HSC Biology Syllabus Notes 

Module 7 / Inquiry Question 2


Overview of Week 10 Inquiry Question – How does a plant or animal respond to infection?

Learning Objective #1 – Investigate the response of a named Australian plant to a named pathogen through practical and/or secondary-sourced investigation for example:

  • Fungal pathogens

  • Viral pathogens

Learning Objective #2 – Analyse responses to the presence of pathogens by assessing the physical and chemical changes that occur in host animals cells and tissues.

NEW HSC Biology Syllabus Video – Response to Pathogens

Week 10 Homework Questions (Essential for Band 5!)

Week 10 Curveball Questions (Moving from Band 5 to Band 6!)

Week 10 Extension Questions

Solutions to Week 10 Questions


Overview of Week 10 Inquiry Question

Welcome back to Week 10 of your HSC Biology Syllabus Notes! 

In this week, we will have a look at the responses of plants and animals that are used to protect themselves against pathogens & infection as per Inquiry Question.

For plants, we will be focusing on virus and fungi pathogens. Specifically, there will be exploration into plants’ first and second line of defence. 

In the case of animals, we will be using humans as an example and be looking into the three lines of defence that makes up our immune system. 

Without further ado, let’s start munching on the delicious knowledge!


Learning Objective #1 - Investigate the response of a named Australian plant to a named pathogen through practical and/or secondary-sourced investigation, for example:


- Fungal pathogens
- Viral pathogens

Plants have both innate and induced disease resistance mechanisms. 

The former is the plants’ first line of defence and the latter can be termed the plants’ second line of defence.

The plant’s innate disease resistance responses involves the:

  • Cell wall & cuticle preventing water loss and act as a physical barrier to prevent pathogens enter leaf.

  • NOTE: Varying properties of cell wall and cuticle can be acquired via adaptation.

  • Antimicrobial chemicals such as nicotine which naturally occurs in some plants.

  • Naturally occurring enzyme inhibitors.

The cell’s second line of defence involves both general (non-specific) and specific immunity. 

In general-induced immunity, it involves pattern recognition receptors that are present on plants’ cell wall which are able to recognise microbe-associated molecule patterns. 

When these microbial patterns are identified by the receptors, various responses are triggered via signalling pathways resulting in: 

  • Production of lignin to reinforce cell wall. Lignin produced also allows the modification of cell wall structure by blocking the plasmodesmata (the channel allowing molecules to through the cell wall) is blocked, thus hindering the flow of pathogen from one cell to another.

  • Production and accumulation of proteins into the cell membrane such as chitinase, glucanase and protease. These proteins are able to inhibit effectors that are secreted by pathogens and stop reproduction & growth of pathogen. We will examine what effector molecules are and what they do soon.

  • Production & secretion of antimicrobial molecules such as nitric oxide (NO) or hydrogen peroxide (H2O2).

  • Production & secretion of signalling hormones such as salicylic acid and jasmonic acid.

  • Activation of genes to produce more antimicrobial enzymes and proteins (e.g. chitinase, glucanase and protease as mentioned earlier) to stop the reproduction & growth of pathogens.

It is important to note that pathogens have adapted to avoid the detection or recognition of microbe-associated molecule patterns which can led to the plant’s general-induced defence mechanism not being triggered. These pathogens can secrete effector molecules.

  • Effectors are molecules secreted by pathogens to suppress the plant’s general-induced defence mechanisms, allowing the pathogen to invade and obtain nutrients from plant cells.

In the specific – induced immunity in plants, the hypersensitive response is involved.

This only occurs when the plant identified and recognises a specific antigen. 

  • NOTE: An antigen is a protein molecule present on the pathogen (or they can be proteins secreted by the pathogen).

There are resistance proteins that are present in the plants’ cell membrane situated near (or guarding) the proteins. These resistance proteins are also found inside plant cells. 

  • The specific-induced immunity response involves resistance proteins recognising the antigen which triggers responses via a signalling pathway. These signals produced as a result of the recognition of pathogen’s effectors by resistance proteins result in the activation of genes in plant that are responsible for the coding and production of enzymes, antimicrobial (e.g. phytoalexins) and oxidative molecules to hydrolyse proteins, nuclear membrane and nucleic acid which breaks them down. This would results in apoptosis.

