Chapter 12 Communicable Diseases Part 2 (defences) Flashcards
What are plant’s way of dealing with a pathogen, is it specific etc?
Not specific but is a rapid response. The idea is to block and kill infected cell before it can spread to other areas, and then regrow later
Plants have physical and chemical defences, what is the physical barrier defence
Physical includes waxy cuticle, cell wall bark ; a barrier against pathogen entry and stops water from staying too long which could be a vector
Describe the cascade of events when a pathogen meets and manages to break cell wall
What does the nucleus do (3)
This is when a pathogen comes in
1) some of the molecules of pathogen may already be detected BUT a pathogenic enzyme breaks down the cell wall of the plant. The BROKEN products of cell wall are then recognised by receptors and start to signal nucleus to attack .
2) NUCLEUS then will respond in 3 ways to deal with situation
- they produce defensive molecules to directly attack pathogen
- produce defensive chemicals to alert other cells to get ready before attacked
- produce LIGNIN AND CALOSE to strengthen and section cells.
Describe the entire mechanical route the nucleus takes :
- what is produced and deposited
- where (3) and why
- what is effect but why good
- nucleus rapidly produces high amount of callose. This is a chemical that strengthens the cell wall and makes it difficult for pathogen to enter
- the callose is deposited at the cell membrane and walls bordering cells next to them - to completely block off infected cell with other
- at the same time lignin is added making the mechanical barrier STRONGER
- callose also deposited between PLASMODESMATA : so pathogens can’t escape through connected cytoplasm to other cells
- callose also deposited in between siege plated in phloem, so that if pathogen here it can’t travel and absolutely kill rest of plant
= effects is cell die, but worth
What about the chemical defence approach the nucleus takes?
Produce powerful chemicals to kill insects, bacteria , fungi, oomcytets general etc
- antibacterial impounds like antibiotics like phenols , lysosomes (enzymes that attack) defending that kill
- anti fungal compounds like phenols , saponins, CHITINASES (enzymes that break chitin cell wall of fungus )
- anti oomcyetes, like GLUCANASE (enzymes that break down glucans which polymers in oomcytes )
- general toxins such as CYANIDE
insect repellants fro, citronella
- insecticides too like caffeine
What are main plant chemical defences
Produce anti fungal chitinases
Produce anti oomcytets glucanses
Produce general toxins like cyanide toxic to most things
Insecticides = caffeine , insect replannts like citronella
Antimicrobial phenols and antibiotics
2) less insects = promoted less spread through vector like something carry fungal spores
What is main difference between specific and non specific defence
Specific is to each pathogen, non is general but FASTER AND ALWAYS PRESENT
What are different non specific defences to KEEP PATHOGENS OUT (4)
+ how
1) barrier = skin
- prevents entry, has biome of microorganisms that outcompete bacteria to live on skin, sebum that oil prevents pathogen from living and can lose pH
2) mucous membranes in airways and openings of body
- in moth nostrils ears, genitals anus have these which secrete sticky mucus to trap them, then after that lysozyme phagocyte destroy
3) lysozyme in tears, urine , acid : kill
4) expulsion reflexes : coughing sneezing for gas exchange system expel, vomiting and diarrhoea in digestive
What about non specific respond of wound repair to prevent them coming in?
How does body seal a wound from one broken (what two main things end up being released)
1) first skin / blood vessel wall breaks, and this releases broken collagen. When this comes into contact with platelets , they become activated and release many substances:
2) one is thromboplastin , an enzyme triggers cascade reaction to make clot, including making fibrinogen into fibrin to make network of fibres to trap blood cells and make a clot
3) but also SEROTONIN , which makes smooth muscle in blood vessels contract, narrowing blood supply to area to stop blood leaking out !
What does the inflammatory response look like
This is a localised response to pathogens at the damage site resulting in inflammation, which is shown by pain, heat and redness and swelling .
What happens in inflammatory response (what two released , how and what they do) !
