How Plants Respond to Pathogens
You'll be able to distinguish physical from chemical plant defences with examples.
Phytophthora cinnamomi ('jarrah dieback') was first identified in the Darling Ranges of Western Australia in 1965. By 2018, a DBCA survey found that 40% of jarrah forest had been exposed; the pathogen kills approximately 40% of WA plant species it encounters. A Banksia has no white blood cells, no antibodies, no fever response, yet its bark, cuticle, cell wall, and phytoalexin chemistry are the only barriers between it and a pathogen that has already destroyed nearly half the jarrah forest.
Orient yourself
Warm up on earlier material, make a prediction, then scan the goals and vocabulary before you read.
Three quick questions from earlier lessons. Pulling old material back to mind before you learn something new makes the new material stick better, so this is not busywork.
Practise this lesson
Four printable worksheets that build from the foundations up to exam-style questions, start at whatever level suits you.
Consider this analogy:
"A castle under siege has two lines of defence: the walls and moat that stop attackers getting in, and the soldiers inside who fight those that breach the walls."
Before reading: apply this analogy to how you think a plant might defend itself against a pathogen. What would the "walls and moat" be? What would the "soldiers inside" represent? Write your predictions before reading on.
Know
- Physical defences plants use to prevent pathogen entry
- Chemical defences plants produce in response to infection
- The hypersensitive response and systemic acquired resistance
- How Banksia responds to Phytophthora cinnamomi infection
Understand
- Why physical and chemical defences are complementary
- How the hypersensitive response limits pathogen spread at the cost of host cells
- Why some plants have greater resistance than others
Can Do
- Distinguish physical from chemical plant defences with examples
- Describe the hypersensitive response and explain its function
- Explain the Banksia–Phytophthora interaction using defence terminology
Walls and weapons
Separate the defences a plant always has from the ones it manufactures only once a pathogen is detected.
Core Content
Structural barriers + antimicrobial chemistry
When Phytophthora cinnamomi reaches the root surface of a jarrah tree, it encounters a cork layer impregnated with suberin, a thick-walled epidermis, and, if it penetrates further, a cascade of antimicrobial compounds including phytoalexins. There are no phagocytes on the way. Every barrier is structural or chemical, not cellular.
These systems are analogous to the castle analogy, but in plant biology, both layers are active and sophisticated.
Physical (Structural) Defences
- Cuticle: waxy, waterproof layer covering leaf and stem surfaces, prevents spore germination and entry of water-borne pathogens
- Cell wall: cellulose and lignin matrix physically blocks hyphal penetration; can be reinforced with extra callose and lignin at infection sites
- Bark: thick outer layer of dead cells in woody plants, physical barrier and desiccation zone that kills pathogens
- Stomatal closure: stomata close in response to pathogen detection signals, blocking the primary entry point for airborne pathogens
- Trichomes: leaf hairs that trap spores and deter insect vectors; some produce sticky or toxic secretions
- Tyloses: balloon-like outgrowths from xylem parenchyma cells that block xylem vessels, prevent vascular wilt pathogens from spreading through the water transport system
Chemical Defences
- Phytoalexins: antimicrobial compounds produced rapidly at infection sites, directly toxic to fungal and bacterial pathogens (e.g. resveratrol in grapes)
- Pathogenesis-related (PR) proteins: produced after pathogen detection, include chitinases (break down fungal cell walls), glucanases, and protease inhibitors
- Reactive oxygen species (ROS): hydrogen peroxide and superoxide produced at infection sites, directly toxic to pathogens and trigger cell wall reinforcement
- Salicylic acid (SA): plant hormone that signals systemic acquired resistance (SAR), activates defences throughout the whole plant
- Tannins and phenolics: constitutive antimicrobial compounds in cell vacuoles, released when cells are damaged
- Resin and latex: sticky, antimicrobial secretions that physically trap and chemically inhibit pathogens in some species
Plants have no specialised immune cells; they defend with two integrated systems. Physical (structural) defences: cuticle, cell wall reinforced with callose/lignin, bark, stomatal closure, trichomes, tyloses. Chemical defences: phytoalexins, PR proteins (e.g. chitinases), reactive oxygen species, salicylic acid, tannins/phenolics. Defences are either constitutive (always present) or induced (activated only on pathogen detection).
Pause, copy the physical vs chemical defences and constitutive vs induced into your book.
Which of these is a chemical plant defence (not a physical one)?
