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Neural Biology 1 > defence against pathogens > Flashcards

defence against pathogens Flashcards

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1
Q

What are the potential pathogens?

A

viruses
bacteria
parasites
fungi

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2
Q

What are the lifestyle of viruses?

A

intracellular infection (also extracellular)

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3
Q

What are the lifestyle of bacteria?

A

largely extracellular (some exceptions)

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4
Q

What are the lifestyle of parasites?

A

extracellular (alo intracellular)

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5
Q

What are the lifestyle of fungi?

A

Extracellular

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6
Q

What are the defence mechanisms against pathogens?

A
  • Anti-bacterial defence mechanism
  • anti-viral defence mechanism
  • defence against parasites
  • ocular defence mechanisms
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7
Q

What is the anti bacterial mechanism/bacterial toxicity-?

A

-Bacteria doesn’t necessarily need to invade tissues to cause an infection - certain types of bacteria that can cause infection just by colonising body surface-these are bacteria that produce toxins- which cause damage as they migrate across the surface tissue of body
-Some bacteria produce damage through the colonisation of the body surface
-Other bacteria cause damage by invasion and subsequent multiplication in the tissues
Most bacterial pathogens fall between these two extremes

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8
Q

What are types of bacterial infection in eye?

A
  1. Bacterial keratitis- bacteria colonised cornea creating lesion in it.
  2. Infiltrate in the periphery of cornea- caused by bacterial toxins that grow on eyelid margins - which instigated an inflammatory reaction in peripheral cornea - inflammatory reaction rather than infection
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9
Q

What are the mechanisms considered for anti-bacterial defence?

A 
Anatomical barriers
Phagocytosis
Antibodies
Complement
T-cells
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10
Q

What are the first way to prevent infection- anatomical barriers?

A

-prevent entry
-Innate defence mechanisms constitute various barriers to prevent
entry
-e.g. skin aided by acidic skin secretions- lowers pH - which limits bacterial growth
-Mucus can trap invading organisms and prevent binding to cells
-External secretions contain anti-bacterial proteins (tears and saliva contain anti-bacterial proteins)

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11
Q

What are some further innate defence mechanisms which prevent entry of infection- anatomical barriers?

A
  • Coughing and sneezing can expel pathogens
  • Healthy humans have many symbiotic organisms (commensals) on internal and external surfaces which compete with pathogens for essential nutrients
  • Acidic secretions in stomach are toxic to some pathogens
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12
Q

What is the phagocytosis defence system ?

A
  • Route of destruction for many bacteria
  • Phagocytosis is enhanced by the coating of bacteria by antibody or complement (or both)-a process termed opsonisation
  • phagocytes have receptors on their surface for the fc component of the antibody molecule and for the C3b component of complement that by the phagocyte can bind specifically to its target
  • once bacteria is taken in by phagocyte it is then destroyed
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13
Q

What is the role of complement ?

A
  • Opsonization- enchanting the process of phagocytosis
  • Chemotaxis and activation of phagocytes- specific complement C5 and C3a are cheomtatis- released at the site of injury / infection-act as chemical signal and establish a chemical gradient along which phagocytes migrate- Anaphylatoxins- molecules which activate phagocytes
  • Formation of the membrane attack complex- able to destroy target cells by breaking down plasma membrane/ membrane of bacterial cell- important in forming lysis.
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14
Q

What is the role of antibody?

A
  • Opsonization
  • Prevention of bacterial binding
  • Neutralization of bacterial toxins
  • IgA( immunoglobulins) important for the defence of mucosal surfaces. Only antibody that can be transported across the epithelium- vast majority of antibody - present in high concentration in tears and saliva
  • IgG and IgM important serum immunoglobulins
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15
Q

What is the process by which IgA cells are able to cross cells?

A
  • cells have receptor on the abluminal surface (basal surface of cell)
  • enables IgA to be taken up and transported off In vesicle and to be secreted across luminal/apical surface- secretory IgA
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16
Q

What are the role of T cells?