  • Apoptosis is essentially programmed death of infected cells and surrounding cells of infected cell so stop the spread of pathogens, effector molecules and infection in general.

  • NOTE: This response is the last defence barrier to defend against pathogen and their effectors that have invaded the cytoplasm and vascular systems.


Response of Potato Plant to Fungi

Host: Ipomoea costata (Potato Plant).

Pathogen: Phytophthora Infestans (Fungi).

Disease: Late Blight (or Potato Blight).

The potato plant’s example is same as the general-induced immunity and specific-induced immunity as we have examined in the above section. 

  • So, you can write them and replace the word ‘pathogen’ with the word ‘Fungi’ in your written response in exams.

However, we will go over some points that are specific to the late blight disease:

We mentioned about microbe-associated molecule patterns detected by pattern recognition receptors in the previous section. Well, the specific response of potato plant is that their pattern recognition receptors can recognise beta-glucans that is present on the phytophthora infestans’ (fungi) cell wall. Here, beta-glucan is a type of microbe-associated molecule pattern.

  • NOTE: There are many more of these microbe-associated molecule patterns that plants may recognise but we, humans, have not yet discovered.

When the pattern recognition receptor recognises the microbial pattern (i.e. beta glucans), the protease protein is produced as a response to inhibit the effectors molecules produced by the fungi’s hyphae and stop the growth of the pathogen. This therefore stop the pathogen’s (or the hyphae) invasion to obtain nutrients from the plant’s cells that are necessary for fungi growth & survival.

NOTE: When asked about plants’ response to VIRUS PATHOGENS, you can use the same notes about general-induced and specific-induced immunity response as explored previous section.

To answer your question, yes, virus also produces effector molecules and plants response to them in the same way, at least at HSC Biology level. 

  • You will learn at university that the type of effector molecules, microbe-associated molecule patterns will differ for fungi and virus due to the pathogen’s difference in chemical composition. However, it’s not necessary to explore such differences at HSC Biology level.

We will provide you a named example of virus affecting a plant that you can use in your exams

Host: Tomato Plant

Pathogen:Tomato Spotted Wilt Virus

Disease: Tomato Spotted Wilt

  • NOTE: If you have another example, you can use that too. It doesn’t really matter.


Learning Objective #2 - Analyse responses to the presence of pathogens by assessing the physical and chemical changes that occur in host animal cells and tissues.



First Line of Defence (Innate Immune Response)

Antigens are molecules (usually proteins) which the host recognise as being foreign and initiate the adaptive immune response (e.g. the production of antibodies to destroy the antigens) and innate immune response (e.g. phagocytosis). 

We will explore both the components of innate and adaptive immune response in detail this week’s notes.

There are two types of antigens being exogenous and endogenous. 

  • Exogenous antigens are basically found on the invading pathogen itself.

  • Endogenous antigens are found in the (harmful and/or toxic) chemicals that are produced by the pathogen when it has entered the host organism.

Lit! Now that we have covered the basis of antigens which will become useful when we explore the second and third line of defence, we can start exploring the first line of defence.

The first line of defence involves the physical and chemical barriers that helps to stop further entry, growth and reproduction of invading pathogens.

The physical barriers constituting to the first line of defence in animals (such as humans) include:

  • Skin

  • Mucous Membranes

  • Cilia

The chemical barriers that makes up the first line of defence are:

  • Acidic conditions in stomach

  • Alkaline conditions in intestines

  • Body secretions – urine, lysozymes, saliva.

NOTE: The first line of defence is non-specific to the invading pathogen. That is, it does not operate differently based on the type of pathogen that is present.


Skin

The skin is a large physical barrier (and an organ) that protects cells from pathogens in the surrounding environment. 

Since the surface of the skin is waterproof, it is able to be maintained at a dry state which hinders the growth of pathogens. 

Sweat glands are also able to produce sweat which naturally occurring bacteria on our skin can breakdown to produce acidic chemicals. This creates an acidic environment that also hinders the growth of pathogens.

NOTE: The skin is a very noice physical barrier <O~O~ 

  • Yes, if you experience a cut, your blood will clot due to the presence of platelets in your blood. This will temporary shield your deeper tissues from being exposed to microbes in the environment. However, that’s not an excuse to not maintain noice, smooth, healthy skin.


Mucous Membranes

The mucous membranes are on the surface of the respiratory, digestive, reproductive and urinary tracts. As the name suggests, they produce thick mucus which is able to trap pathogens and antigens. 

Saliva that travel across these membranes contain enzymes such as lysozymes that is able to breakdown pathogens. 

The moist and nutrient-rich environment of the mucus membranes are able to support the growth of natural, beneficial microbes that produces chemicals capable of hindering the growth and entrance of pathogen.


Cilia

These are tiny-like structures that are located along the respiratory tract. 

They vibrate or move at upright direction, resulting mucus (containing trapped pathogens) being propelled to the throat which can be coughed or sneezed out.


Acidic & Alkaline Environments

Our stomach contains hydrochloric acid which is very acidic . 

This high level of acidic is able to dissolve pathogens or mucus that contains any trapped pathogens.

Similarly, the alkaline environment in our intestines are able to decompose and kill pathogens. 


Body Secretions - Urine, Lysozymes and Saliva

Urine that produced from the kidney passes through the walls of the ureter and bladder. As urine is acidic, this washing of the walls of the ureter and bladder helps kill and hinder the growth of microbes (e.g. pathogens).

Saliva in our mouth are contains enzymes called lysozymes that is capable of decomposing their protective cell wall of bacteria which led to their eventual decomposition. This therefore prevents infection from the pathogen. Tears also contain lysozymes that allow us to flush off any pathogens on the surface of our eye (cornea). 

  • We will explore more about the eye soon in Module 8!


Second Line of Defence (Innate Immune Response)

Moving onto the second line of defence! 

For humans, the second line of defence deal only physiological adaptations of the organism. 

The physiological defence adaptations that makes up the second line of defence include:

  • Phagocytosis

  • Lymphatic System

  • Inflammation Response

  • Cell death to seal off pathogens & Antigens

  • Interferons & complement proteins

NOTE: Similar to the first line of defence, the second line of defence is also non-specific to to the invading pathogen. 

Let’s explore each of the physiological adaptations that makes up the second line of defence in our body.


Phagocytosis

Phagocytes are a type of leucocytes (i.e. specialised white blood cells) that is responsible for phagocytosis. 

There are two types of phagocytes, these being neutrophils and macrophages. 

Phagocytosis can be defined as the defence mechanism whereby phagocytes modify to their shape to envelope or enclose a non-specific antigen (e.g. a pathogen). 

  • The advantage of phagocytes is that it is able to distinguish self markers and non-self (not belonging to the host) markers.

  • Therefore, phagocytes will only operate or engulf matter that are foreign to the body.

When the phagocyte has ‘engulfed’ the antigen, it will combine with a lysosome, which contains digestive enzymes (e.g. protease) produced by Golgi Apparatus, to breakdown the microbe or antigen.

 

Following this, the decomposed matter derived from the antigen is let out by the phagocyte. As the chemical structure of the antigen has been largely altered due to the action of enzymes in lysosome, the decomposed matter of antigen is not toxic or harmful to the host’s cells.

Phagocytosis is useful because when the antigen is engulfed by the phagocyte (e.g. macrophage), any of the toxins that it secretes will be contained in the macrophage and not be secreted to harm other cells. Also any reproduction will occur inside the macrophage will be destroyed by lysosomes’ enzymes upon combination.

Another benefit of phagocytosis (and other mechanisms in the 2nd line of defence that we will explore soon) is that minimises the reproduction of the pathogen & harmful effects caused by pathogen before the adaptive immune response (3rd line of defence) is initiated. 

  • You will see later that the third line of defence involves B and T cells involved in initiating the adaptive immune response need to bind with a specific antigen. This binding process is not immediately and so the 2nd line of defence is good at minimising the quantity and damage caused by invading pathogen before the adaptive immune response hopefully ‘saves the day’.

  • NOTE: In some scenarios, the antigen may avoid being engulfed and phagocytosis is unsuccessful.

Phagocytes assist the 3rd line of defence as the phagocyte that engulfed the antigen will move & display some of the antigen on its surface. The phagocyte can then present this antigen to cells (lymphocytes) that make up the 3rd line of defence and activate lymphocytes.

Lymphatic System (Lymph System)

The role of the lymph system is to filter and return intercellular fluid to the blood using lymph nodes connected by lymph vessels. 

The lymphatic system therefore is comprised of lymph vessels that joins lymph nodes together. 

  • NOTE: The fluid that flows through the lymph vessels is known ‘lymph’.

The lymph nodes in the lymphatic system has the ability to filter and trap antigens. It is within the lymph nodes where B and T lymphocytes are stored.

  • NOTE: Lymphocytes is a type of specialised white blood cell (e.g. leucocyte).

  • We will explore more about lymphocytes when we examine the third line of defence.

So, essentially, the lymph nodes in the lymph system facilitate the lymphocytes to bind with antigen and initiate an adaptive immune response.

  • It is important to note that the interaction of lymphocytes with antigens is NOT a second line of defence mechanism, rather it is 3rd line.

  • We are ONLY dealing with filtering and trapping antigens when we are talking about the lymph system.


Inflammation Response

Alright, now we have arrived to explore the inflammation response as a defence mechanism in the second line of defence. 

Let’s see how this works!

Again, like all other defence mechanisms that makes up to the second line of defence, the inflammation response is non-specific to an antigen or a pathogen. 

The inflammation response is initiated by infected cells releasing chemicals known as histamines and prostaglandins. These chemicals act on blood vessels causing vasodilation (e.g. dilation of blood vessel), resulting in higher level of blood flow through the site of infection. 

Remember that our blood contains red blood cells which are red in colour. Due to vasodilation, a higher blood flow would mean that there are more red blood cells at the site of infection. As a result of this, the site of infection appears to be red and swollen (and hot). 

  • So, inflammation responses occur at sites of infection.

As our blood is hot, this increased blood flow to the site of infection would increase the temperature of the environment surrounding the infected cells at the infected site. 

Due to this increase in temperature, it slows the rate at which pathogens reproduce their enzymes and protein such as effector molecules that are required for the pathogen’s invasion, survival and successful reproduction.

On top of dilating the blood vessels, histamine also increases the permeability of capillaries which allows more white blood cells to move to the infected cells. These white blood cells include macrophages which can engulf antigens (e.g. toxins produced by pathogen) or pathogens themselves at the site of infection.


Cell death to seal off pathogens & Antigens

When the infected cell(s) is not suppressed from transmitting disease, the second line of defence have the mechanism involving neighbouring cells dying to form a wall of dead cells surrounding infected cell(s), forming a capsule structure known as granuloma. 

The granuloma has a three-layer structure.

  • The first layer involves different types of phagocytes surrounding the infected cells.

  • The next outer layer is comprised of lymphocytes surrounding the phagocytes.

  • The final layer is made up of fibre cells to consolidate and envelope the structure.

Since the pathogens are deprived from food supply by being contained in the granuloma, it will die. The death of antigens & pathogen prevents the transmission of the disease to healthy cells.


Interferons & Complement Proteins

When cells are infected by a virus, they are able to secrete proteins called interferons.

The effect of interferons is that they induce neighbouring unaffected cells to produce antiviral chemicals which help reduce protein synthesis activity. This means that the amount of viral particles that are reproduced is reduced. This limits the transmission of disease between cells. 

If the neighbouring cells are infected with the virus, it would signal the infected cells to perform apoptosis. 

Complement proteins are produced by liver cells and makes up the complement system comprised of a collection of 20 types proteins that circulate the blood. 

These proteins stimulate phagocytes activity to allow more phagocytes to travel towards site of infection. We will discuss more about how these proteins when we discuss about antibodies soon.


Third Line of Defence (Immune Response)

NOTE: The ‘adaptive immune response’ refers to the third line of defence. 

The term ‘adaptive immunity’ refers to the host cells’ ability to recognise and defend against invading antigens. 

NOTE: This section will be covering next week’s notes which is about the adaptive immune response (third line of defence).

The adaptive immune response in humans involves three different biological molecules, these being:

  • T – Lymphocytes (T cells)

  • B – Lymphocytes (B cells)

  • Antibodies

They play a role in the third line of defence in humans and have interactions with each other which we will explore now.


T - Lymphocytes

As we have mentioned earlier, lymphocytes are a type of specialised white blood cells (i.e. leucocyte).

In the case of T lymphocytes, they are manufactured in the bone marrow and mature in thymus gland (located near your lungs). 

Upon maturation, the cells are released into the bloodstream whereby it is transported into the lymph vessel and stored in the lymph nodes. 

  • T cells are also stored in lymphatic tissues in the spleen, thymus, tonsils and liver.

T lymphocytes have a surface receptor protein that can recognise a specific antigen. For instance, often after phagocytosis, some parts of the pathogen or antigen is re-located or moved to the surface of the phagocyte
(e.g. macrophage). These phagocytes will move into the lymph (fluid) whereby they will encounter lymphocytes stored in the lymph node. 

The lymphocyte may have surface receptor proteins that matches with the protruding antigen which the phagocyte engulfed. 

If we assume that the lymphocyte’s surface receptor proteins matches the antigen, the T lymphocyte will then be activated. 

There are many types of T lymphocytes, these include:

  • Helper T cells.

  • Cytotoxic T cells (also known as Killer T cells).

  • Memory T cells.

  • Suppressor T cells.

It is Helper T cell that activates other types of T cells via cytokines, so usually we start with T helper cells when examining the interaction between T cells and antigens.

NOTE: You should always be specific in your response when talking about T cells. That is, you should not say that ‘T cells are activated’. Rather, you should say the specific name of the T cell that you are talking about, for example, ‘Helper T cells are activated’ or ‘Cytotoxic T cells are activated’.

Anyways, let’s get back on the topic of activated Helper T cells after its surface receptor protein matches and binds with the antigen. 

When Helper T cells are activated, it will clone and differentiate sub-types of Helper T cells that differ in the cytokines that they produce. These cytokines that Helper T cells produce will help clone and activate other specific T cells such as cytotoxic T cells, memory T cells and suppressor T cells. 

These different types of T cells that are produced all have the SAME specific receptor protein that is present in the original Helper T cell which they are derived from. 

Hence, the different types of T cells produced are specific to the same antigen which the original Helper T cell was activated by. 

The cytotoxic T cells that are produced will travel towards infected cells and release cytotoxins to eliminate the infected cells which thereby destroys the antigen(s).

The activated helper T cells will also secrete cytokine molecules that activates B lymphocytes, causing them to divide and differentiate into plasma cells and memory B cells. 

NOTE: Plasma cells will produce antibodies as we will learn later.

Moreover, cytokine molecules have the function to increase the rate at which macrophages is able to phagocytose antigens as well as enhancing the inflammation response (2nd line of defence).

Lastly, the increase in cytotoxic T cells being produced (from Helper T cell activation) is also caused by cytokines.  

When all the antigen has been destroyed, suppressor T cells are responsible to bind with matching antigen with its surface receptor protein in order to suppress B lymphocytes and cytotoxic T cells and other T cells that recognises the same antigen.

So, in essence, suppressor T cells regulate the adaptive immune response.

We will now explore the role of B lymphocytes in the human’s adaptive immune response. 


B - Lymphocytes

Like T lymphocytes, B lymphocytes are also a type of specialised white blood cells (leucocyte).

  • They are manufactured in the bone marrow and also mature there. In the case of T-cells, we mentioned that they are produced in the bone marrow but mature in the thymus gland.

  • After maturation, the B cells will move form the bone marrow to lymph nodes and lymphatic tissues via blood.

Again, similar to T cells, B lymphocytes also have a specific surface antibody protein that can recognise and is specific to a particular antigen.

Suppose that we have B lymphocyte’s surface antibody successfully binding with an antigen. If this occurs, the B cell, bounded to the antigen, will travel and present the antigen to a Helper T cell. The Helper T cell, which the B cell presents antigen to, will also have a surface receptor protein that is specific to (i.e. matches) the antigen.

If the Helper T cell, which the B cell presented the antigen to, has matching surface receptor protein to the antigen, it will become activated. 

Upon activation, the helper T cell will perform the activities that we have mentioned previously. For instance:

  • They will secrete cytokines to activate more Helper T cells with the same surface receptor protein that’s specific to the antigen.

  • The cytokines that Helper T cells produce will help clone and activate other T cells – e.g. cytotoxic, memory T cells, suppressor T cells, etc.

  • Etc … Please review the previous section about ‘T Lymphocytes’ to review on all other activities.

Now, we did mention in the previous section when we examined T Lymphocytes where we said that activated Helper T cells will secrete cytokine molecules that will stimulate or activate B lymphocytes that has surface antibody that is matching the antigen that caused the Helper T cell to be activated. 

As a result of the B cell being activated due to cytokine (i.e. interleukin-2), it will divide and differentiate into plasma cells and memory B cells. Again, these plasma and memory B cells also have surface antibody proteins that are specific to the antigen which the Helper T cell was activated by. 

These plasma cells is responsible for producing antibodies that has a surface receptor protein that capable of binding to the antigen that was activated the Helper T cell that ultimately gave rose to the the antibodies via B cell activation. 

These antibodies that are produced by the plasma cells are secrete into the lymph and blood to bind with an antigen. 

An antigen-antibody complex is formed when the antibody produced by the plasma cell binds to a matching antigen. Upon successful binding, the pathogen or antigen is inhibited from being harmful other cells. 

  • We will examine several ways the antibody can inhibit the harmful activities of pathogen in the next section.

Phagocytosis can then be performed on the antigen-antibody complex whereby a phagocyte can enclose or engulf the complex. The antigen is digested upon combination of phagocyte with lysosome whereby the lysosome secretes lysozymes as we have mentioned earlier in the second line of defence.

Now, you may ask what Memory B cells does?

Memory B cells will remain in the lymph nodes and lymphatic tissues and have similar properties to B cells. That is, they also have surface antibodies that can recognise a specific antigen. 

When memory B cells are activated by the same antigen (e.g. individual’s re-exposure to same pathogen few years later), the memory B cell will undergo mitosis and differentiate into plasma cells in about 4 days where the plasma cells will then produce antibodies. Due to memory B cells, a secondary exposure to the same antigen means that the individual will not experience the symptoms!

Memory B cells also undergo somatic hypermutation which results more antibodies are produced in the secondary exposure to the same antigen (secondary immune response) than during primary immune response (i.e. when individual gets exposed to the antigen for the first time).

Memory B cells are also more abundant than B cells. This along with the fact that memory B cells have higher affinity surface receptor proteins than B cells after memory B undergoing somatic hypermutation, it allows memory B cells to be more quickly activated than B cells.

Memory T Cells 

Recall that we also mentioned about memory T cells earlier. When the host organism is exposed to the same antigen again (perhaps could to due to exposure to the same pathogen), these memory T cells will have the same surface receptor protein that activated the Helper T cells the first time that produced the memory T cells. 

The memory T cells with matching surface receptor protein to the antibody will clone and differentiate into other T cells such as cytotoxic T cells and Helper T cells. We have already talked about the role of these T cells earlier.

NOTE: There are more memory T cells than Helper T cells which is why the secondary exposure to the same pathogen (with same antigen) is quicker than when the individually exposed to the pathogen for the first time. It also easier to activate, thus taking less time, for memory T cells to differentiate into other T cells (e.g. cytotoxic cells) compared to Helper T cells. 

Due to memory T cells, a secondary exposure to the same antigen means that the individual will not experience the symptoms!


Antibodies

Lastly, we have antibodies which we have already discussed in the above ‘B lymphocytes’ section. 

In summary, antibodies are also called immunoglobulins which are proteins produced by plasma cells. 

  • Antibodies are Y-shaped, each with two antigen binding sites.

We mentioned earlier that plasma cells are produced via the activation of B cells or Memory B cells and the produced antibodies will have antigen binding sites that matches the antigen that activated the B cells and Memory B. 

Upon successful binding, antibody is able to immobilise the antigen or block their receptors that are used in host cell entry. 

Antigen-antigen complex provides a site for complement proteins to bind to which is able to attract phagocytes to bind to them and destroy the antigen. 

  • NOTE: We have talked about the nature of complement proteins in the 2nd line of defence.


Basic Flowchart To Summarise Adaptive Immunity

(3RD LINE OF DEFENCE)

Adaptive-Immunity-Flowchart-Editedx.png

Remember that there are many ways which Helper T cells can be activated by antigen. 

For example, as we have already mentioned in the T Lymphocytes section, phagocytes can present some fragments of its engulfed antigen on their surface and move to present the antigen to activate Helper T cells.

We will make a prettier flowchart soon! :)