Compare what is already present before attack with what is switched on after pathogen recognition, then classify each example as physical or chemical.
Deliberate cell suicide
Work out why killing its own cells is one of the most effective moves a plant can make.
Deliberate cell suicide to contain a pathogen
We just saw the physical and chemical barriers that block or poison a pathogen. That raises a question: what does the plant do when a pathogen breaks through and infects living cells? This card answers it → the hypersensitive response, a deliberate sacrifice of cells at the infection site.
The hypersensitive response is counterintuitive, the plant deliberately kills its own cells at the infection site to stop the pathogen spreading.
When a pathogen breaches initial physical barriers and begins to infect plant cells, one of the most powerful plant defence responses is the hypersensitive response (HR).
The HR works because most plant pathogens are biotrophs (they require living host cells to survive and reproduce) or hemibiotrophs. By rapidly killing the cells around the infection point, the plant creates a zone of dead tissue that the pathogen cannot exploit.
HR is a downstream response that can follow different recognition pathways, not an exclusive marker of one receptor class. Cell-surface PRRs recognise PAMPs; intracellular resistance proteins, often NLRs, can recognise pathogen effectors or the changes they cause. These pathways can activate overlapping defences, including ROS and, in some interactions, localised programmed cell death (HR). HR can limit biotrophs that need living cells; adjacent cells may reinforce the boundary, and salicylic-acid signalling can contribute to whole-plant SAR.
Pause, copy the HR steps and why killing cells stops biotrophs into your book.
In the hypersensitive response, the plant deliberately kills its own cells around the infection site.
The hypersensitive response (HR) in plants involves rapid, localized programmed cell death to prevent pathogen spread.
Plants have no defence mechanisms against pathogens because they lack an immune system.
Hypersensitive Response
Alerting the whole plant
Follow the salicylic acid signal from one infected leaf out to tissue the pathogen has never touched.
The plant equivalent of immunological memory, by a different mechanism
We just saw the HR contain a pathogen locally and release salicylic acid. That raises a question: what does that salicylic-acid signal do once it leaves the infection site? This card answers it → systemic acquired resistance, which primes the whole plant against future attack.
After a local infection triggers the HR, the plant sends a chemical signal, salicylic acid, to the rest of its body, priming defences everywhere.
Systemic acquired resistance (SAR) is the plant equivalent of immunological memory, though the mechanism is entirely different. After a localised infection triggers the HR, signalling molecules (primarily salicylic acid) travel through the phloem to uninfected parts of the plant.
In those uninfected tissues, SAR activates the expression of pathogenesis-related (PR) genes, producing PR proteins that prime the plant's defences against future infection. The entire plant becomes more resistant, not just the site of the original infection.
SAR can last for days to weeks after the initial infection signal. Unlike animal immunological memory, it is not pathogen-specific, it provides broad-spectrum resistance. This is both an advantage (broad protection) and a limitation (no targeted antibody-like response).
The HR can be a localised sacrifice: dead host cells may limit pathogens that require living tissue. A visible necrotic lesion can indicate local cell death, but does not alone establish that pathogen spread was contained.
Systemic acquired resistance (SAR) = whole-plant defensive priming after a local infection. Signal = salicylic acid travelling via phloem → activates PR genes plant-wide. It is broad-spectrum (not pathogen-specific) and lasts days to weeks. SAR is analogous to animal immunological memory but mechanistically different, it is not antibody-specific and not heritable.
Pause, copy the SAR definition, its salicylic-acid signal, and how it differs from animal memory into your book.
The hormone _____ acid travels through the phloem to trigger systemic acquired resistance.
Systemic Acquired Resistance (SAR) Pathway
Banksia versus Phytophthora
Put every defence together on the named Australian example, then work out why they are often not enough.
Phytophthora dieback, root invasion and Banksia's response
We just saw the full plant defence toolkit, barriers, HR, and SAR. That raises a question: what happens when those defences meet a pathogen the plant never evolved against? This card answers it → Banksia versus introduced Phytophthora cinnamomi, where the same defences are only partially effective.
Phytophthora cinnamomi is an oomycete, a water mould, not a true fungus, and it causes one of Australia's most ecologically devastating plant diseases.
Phytophthora cinnamomi causes Phytophthora dieback, infecting the roots of a vast range of native plants including Banksia, jarrah, grass trees (Xanthorrhoea), and many heathland species. It spreads primarily through water movement in soil, zoospores (swimming spores) move through water films between soil particles. Human activity (vehicles, boots, contaminated soil on equipment) dramatically accelerates spread.
How Phytophthora Attacks Banksia Roots
Zoospores are attracted by chemical signals (root exudates) from living roots. They attach to root surfaces, germinate, and penetrate root cells using enzymatic degradation of the cell wall. Hyphae then grow through root cortex tissue, destroying cells and blocking water and nutrient uptake through the xylem. Above ground, the first visible sign is yellowing and wilting of leaves, a consequence of root failure, not direct above-ground attack.
Banksia Defence Responses
Most Australian Banksia species have limited resistance to Phytophthora cinnamomi, the pathogen is introduced from Southeast Asia and Australian plants have had limited evolutionary exposure. Banksia species that do show some resistance typically have stronger hypersensitive responses and produce more effective phytoalexins. Research into naturally resistant individuals is ongoing as part of conservation management.
Phytophthora cinnamomi is an oomycete (water mould), NOT a true fungus, it spreads via soil-water zoospores and human movement of soil. It invades roots, destroys the cortex and blocks the xylem, causing above-ground yellowing and wilting. Banksia responds with callose/phenolics, phytoalexins and HR, but this is often insufficient because limited evolutionary exposure means weak pathogen recognition.
Pause, copy that Phytophthora is an oomycete, how it attacks roots, and why Banksia's defences often fail into your book.
Phytophthora cinnamomi is best classified as:
Phytophthora cinnamomi has been described by the IUCN as one of the world's 100 worst invasive species. In Australia, it threatens an estimated 5,000 plant species, including 40% of native plant species in south-western Western Australia, a global biodiversity hotspot. Banksia woodlands in the southwest are particularly affected: entire communities of Banksia, jarrah, grass trees, and orchids can be eliminated as the disease front moves through. The disease spreads along vehicle tracks and walking paths, meaning that human recreation in national parks is a significant transmission vector, hence the boot-wash stations and track closures at many WA parks. There is no effective broad-scale treatment. Phosphonate (phosphite) fungicide applied by stem injection or foliar spray can suppress Phytophthora and boost plant immune responses (including SAR), but it cannot eradicate the pathogen from soil. Management focuses on hygiene (preventing introduction to new areas), phosphonate treatment of high-value or critically endangered plants, and identifying naturally resistant genotypes for conservation seed banking. You will apply your knowledge of plant defences to this system in the practice questions.
Physical Plant Defences
- Cuticle, waxy layer preventing spore entry.
- Cell wall reinforcement, callose and lignin deposited at infection sites.
- Stomatal closure, blocks entry of airborne pathogens.
- Tyloses, block xylem to prevent vascular pathogen spread.
Chemical Plant Defences
- Phytoalexins, antimicrobial compounds produced at infection site.
- PR proteins, chitinases, glucanases; degrade pathogen structures.
- Reactive oxygen species (ROS), toxic burst at infection site.
- Salicylic acid, signals systemic acquired resistance throughout plant.
Hypersensitive Response
- Recognition by cell-surface PRRs of PAMPs, or by intracellular resistance proteins (often NLRs) of pathogen effectors or their effects, can trigger overlapping defence responses.
- ROS burst → toxic to pathogen and local signal.
- Programmed cell death → necrotic zone starves biotrophs.
- Callose/lignin reinforcement → seals the necrotic zone.
Banksia and Phytophthora cinnamomi
- Pathogen: oomycete (not a true fungus); spreads via soil water zoospores.
- Mechanism: invades roots, destroys cortex, blocks xylem → above-ground wilting.
- Banksia responses: cell wall reinforcement, phytoalexins, HR (in resistant individuals).
- Management: phosphonate injection, hygiene, seed banking of resistant genotypes.
Explain how a named Australian plant responds to infection by a named pathogen.
The dot point instructs you to investigate the response of a named Australian plant to a named pathogen — a scoping instruction — so it is examined with Explain: investigate → explain. Both names are required by the dot point itself.
Plan: name the principle, take each layer of response as a linked pair, then close on why the response often fails.
Plants have no circulating immune cells and no antibodies, so every defence is either a pre-existing structural barrier or a chemical response mounted by the infected cells themselves and signalled outwards. Defence is therefore local first and systemic second, and it works by containment rather than by pursuit.
Banksia species facing Phytophthora cinnamomi meet the pathogen first at physical barriers that exist before any infection: a waxy cuticle over the leaves, lignified and suberised cell walls in the roots, and bark. Phytophthora is a soil-borne water mould whose motile zoospores swim through wet soil to root tips, so the barrier that matters here is the root, and the fine feeder roots where uptake occurs are the least protected part of it.
Once a pathogen breaches the barrier, plant cells detect molecules characteristic of it and respond. The hypersensitive response is the most striking: cells immediately surrounding the infection site undergo programmed death, killing the tissue and, with it, the pathogen's supply of living cells. For a biotroph that requires living tissue this is effective containment — the visible dead lesion is the defence working, not the damage.
Alongside this, infected tissue produces antimicrobial compounds — phenolics, phytoalexins and enzymes such as chitinase that degrade fungal cell walls — and deposits callose to plug plasmodesmata and phloem, physically isolating the infected region. Salicylic acid then travels through the plant and triggers systemic acquired resistance, so distant uninfected tissue raises its defences before the pathogen arrives, giving a whole-plant response from a local infection.
Against Phytophthora cinnamomi these defences frequently fail, and the reason explains the scale of the damage. The pathogen attacks the root system, so containment sacrifices the tissue the plant needs for water uptake; it has a very wide host range, so it is not held in check by any single species' resistance; and Australian plants including many Banksia have no long evolutionary history with it, since it was introduced. The response is therefore a genuine defence that is simply outmatched, which is why dieback has reshaped whole plant communities in southern Australia.
Plants have no circulating immune cells and no antibodies, so every defence is either a pre-existing structural barrier or a chemical response mounted by infected cells and signalled outwards — defence is local first and systemic second, and works by containment rather than pursuit. Banksia species facing Phytophthora cinnamomi meet the pathogen first at barriers present before any infection: a waxy cuticle over the leaves, lignified and suberised cell walls in the roots, and bark — and because Phytophthora is a soil-borne water mould whose motile zoospores swim through wet soil to root tips, the barrier that matters is the root, whose fine feeder roots are the least protected part. Once breached, plant cells detect molecules characteristic of the pathogen and respond, most strikingly through the hypersensitive response, in which cells surrounding the infection site undergo programmed death, killing the tissue and with it the pathogen's supply of living cells — for a biotroph requiring living tissue this is effective containment, so the visible dead lesion is the defence working rather than the damage. Alongside this, infected tissue produces antimicrobial phenolics and phytoalexins and enzymes such as chitinase that degrade fungal cell walls, and deposits callose to plug plasmodesmata and phloem and isolate the infected region, while salicylic acid travels through the plant and triggers systemic acquired resistance so that distant uninfected tissue raises its defences before the pathogen arrives. Against Phytophthora cinnamomi these defences frequently fail, and why explains the scale of the damage: the pathogen attacks the root system, so containment sacrifices the tissue needed for water uptake; it has a very wide host range, so no single species' resistance holds it; and Australian plants including many Banksia have no long evolutionary history with it, since it was introduced — so the response is a genuine defence that is simply outmatched, which is why dieback has reshaped whole plant communities in southern Australia.
Compare the defences of plants and animals against pathogens.
Compare requires similarities and differences against stated criteria. These two are often treated as opposites and they share more than that suggests, so the shared ground has to be established honestly.
Plan: state the criteria and what they share, compare on each, then close on what explains the differences.
Both defend in layers, both begin with physical and chemical barriers, both recognise molecules characteristic of pathogens rather than the pathogen as a whole, and both respond by isolating and destroying infected tissue. They will be compared on whether defence is carried out by mobile cells, on whether specific memory exists, and on how a local infection triggers a whole-organism response.
This is the decisive difference. Animals have a circulatory system and mobile immune cells — phagocytes, lymphocytes — that travel to the site of infection, so defence can be concentrated wherever it is needed. Plants have neither: their cells are fixed in place by cell walls, so every cell must be capable of defending itself, and defence is distributed rather than deployed. This is why an animal's response converges on the infection and a plant's response radiates outward from it.
Animals possess adaptive immunity: lymphocytes with receptors for one specific antigen are selected and multiplied, and memory cells persist, so a second exposure produces a faster, larger response. Plants have no equivalent — no antibodies, no lymphocytes, no cells dedicated to memory. They do have systemic acquired resistance, which raises defences across the whole plant for weeks after an infection, so there is a form of induced protection, but it is broad rather than pathogen-specific and it is not inherited by the next generation.
Both isolate infected tissue, but at very different cost. An animal's inflammatory response increases blood flow and delivers cells to the site while the tissue survives, and the animal repairs it afterwards. A plant kills the infected region outright through the hypersensitive response, and because plants cannot heal damaged tissue they compartmentalise it and grow around it instead. Sacrificing tissue is affordable for a plant with indeterminate growth and would not be for an animal.
The differences follow from body plan rather than from sophistication. An organism that cannot move must defend every part of itself independently and can afford to lose parts; one that moves has a transport system that can carry defenders and a body it must keep intact. Neither strategy is more advanced — each is what the other's anatomy would not permit.
Both defend in layers, both begin with physical and chemical barriers, both recognise molecules characteristic of pathogens rather than the pathogen as a whole, and both isolate and destroy infected tissue; they will be compared on whether defence is carried out by mobile cells, on specific memory, and on the response to a local infection. Mobile cells are the decisive difference: animals have a circulatory system and mobile phagocytes and lymphocytes that travel to the site, so defence is concentrated where needed, while plant cells are fixed in place by cell walls so every cell must defend itself and defence is distributed rather than deployed — which is why an animal's response converges on the infection and a plant's radiates outward from it. Animals also possess adaptive immunity, selecting and multiplying lymphocytes whose receptors match one specific antigen and retaining memory cells so a second exposure is faster and larger, whereas plants have no antibodies, lymphocytes or memory cells; they do have systemic acquired resistance, which raises defences across the whole plant for weeks after infection, but it is broad rather than pathogen-specific and is not inherited. Both isolate infected tissue at very different cost: an animal's inflammatory response increases blood flow and delivers cells while the tissue survives and is repaired afterwards, whereas a plant kills the infected region outright through the hypersensitive response and, unable to heal damaged tissue, compartmentalises it and grows around it — sacrificing tissue being affordable for a plant with indeterminate growth and not for an animal. The differences therefore follow from body plan rather than sophistication: an organism that cannot move must defend every part independently and can afford to lose parts, while one that moves has a transport system to carry defenders and a body it must keep intact — neither strategy more advanced, each being what the other's anatomy would not permit.
Practise independently
Attempt at least one response in your own words. Model answers support checking; they do not replace the attempt.
A fresh set drawn from this lesson's question bank, feedback shown immediately. +5 XP per correct · +25 XP all correct
Pick your answer, then rate your confidence, that tells the system what to drill next.
UnderstandBand 3(3 marks) 1. Distinguish between constitutive and induced plant defences. Give one example of each and explain how each type contributes to plant protection against pathogens.
1 mark: constitutive defence with example · 1 mark: induced defence with example · 1 mark: explanation of how the two types are complementary
UnderstandBand 4(3 marks) 2. Describe the sequence of events in the hypersensitive response (HR) in plants. In your answer, explain why programmed cell death is considered an adaptive defence rather than a sign of disease.
1 mark: HR sequence (recognition → ROS → programmed cell death → reinforcement) · 1 mark: salicylic acid signalling and SAR · 1 mark: why cell death is adaptive, not pathological
EvaluateBand 5(4 marks) 3. Investigate the response of Banksia to infection by Phytophthora cinnamomi. In your answer, describe how the pathogen causes disease, explain both the physical and chemical responses the Banksia mounts, and explain why these responses are often insufficient to prevent plant death in susceptible species.
1 mark: mechanism of infection in roots · 1 mark: physical responses · 1 mark: chemical responses including HR · 1 mark: why responses are insufficient in susceptible individuals
Show all answers
Multiple choice
MC answers and full explanations are shown inline as you complete each question. Use the retry button to attempt a fresh set from the lesson bank.
Short Answer Model Answers
Q1 (3 marks): Constitutive defences are always present in plant tissues regardless of whether infection is occurring, they do not need to be activated. An example is the cuticle: a waxy layer covering leaf and stem surfaces that physically prevents spore germination and the entry of waterborne pathogens at all times. Constitutive defences contribute to plant protection by providing an immediate, continuous barrier that pathogens must overcome before any infection can begin. Induced defences are activated only after the plant detects pathogen presence. An example is phytoalexins: antimicrobial compounds synthesised at infection sites within hours of pathogen detection. Induced defences contribute by providing a targeted, high-concentration response exactly where it is needed. Together they are complementary: constitutive defences provide the first barrier that reduces pathogen entry, while induced defences provide a second, more powerful response against any pathogens that breach the initial barrier.
Q2 (3 marks): The hypersensitive response (HR) is a localised defence response that can follow more than one recognition pathway. Cell-surface pattern-recognition receptors (PRRs) recognise pathogen-associated molecular patterns (PAMPs), while intracellular resistance proteins, often NLRs, can recognise pathogen effectors or the changes they cause. These pathways can converge on overlapping responses, including reactive oxygen species (ROS) and, in some interactions, HR; HR is not an exclusive signature of one receptor class. In an interaction that activates HR, a rapid ROS burst at the infection site can act as a local signal and contribute to defence. Infected cells and immediately surrounding cells then undergo rapid programmed cell death, forming a visible necrotic lesion. Surviving adjacent cells deposit callose and lignin, sealing off the dead zone, while salicylic acid travels through the phloem to activate systemic acquired resistance throughout the plant. Programmed cell death is adaptive rather than pathological because most biotrophic pathogens require living host cells to survive and reproduce, by killing infected cells, the plant creates a zone of dead, nutrient-poor tissue the pathogen cannot exploit. A visible lesion can indicate localised cell death, but its presence alone does not show that pathogen spread was contained. Likewise, absence of a lesion alone does not establish susceptibility or uncontrolled spread.
Q3 (4 marks): Phytophthora cinnamomi causes disease in Banksia through root infection. Zoospores, motile swimming spores, are attracted by root exudates and move through water films between soil particles. They attach to root surfaces, germinate, and penetrate root cells by enzymatically degrading the cellulose cell wall. Hyphae grow through the root cortex, destroying cells and blocking xylem vessels, preventing water and nutrient uptake; the first visible symptom above ground is yellowing and wilting. Physical defence responses include deposition of callose and phenolic compounds in root cell walls to slow hyphal penetration, and in some species, growth of cluster roots away from infected zones. Chemical defence responses include production of phytoalexins (antimicrobial phenolics) and, in resistant individuals, a hypersensitive response that kills infected root cells to create a necrotic containment zone. These responses are often insufficient in susceptible Banksia because (1) most Australian Banksia have had limited evolutionary exposure to Phytophthora, so their immune recognition may be less effective and the HR is delayed or absent; (2) phytoalexin concentrations may be too low to inhibit the pathogen; and (3) Phytophthora spreads rapidly through soil water, establishing infections at multiple points simultaneously and overwhelming the plant's localised root defences.
Retrieve and reflect
Use the Review session first, then compare how your thinking changed.
A full module quiz covering every lesson in this module, not just this one. Set aside a decent block of time and treat it like a real assessment.
Start the module quiz →Defend your ship by blasting the correct answers for How Plants Respond to Pathogens. Scores count toward the Asteroid Blaster leaderboard.
☄️ Play Asteroid Blaster →You were asked to apply the castle analogy, walls and moat versus soldiers inside, to plant defences against pathogens. The analogy is particularly apt for Phytophthora cinnamomi, first identified in WA's Darling Ranges in 1965 and now present in 40% of jarrah forest (DBCA, 2018): for jarrah and banksias, the cuticle, bark, and cell wall are literally all that stands between the plant and a pathogen that kills approximately 40% of WA plant species it encounters. There are no mobile immune cells to call in once the wall is breached, only chemistry.
The mapping works well. The "walls and moat" are the plant's physical (structural) defences: the cuticle (outer wall), cell wall (inner fortification), stomatal closure (closing the gates), and bark (the moat, a zone the pathogen must cross). These are largely constitutive, always in place, whether an attack is occurring or not.
The "soldiers inside" are the chemical and cellular responses activated when a pathogen breaches the physical barriers: phytoalexins and PR proteins (chemical weapons), the hypersensitive response (soldiers sacrificing themselves to create a firebreak), and systemic acquired resistance (dispatching messengers to alert the rest of the castle).
Where the analogy breaks down: unlike soldiers, the HR doesn't fight the pathogen directly, it removes the resource the pathogen needs (living cells). It's less "soldiers fighting" and more "burning your own stores to deny them to the enemy." Also, SAR is more like a general alertness upgrade across all soldiers than a specific counter to the known attacker.
If you predicted something like "thick walls prevent entry, internal chemicals fight what gets through", you had the essential structure exactly right.