A
  • Some bacteria e.g. Mycobacterium tuberculosis ( causes respiratory infection)can survive and divide inside macrophages- immune system must have capacities to identify these macrophages-
  • Specific T-cells recognise bacterial peptides expressed on macrophage surface associated with MHC molecules- cytotoxic T cells have the ability to recognise these abnormal peptidce- cell destruction
  • T-cells produces cytokines which stimulate the macrophage to destroy intracellular pathogens- that are growing inside cells
  • 2 types of t lymphocytes have an anti-bacterial role
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17
Q

What is the viral life cycle?

A
  • structure of virus has- nucleic acid (either DNA or RNA) and protein
  • Nucleic acid surrounded by a protein envelope that encloses it
  • virus can’t reproduce itself- it infects a host/target cells which causes infection
  • cell surface receptor where virus attaches to
  • virus penetrates inside cells- intracellular
  • protein envelope of nucleic acid dissocitaes
  • nucleic acid used as blue print- produce more copies of itself- multiple copies in cytoplasm of cell
  • viruses assembled and released in surrounding tissues then infects other tissues
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18
Q

What are the anti- viral mechanisms?

A 
Anatomical barriers
NK cells- natural killer cells
Antibody
Interferon
T-cells
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19
Q

What are Nk cells?

A

natural killer cells

  • Large granular lymphocytes
  • Similar to cytotoxic T-cells
  • Destroy virally infected cells
  • role in defence of tumour - destroy cancerous cells
  • abiltiy to recognise abnormal pr virally infected cells
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20
Q

What are the roles of antibodies in viruses?

A
  • IgA synthesised locally in the nose and lung protects against viral infection
  • IgG and IgM effective against blood-borne viruses
  • Antibodies neutralise viruses by binding to key viral surface antigens and thereby blocking their entry into their target cells
21
Q

When is antibodies effective?

A

when the virus is in its extracellular phase of its life cycle.
-Once virus gets inside cll it evades the antibody system of defence as antibodies can’t penetrate cells in order to target the virus in the cell however just good in extracellular components of life cycle

22
Q

What are the interferons?

A

-mechanism which recognise virally infected cells
-also a mechanism that limit the replication of virus inside a cell or some antiviral resistance
-The interferons are a group of molecules which limit the spread of viral infections
Interferon alpha and beta

23
Q

What are the3 classes of interferon?

A
  • Interferon alpha and beta and gamma.
  • Interferon alpha and beta produced by leukocytes fibroblasts and virally infected cells
  • Interferon gamma produced by activated T-cells
24
Q

What is the role of the interferon ?

A
  • as a cell becomes infected with a virus it is stimulated to produce alpha and beta interferons which signal neighbouring cells to produce anti-viral proteins (to generate anti-viral resistance)
  • Interferon gamma produced by activated T-cells stimulates the upregulatation- the increase production of MHC class I proteins which present viral peptides to cytotoxic T-cells
  • If there is a lot more MHC 1 proteins on surface of cell - there will be a lot more viral presentation and viral antigens which increases the likelihood of cytotoxic t -cells recognising that cell is infected.
25
Q

What is the role of T- lymphocytes in viruses?

A
  • 2 populations of T- cells
  • Cytotoxic T cells- recognise cell is infected via viruses - through recognition system which occurs through presentation of viral peptide through class 1 MHC molecules- when cytotoxic T cell sees viral antigen can then recognise cell is infected and then triggers apoptosis occurs (programmed cell death) destruction of infected cell
  • T helper cells- also recognise infected cells and produce interferon gamma
26
Q

What is anti parasitic mechanisms ?

A
  • Innate (the alternative complement pathway, phagocytosis)

- T-cells (specifically Th)

27
Q

What is the Immune response to parasitic worms?

