a CRITICAL first step in the process of phagocytosis.

Pathogenic bacteria often have a capsule to combat phagocytosis.

However, hosts have developed various means of enhancing uptake of even encapsulated bacteria.

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

OPSONISATION

A

The process by which opsonins- a variety of protein molecules are added to the surface of bacteria to enhance uptake by phagocytes.

Phagocytes have opsonin receptors on their surface to allow binding with opsonins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

INNATE OPSONINS

A

The most important innate opsonins are COMPLEMENT components.

Complement activates the complement cascade.

Also important are ACUTE PHASE PROTEINS (C-reactive Protein, Mannose Binding Lectin)

Also LPS (lipopolysaccharide) binding protein.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

ACQUIRED OPSONINS

A

IMMUNOGLOBULINS, particularly** IgG**

Bind to bacterial surface then is detected by high affinity receptors on the phagocyte

The phagocyte then binds with high affinity due to this opsonisation.

Complement, an innate opsonin, can enhance IgG opsonisation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

COMPLEMENT

A

Comprised of serum proteins, which are enzymes in their inactive form.

As one complement protein is activated, so a cascade of activation forms.

There are three different pathways:

  1. CLASSICAL PATHWAY
  2. LECTIN PATHWAY
  3. ALTERNATIVE PATHWAY
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

COMPLEMENT CASCADE- CLASSIC PATHWAY

A

Distinct stages, beginning with antigen binding to antibody.

Leads to complement activation by C3/C5 CONVERTASE

-> PHAGOCYTE RECRUITMENT/INFLAMMATION (recruitment of inflammatory cells)

C3a, C5a, C4a.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

COMPLEMENT CASCADE- LECTIN PATHWAY

A

MBP (Mannose Binding Protein/Lectin) binds to bacterial surface.

This leads to complement activation by C3/C5 convertase.

-> OPSONISATION (C3b, iC3b, C3dg, C4b)

20
Q

COMPLEMENT CASCADE- ALTERNATIVE PATHWAY

A

Bacterial surfaces activate pathway, allowing conversion of complement to active forms by C3/C5 convertase.

MEMBRANE ATTACK COMPLEX (MAC), a multimeric protein, forms pores in bacterial membranes, to kill them.

C5b, C6, C7, C8, C9

Non pathogenic bacteria have developed ways to avoid the effects of MAC.

21
Q

“Host cells recognise (potential) pathogens due to their characteristic components…”

A

PAMPs- PATHOGEN ASSOCIATED MOLECULAR PATTERNS.

These are also present on non pathogenic molecules.

Often essential components of bacteria; there is little variation between bacteria, which allows recognition by host.

22
Q

LIPID A

A

Acts as a PAMP for GRAM NEGATIVE BACTERIA.

23
Q

PEPTIDOGLYCAN

A

Acts as a PAMP for GRAM POSITIVE BACTERIA, where it is exposed on the surface.

24
Q

BACTERIAL DNA and BACTERIAL LIPOPROTEINS

A

Can also act as PAMPs.

25
Q

PATTERN RECOGNITION RECEPTORS

A

An area of current research.

  1. TOLL LIKE RECEPTORS (TLRs)- Originally recognised in Drosophila. Highly conserved between species. Different TLRs recognise different molecules.

TLR 2- Peptiodoglycans, lipoproteins

TLR 4- LPS, Lipid A

TLR 5- Flagellin

TLR 9- Bacterial DNA.

PRRs/TLRs are present on the SURFACE of bacteria, so act when bacteria is outside of the cell. However, intracellular Pattern Recognition Receptors also exist.

PRRs are HIGHLY SENSITIVE.

26
Q

“Response to PRR activation occurs in a number of ways…”

A
  1. CYTOKINE PRODUCTION BY MACROPHAGES- Affects innate and adaptive immune response.

Causes inflammation, pyrexia, acute phase response, activation of macrophages, attraction of monocytes, neutrophils and T cells.

Adaptive- TH1 and TH2 cells, B cells develop, helper T cell activity is enhanced.

  • “Recognition via PRR allows host cells to respond rapidly and produce messenger molecules to alert other parts of the defence system and allow the above responses”*
    2. INFLAMMATORY RESPONSE- Produced by cytokines and chemokines, useful on a local level to increase blood flow to affected area, delivering phagocytes and other cells.

Capillary wall become leaky to allow cell delivery to tissues.

Serum protein moves in to tissues and acts.

Local coagulation limits spread of bacteria.

27
Q

SHOCK

A

Can be caused by a massive inflammatory response (for example, in response to systemic infection)

  • Massive fluid loss
  • Massive coagulation- DISSEMINATED INTRAVASCULAR COAGULATION- can lead to organ failure and death.
  • It is important for the host to control and feed back on defense responses (via. Pattern Recognition Receptors)
28
Q

INDUCTION OF THE ADAPTIVE IMMUNE RESPONSE

A
  1. Leukocytes encounter bacteria
  2. Antigen processing occurs in specialised cells
  3. Antigen presentation on surface of Antigen Presenting Cells
  4. Antigens are presented with MHC Class I and II.
  5. Cytokine and chemokine secretion is also occuring from cells that have come in to contact with bacteria (macrophages, dendritic cells, NK cells etc)

This all causes ACTIVATION, PROLIFERATION AND DIFFERENTIATION OF LYMPHOCYTES.