Two for h
One for c
Mast cells are activated in the damaged tissue and release HISTAMINES AND CYTOKINES
1) histamines
- histamines make the blood vessles near VASODILATE, causing more blood to the area and thus redness shown, but this increases temperature here which stops pathogens from REPRODUCING
- histamines make blood vessel walls more Leaky so blood plasma is forced out, and tissue fluid causes swelling and pain but essentially diluted the pathogen rendering it harmless (ya solution pollution dilution )
2) cytokines
- these attract white blood cells phagocytes to the site and they dispose of pathogens by PHAGOCYTOSIS
- How the non specific gets rid of pathogens
Two ways
1) fevers
- cytokines stimulates hypothalamus in brain to increase bidy temo from 37° to stop pathogens reproducing
- make immune system work faster as they do at higher temp
2) phagocytosis
- phagocyte like neutrophil macrophage dendrite recognise non self
- engulfs pathogen and invaginate making phagosome
- combines with lysosome to make phagolysome
- enzymes digest and it dies
Phagocytosis process again
What happens to neutrophils tho
phagocytosis
- phagocyte like neutrophil macrophage dendrite recognise non self
- engulfs pathogen and invaginate making phagosome
- combines with lysosome to make phagolysome
- enzymes digest and it dies
Neutrophils die too once digest by doing apoptosis
How do phagocytes and what then become APC
only macrophage dendeite because neutrophil dies
1) . After digest, process products of digestion
2) combines antigen found here with major histocompatibility complex
3) moved this using cytoskeleton to the csm
Now oresents antigen to start the specfic response
What effect does phagocytes releasing cytokines do
How can they use opsonins
Finally phagocytes release cutokines to alert other phagocytes under attack and come
They have couple common receptors to common opsonins which are antibodies and attach to the constant region which essentially Tage them for them and tells them to attack .
Where are t lymphocytes MATURE and where b
T in thymus
B in bone marrow
What is difference between cell mediated and humoral response
- what ways cause a cell mediated
What is humour
- what cause a humoral
1) Cell mediated is response to bodies OWN cells thst have been changed , for example
- by a virus
- antigen processing
- mutation like cancer
- transplanted tissue cells
Cell mediated is vital for cancer and viruses
However humoral is defence against Antigens found on cells OUTSIDE the body cells
- so bscteria, fungi
APCs
These are found in thr humour = body fluid
-
Describe cell mediated all steps
1) An APC releases cytokines in order to attract and find the correct complimentary receptor T helper celll, this is clonal selection and can take a decent amount of time
2) once found the correct receptor complimentary t helper cells binds to the APC and then released interleukins. These Signal to other t helper cells to divide by mitosis and differentiate into other t helper cells - this is clonal expansion .
This becomes
- cytotoxic t killer cells (these kill, they release perforins and gransozymes which create pores and breakdown )
- normal t helper cells
( needs more to repeats profess faster rate)
- t memory cells
(These keep note of the receptor in order to mass produce in case same pathogen appears again)
- t regulatory cells
( this is to regulate and stop an auto immune response after (as some antigens looks the same ))
Regulated and stored in memory . Now t helper cell can cause a humoral response too
Now describe humoral responses
How t helper cells involved
1) instead of macrophage dendrite, now B cell engulf snd processed antigens snd becomes APC
2) they release cytokines that activate t helper cells. They do this and once a t helper cell that is complementary to antigen binds, this is clonal selection and takes time
3) once binded now T cells activwted produced interleukins that stimulate b helper cells to divide by Mitleid and differentiate = clonal expansion
This becomes
- b plasma cells
- b memory cells
4’ b plasma cells receptors are still comolemtary to the pathogen , but can detach - these sre now antibodies l they are soluble and can deal with pathogens on their own . This is the primary response !
B memory cells re,Eber receptors to madd produce on second infection , secondary reponse
Primary vs secondary response
Primary response involves the time it takes to Clonal select and expand firdt time around , for cell mediated time to make cytotoxic t killer and also intimate humoral and humoral Time it twkes to make plasma cells. This can take weeks and this is why we feel symptoms, because that is effect of pathogens before body deals wothnit
Seojcdwry response insane quick because selection is very quick due to memory cells. As a result pathogen dealt with even before symptoms have chance to show
When do autoimmune response occur and why
Treatment but what bad
Don’t know, but maybe because some antigens are very similar to human one so mismatch
Also happens because t regulatory cells don’t work effectively
- bad is immunosuppressive can be used but thst stops bidy from natural defence for other basic disesdes
Types of autoimmune disease
Rheumatoid arthritis = joints
Type 1 diabetes = insulin producing cells
Vitiligo = melanocytes
Example for natural active immunity and natural passive
How do baby digestive system allow antibdoeis
Key difference between two?!!
1) active = the immunity you make yourself from specific immune response humoral and cell mediated. This aquifer immunity’s active because your own body made antibodies and memory
2) natural but passive
- baby immune system not work at birth
- but they passively acquire immunity through transfer of antibodies from placenta while in uterus + antibodies from breast fed milk l
- baby digestive system don’t digest So they just go to blood stream
As a result baby has same immunity as mother BUT ONLY TEMPORARILY (key difference )
Artificial passive ?
- what advantage but what disadvantage
#where do these even come from Why passive aswellm
- body cannot sometimes produce own antibodies fast enough before pathogen kill you
- so you are transferred antibodies already produced to counter
- this gives you TEMPORARY but lifesaving immunity they won’t be long term
2) antibodies come from like an animal thst was injected with snd produced their own antibodies disease and then transferred to you by drop = artificial but passive
(passive because you didn’t contribute at any stage yourself )