A

Immune activity is directed by Th cells (triggering B cells to produce antibodies and also produce cytokines which control …) macrophages which control activation and degranulation of eosinophils

  • Eosinophil granules contain substances that are toxic to parasitic worms- produce chemicals which limit growth of these parasitic worms
  • Mast cell and basophil degranulation also occurs
28
Q

What are the ocular defence mechanisms ?

A
  • The ocular surface is exposed to the external environment and so is potentially vulnerable to pathogenic microorganisms
  • The ocular surface consists of the cornea and conjunctiva
  • A variety of mechanisms have evolved to protect the ocular surface
  • Although the cornea and conjunctiva possess inherent defences, the eyelids and tear film also play important roles
29
Q

What can the ocular defence mechanisms be classified as?

A
  • mechanical,
  • anatomical
  • immunological systems
30
Q

What are the roles of the eye lids?

A
  • Blinking is an effective cleansing mechanism- micro-organism needs to bind to a surface in order to penetrate - so just movement of eyelid prevents attachment
  • Lashes trap microbes preventing access to the globe
  • The lids (and mucosal surface) possesses a normal population of microbes (commensals bacteria ) which limit colonisation/growth by pathogens by competing for nutrients. - so presence of commensals play an important defence role in relation in limiting colonisation by potential pathogens- however could rarely cause ocular disease
31
Q

What is the role of tear film ?

A

The washing action of the tears reduces microbial adhesion and removes desquamated cells- cells of ocular surface constantly replicated and lost form surface- washing action of tears remove the desquamated cells

  • Tear film mucins have anti-microbial properties
  • Tears contain several proteins with antimicrobial properties: lysozyme, lactoferrin, IgA, beta lysin and lipocalin
32
Q

What is a lysozyme ?

A
  • important enzyme - present in tears and saliva
    -Lysozyme is produced by the lacrimal gland and represents approximately 25% of total tear protein
    Lysozyme has the ability to lyse the bacterial cell wall (particularly Gram +ve bacteria)
  • enzyme which cuts the polypeptide chain that is involved in the construction of the bacterial cell wall particular gram +.
33
Q

What is IgA in the eye?

A
  • IgA is the predominant antibody in tears- antibody gets into the tears across the secerteiry cells of the lacrimal gland
  • Ig A is produced by plasma cells within the connective tissue surrounding lacrimal acini
  • then it is IgA is transcytosed across the acinar cells/ basal surface and taken up into vesicle and secreted in tears
  • Ocular surface mucin may concentrate IgA at the mucosal surface
34
Q

What is the role of IgA in ocular ?

A
  • IgA prevents infection by binding to bacteria and viruses and prevents their attachment to the ocular surface
  • also binding of antibody enhances phagocytosis through the process of opnosization
  • Inactivates bacterial toxins
  • Although IgA is the principal tear immunoglobulin levels of IgG and IgM are found during inflammation music higher (probably derived from the blood vessels of the conjunctiva)- which gets into the tears
  • if taken a tear sample- the antibody present in that sample would be universally IgA with low levels of IgG and IgM.
35
Q

What does the experiment of sampling tears from eye opening to eye closing show?

A
  • Closed eye tears show a 50 fold increase in sIgA (secretory IgA) - thought to be mechanism which protects the eye during eye closure.
  • Eye closure is associated with an increased recruitment and activation of PMNs
  • There is evidence of increased complement activation during eye closure (increased C3 conversion)
36
Q

So what does eye closure suggest ?

A

It has been suggested that eye closure results in a shift from the passive defence barrier of the open eye to an active immune,inflammatory phagocytic-mediated process

37
Q

What is the role of the conjunctiva ?

A
  • It is a Mucous membrane - provide protection with their tissues
    -The conjunctiva forms part of the eye-associated lymphoid tissue (EALT)
    -It plays an important role in the immune protection of the ocular surface and its mucosal adnexa.
    It is anatomically continuous from the lacrimal gland throughout the conjunctiva- and lacrimal drainage-associated lymphoid tissue
38
Q

What does the EALT consist of ?

A
  • of a diffuse lymphoid tissue of T lymphocytes and IgA-secreting plasma cells (which are derive from B-cells) (in the drawing, large blue cells represent plasma cells, small blue cells represent B cells and small black cells represent T cells)- shows distribution of those lymphocytes throughout the lacrimal gland in terms of Lacrimal gland associated lymphoid tissue, then conjunctiva in terms of conjunctiva associated lymphoid tissue and then extending down the nasal lacrimal drainage and into nose
  • The system connects with the rest of the immune system via lymphatics
39
Q

What is the role of the conjunctiva further ?

A
  • lymphoid follicle wihtin conjuctiva - aggregate of immune cells - can see it is a predominately a lymphocyte population
    -In the conjunctival epithelium cytotoxic T cells (Tc) predominate
    -In the stroma T-helper cells (Th) predominate
    -Stromal lymphocytes are often present in aggregates termed follicles with a modified overlying epithelium (M cells)- thought to be a portal which antigens are directed across the ocular surface so they intercept the immune cells.-
    -
40
Q

What happens in the lymphoid follicle system ?

A

activation of immune system - activation of t-lymphocytes, b lymphocytes

41
Q

What is CALT?

A

CALT provides a mechanism for the local production of IgA to augment lacrimal IgA
- Although a vast majority of IgA is from the lacrimal gland it appears that it can cross the conjunctival surface from the storm of the conjunctiva .

42
Q

What is the role of the cornea ?

A
  • effective anatomical barrier
  • Few micro-organisms can penetrate an intact corneal epithelium- relies on a breach in the corneal eptheilum for potential pathogens to penetrate the cornea .
  • Membrane bound mucins prevent attachment of micro-organisms- cells on surface have a glyococalyx - which prevent attachment ion micro-organisms
  • Frequent shedding limits contact time for micro-organisms
  • The integrity of the surface layer is important in maintaining polarity and creating an effective barrier to infection-
  • Absence of blood vessels
43
Q

What are the cells in cornea?

A

-Cells of the innate immune system: neutrophils and macrophages are found in the corneal epithelium- phagocytic system
-cornea contains a type of antigen presenting cell-
Langerhans cells -are concentrated in the peripheral cornea- important in presenting antigens to immune cells.
They act as antigen presenting cells and generate an adaptive immune response

44
Q

What are the corneal defences to infection ?

A
  • Each microorganism provokes a different defensive response
  • The initial response consists of neutrophil infiltration
  • Langerhans cells identify the organism and initiate an adaptive response- through process of antigen presentation activation of immune cells (although this generally takes at least 24h)-
  • Cytokine release leads to an influx of lymphocytes and macrophages (2nd wave response)
45
Q

Why does corneal transplantation occur?

A
  • in cases of corneal opacification
  • High success rate due to avascularity of cornea and lack of immune activation.
  • Success rate reduced in high-risk patients (e.g. neovascularisation). Where the immune system responds to attack foreign (donor) antigens,
  • process occurs - cutting out a circle of the host cornea - which becomes opaque through scarring or experienced corneal disease which leads to reduced vision - sight saving procedure.
46
Q

What can happen to corneas occasionally ?

A

can become vascularised hence represent the high risk grafts - success rate much lower - need to be much more tissue matched between host and antigens.

47
Q

What are the 2 strategies in high risk grafts that are used?

A
  • HLA molecules matching of donor and recipient

- immunosuppressive therapy- cortico steroids can be given as eye drops

48
Q

How can corneal graft rejection occur?

A

T cells and macrophages infiltrate the tissue and secrete a variety of cytokines and corneal graft rejection can occur
can have drugs - steroids to prevent rejection.

Neural Biology 1 (58 decks)

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