29
Q

ANTIGEN PRESENTING CELLS

A

Macrophages

Dendritice cells

B cells

30
Q

MAJOR HISTOCOMPATABILITY COMPLEX CLASS I

A

Presents antigen to CD8 T CELLS- CYTOTOXIC.

Causes LYSIS OF INFECTED CELLS.

31
Q

MHC CLASS II

A

Presents antigens to CD4 T CELLS- HELPER T CELLS.

These provide help for B cells, macrophage activation and cytotoxic T cells.

Most important T cell in microbiology.

32
Q

B CELLS and PLASMA CELLS

A

Produce antibodies.

33
Q

HELPER T CELLS

A

Antigens are presented to helper T cells by MHC class II and CD4.

They can be divided in to TH1 and TH2 cells, which have distinct functions, producing different patterns of cytokines.

TH1 CELLS- ACTIVATION AND ATTRACTION OF MACROPHAGES.

Important for dealing with INTRACELLULAR pathogens

Produce cytokines- TNFa, B, IFN gamma etc.

TH2 CELLS- IMPORTANT FOR PROLIFERATION AND SECRETION OF ANTIBODY BY B CELLS.

Produce interleukins.

34
Q

Th17 CELLS

A

These helper T cells are important for combatting extracellular bacteria and fungal pathogens at mucosal surfaces.

They produces cytokine IL17 and others.

Attract neutrophils to mucosa, causing mucosal cells to produce antimicrobial peptides and antibacterial proteins.

The are known to play a role in protection against intracellular pathogens.

35
Q

IMMUNOLOGICAL SYNAPSE

A

The gap between interaction of T cells and B cells.

36
Q

ANTIBODY MEDIATED IMMUNITY

A

The constant region determines what receptor is recognised on the phagocytic cell etc.

Antobodies combat bacteria in many ways:

OPSONISATION

TOXIN NEUTRALISATION- Via antitoxins

ADHESION AND INVASION INHIBITION- Via antiadhesins and antiinvasins

INHIBITION OF BACTERIAL NUTRIENT UPTAKE- Via antitransporter

37
Q

TRANSPLACENTAL TRANSFER

A

Neonates have no acquired immunity; it must be passed on from the mother.

In PRIMATES, this occurs by TRANSPLACENTAL TRANSFER of IgG via a specific transporter.

In other mammals, LITTLE transplacental transfer occurs. Most transfer of IgG is TRANSMAMMARY, via COLOSTRUM.

38
Q

IgA

A

Important for protection at MUCOSAL SURFACES.

Produced in the gut by PEYER’S PATCHES.

Produced in dimeric form with a dimeric receptor at the base of epithelial cells.

Receptor allows transfer from gut wall to gut lumen.

IgA combines with mucus and undertakes NEUTRALISATION, PREVENTION OF BACTERIAL ADHESION AND AGGLUTINATION.

IgA is POOR at stimulating an inflammatory response, as it has poor complement activation and phagocyte attraction.

This is probably due to the requirement for maintenance of mucosal surfaces- a large inflammatory response would damage mucosa and compromise function.

39
Q

CELL MEDIATED IMMUNITY- ACTIVATION OF MACROPHAGES.

A

Macrophages are important in defence against intracellular pathogens.

They must be ACTIVATED by TH1 cells, which bind to macrophages.

IFNy and TNFa are important in activation.

Signals are delivered by the membrane bound CD40 LIGAND.

40
Q

ACTIVATED MACROPHAGES

A

Cause:

ENHANCED ROI PRODUCTION

PRODUCTION OF REACTIVE NITROGEN INTERMEDIATES VIA NOx

ENHANCED PHAGOLYSOSOME FUSION

ENHANCED ANTIBACTERIAL ACTIVITY

ENHANCED SECRETION OF PROINFLAMMATORY CYTOKINES, which attract monocytes and macrophages to the site of infection.

41
Q

NITROUS OXIDE PATHWAY

A

Activated macrophages produce nitrous oxide to kill pathogens.

Appropriate stimulation (eg. by cytokines) will cause increased induction of NITRIC OXIDE SYNTHETASE enzyme (iNOS)

This converts L-ARGININE and OXYGEN to NITROUS OXIDE.

NOx itself has a low antibacterial activity, but it can be converted to a variety of Reactive Nitrogen Intermediates, which have much enhanced antibacterial properties.

Important in combatting parasites as well as bacteria.

It is not certain at present whether all animals use the NOx pathway.

42
Q

GRANULOMAS

A

Multicellular lesions.

Lymphocytes and macrophages plus other cells fuse to form Multinucleated Giant Cells.

Central area of necrosis.

Central mycobacteria may be dead or dormant, but are walled off from the rest of the tissue.

43
Q

CROSS REGULATIO whicN OF T CELLS

A

TH1 and TH2 cells can reciprocally regulate the activity of each other.

TH1 cells produce IFNy which inhibits TH2 cells.

TH2 cells produce IL4 and IL10, which inhibit TH1 cells.

It is theoretically possible to get a very polarised immune response eg. Entirely TH1 cells (macrophage attraction and activation)

Entirely TH2 cells (antibody production)

44
Q
A
45
Q
A

Microbiology (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions