Task Solutions-Human Immune Response towards Pathogen: BIOL20982

Task Solutions-Human Immune Response towards Pathogen: BIOL20982

Running Head: HUMAN IMMUNE SYSTEM TOWARDS PATHOGEN
Human Immune Response towards Pathogen
Name of the student
Name of the University
Author Note

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Running Head: HUMAN IMMUNE SYSTEM TOWARDS PATHOGEN
Human Immune Response towards Pathogen
Name of the student
Name of the University
Author Note
1 HUMAN IMMUNE RESPONSE TOWARDS PATHOGEN
Table of Contents
TASK 1 2
TASK 2 3
TASK 3 6
TASK 4 7
References 10
2 HUMAN IMMUNE RESPONSE TOWARDS PATHOGEN
TASK 1
1. A. Any organism that causes the disease is called apathogen [1].
B. Microorganisms responsible for MRSA are methicillin-resistant Staphylococcus
aureus. The causative factor of NOROVIRUS is the RNA virus of the family Caliciviridae.
The athlete’s foot is caused by a fungus known as dermatophyte; T. rubrum is the
dermatophyte mostly associated with the athlete’s foot. Malaria is caused by asingle-celled
parasite of the genus plasmodium.
C. Staphylococcus aureus comprises athick peptidoglycan layer and acapsule made
of polysaccharides. These virulence factors are involved in toxin production, adherence to
and invasion within the host tissue, and destroy the host’s immune system. Norovirus is a
small virion with adiameter of 27 to 32 nm. It has no envelope, single-stranded, RNA virus,
or positive sense. T. rubrum is cottony and white on the surface. The underside of the fungus
may be red or yellowish, or brownish. Plasmodium is aunicellular eukaryote. Attached to the
nucleus, there are the endoplasmic reticulum and Golgi apparatus.
D. The entry route of MRSA causing agent is via skin-to-skin contact, contact with
the infected scrapes, and cuts. NOROVIRUS spreads through contaminated foods, water, and
direct contact with the infected person through a faecal oral route. T. rubrum spreads via
direct contact with infected skin, hair retained in combs, and using towels of the infected
person. Entry routes of malaria parasites are the bite of amosquito from an infected person,
blood transfusion, and use of contaminated needles.
2. A. Resident flora are the microorganisms that naturally reside in the site of the
body.
3 HUMAN IMMUNE RESPONSE TOWARDS PATHOGEN
B. In an animal, normal flora behaves as an antigen. It helps to induce alow level of
antibiotics. These antibiotics, in turn, react with similar pathogens or antigens and prevent the
invasion of the pathogen. Gastrointestinal tract flora Helicobacter pylori help in vitamin K,
ammonia production, etc. Resident flora sometimes causes infection [2]. Infection under the
skin is caused by resident skin flora if a cut on the skin. Serious conditions result from
spilling resident flora from the large intestine during surgery into the sterile areas of the
abdomen. Caries, abscesses, endocarditis, and foul-smelling are examples of infections due to
normal flora. Impairment of the host or host defence may lead to a condition where the
normal flora cannot suppress the pathogens or invade the host themselves, causing acritical
condition.
3. Skin and mucous membrane act as the body’s innate immune system [3]. The skin
epidermis prevents the entry of germs by making a physical barrier. The keratin of the
epidermis makes the surface of the skin so tough that itresists the action of bacterial enzymes.
Along with that, epidermis cells frequently shed with the attached microorganisms. The
basement membrane between the dermis and epidermis releases cytokines that regulate
wound healing and prevent infection. On the other hand, mucus secreted from the mucus
membrane help restrict the microorganism’s entry [4]. For example, tear fluid contains
lysozyme that helps to protect the eye from infection. Microorganisms in the air become
stuck to the mucus of airways and blown out of the nose. The mucus membrane of the
stomach secretes acid, and the digestion of food particles also helps kill bacteria and prevent
them from multiplying.
TASK 2
4. Cellular components that help clotting are platelets, proteins, ions, enzymes, and
endothelial cells. The clotting mechanism is involved in 2 stages. Primary homeostasis
4 HUMAN IMMUNE RESPONSE TOWARDS PATHOGEN
consists of vasoconstriction, adhesion of platelets, activation of platelets, and aggregation of
platelets [5]. Vessel injury leads to vasoconstriction mediated by a potent vasoconstrictor
endothelin 1, secreted from the damaged endothelium. Sub endothelial collagen, von
Willebrand factor, inflammatory mediators, and ATP are exposed to damaged endothelium.
Combining these factors leads to the second phase of primary homeostasis, platelet adhesion.
It is mediated by thrombin. Platelet adhesion leads to aggregation of the platelets. Receptors
Of activated platelets adhere to fibrinogen and Vwf and form weak platelet plugs. This is the
temporary protection from bleeding. This leads to secondary homeostasis by further
stabilizing fibrinogen to fibrin via thrombin.
Secondary homeostasis is accomplished by activating clotting factors, transforming
prothrombin to thrombin, and transforming fibrinogen to fibrin. There are extrinsic and
intrinsic pathways [6]. Many tissue and clotting factors play an active part in this clotting
mechanism. FXa from both the extrinsic and intrinsic pathways then react with FVa, and
calcium on the phospholipid surface creates prothrombinase enzyme, which activates
prothrombin to thrombin. Thrombin activates FXIIIa, which reacts with fibrin to form a
stabilized clot.
5. Macrophages secrete enzymes to destroy the ingested particle [7]. Macrophages
consist of receptors that help distinguish between self and nonself in the nonspecific
recognition of foreign substances. At the time of inflammation, monocytes are transformed
into macrophages and engulfed to eliminate the causative agent. Cellular enzymes inside the
macrophages destroy the ingested particles. Some macrophages remove dead or necrotic cells,
whereas others engulf the microbes and provide host immunity. Ingested microbe in the
phagosome fuses with the lysosome, where digestive enzymes of the lysosome help digest the
microbial protein. Some macrophages are long-lived, and they can kill hundreds of different
5 HUMAN IMMUNE RESPONSE TOWARDS PATHOGEN
bacteria before their death [8]. Thus, they provide nonspecific or innate immunity.
Macrophages play agreat role in adaptive immunity by activating the T helper and cytotoxic
cells to destroy the pathogens.
ACTIVE IMMUNITY PASSIVE IMMUNITY
It is permanent It lasts for only afew weeks and months.
In response to direct contact with the
antigen, the body produces antibodies
Antibodies are introduced to the host from
outside
Produces immunological memory Does not related to immunological memory.
After entry of the antigens, the host
immune system produces antibodies
and other specialized lymphocytes
Passive immunity can be transferred from
mother to foetus by the placenta in the form of
antibodies or from mother to baby via the milk
of amother
No side effects May cause reactions
6 HUMAN IMMUNE RESPONSE TOWARDS PATHOGEN
TASK 3
6. When apathogen enters the host body, active immunity is attained by producing antibodies.
When antibodies are introduced into the body from an external source, passive immunity
toward an antigen occurs.
Table 1: Difference between active and passive immunity
Table 2: Difference between Natural and Artificial immunity
Natural immunity grows when aperson, after exposure to alive pathogen, develops
disease and immunity. In natural passive immunity, immunity is transferred in antibodies
from mother to fetus via the placenta and breast milk. In artificial immunity, pathogens are
inserted into the body from outside, which helps to generate immunity against that pathogen.
The active form of artificial immunity comes in the form of vaccination, whereas antibodies
are introduced in the body when the person is already affected by the disease [9].
NATURAL IMMUNITY ARTIFICIAL IMMUNITY
Response to an infection Response to vaccination
Formation of memory cells There are no memory cells formation
7 HUMAN IMMUNE RESPONSE TOWARDS PATHOGEN
TASK 4
7. Antigens and antibodies are two different things. The antibody is a glycoprotein
molecule. It is activated and reacts with antigens. On the other hand, antigens, when they
enter the host body, activate the host immune system and thus induce the production of
antibodies.
Table 3: Difference between antigens and antibody
TOPIC ANTIGENS ANTIBODIES
Also Called Immunogens Immunoglobulins
Molecular type Usually lipid. They can also
be proteins, nucleic acids,
All are protein
8 HUMAN IMMUNE RESPONSE TOWARDS PATHOGEN
Generally, antibodies are 10nm in size [10]. There are four polypeptide chains in an
antibody of humans and most mammals. These four polypeptide chains consist of two
identical light chains and two identical ones. Disulphide bonds connect them. Each chain has
aseries of domains. There are one constant domain (C L)and one variable domain (V L)in the
light chain, whereas the heavy chain contains one variable domain (V H)and three to four
constant domains (C H). An antibody molecule can also be divided into two antigen-binding
and crystallizable fragments. Each antigen binding domain (Fab) contains One VL,VH,CL,
CH1. Crystallizable fragment (Fc) of antibody forms the trunk of the Y shape.
Difference between Humoral and cell-mediated immunity
Cell-mediated immunity Humoral immunity
Mediated by T cells Mediated by B cells
Antibodies are not formed Antibodies are formed
To identify the antigens, receptors are used To identify antigens, antibodies are used
It protects against fungi, viruses and other
intracellular bacterial pathogens
Protects against bacteria and virus
Protects against cancer by eliminating Tumour cells cannot be eliminated by
carbohydrates
Effect May cause allergic
reactions or illness
Lysis or immobilization of the
antigen
Specific binding site Epitopes are the binding
site with the antibodies
Paratopes of antibodies bind
with an epitope of an antigen
9 HUMAN IMMUNE RESPONSE TOWARDS PATHOGEN
tumour cells humoral immunity
Participants are CD4+ and CD8+ cells Participants are TH cells
Hypersensitivity type IV is mediated Hypersensitivity types I, II, and III are
mediated
Delayed response Quick response
Table 4: Difference between cell-mediated and humoral immunity
Humoral immunity is antibody-mediated immunity[11]. Secreted antibodies,
complement proteins, and antimicrobial peptides participate in this immune mechanism.
Humoral immunity refers to all the mechanisms that assist the production of antibodies. The
mechanisms are activating Th2, cytokine production, germinal center formation and isotype
switching, affinity maturation, and generation of memory cells. Humoral immunity also
denotes the effector function means neutralization of pathogens and toxins by antibodies,
activation of classical complement, promotion of opsonin of phagocytosis, and elimination of
pathogens.
In cell-mediated immunity, apoptosis is induced by antigen-specific cytotoxic T cells
[12]. Virus-infected cells, cancer cells, and intracellular bacteria display foreign antigens on
their surface. These surface antigens are detected by T cells, and apoptosis takes place.
Macrophages and natural killer cells destroy the pathogens via recognition and cytotoxic
granule secretion (natural killer cells) and phagocytosis(macrophages). T helper cells are
differentiated into TH1 cells, which produce interferon-gamma and lymphotoxin alpha,
whereas TH2 cells produce IL 4, IL 5, and IL 13 to destroy the infected cells.
10 HUMAN IMMUNE RESPONSE TOWARDS PATHOGEN
8. The clonal selection hypothesis states that individual lymphocyte, mainly the B
cells, produces receptors specific to an antigen [13].
Immunological memory helps the body’s immune cells respond rapidly on the second
exposure to an antigen. Natural immunity and artificial immunity are based on
immunological memory. In asoluble antigen, the antigen binds to the B cells, which have
specific antibodies against that antigen. Then B cells transform into plasma cells and memory
cells. After the initial exposure to antigens, antibody production is stopped by the plasma
cells, and they die gradually. Memory B cells take an active part in the second exposure of
that antigen.
In secondary response, the ability of antibodies to bind with the antigens increases
more than the first one. By clonal selection, alteration occurs of variable regions of heavy and
light chains of memory cells by somatic mutation. This increases the antigen-binding affinity
and immune response of the antibodies.
References
[1] Pirofski LA, Casadevall A. Q&A: What is apathogen? A question that begs the point.
BMC biology. 2012 Dec;10(1):1-3.
[2] Biancone L, Monteleone I,Blanco GD, Vavassori P, Pallone F. Resident bacterial flora
and immune system. Digestive and Liver Disease. 2002 Sep 1;34:S37-43.
[3] Proksch E, Brandner JM, Jensen JM. The skin: an indispensable barrier. Experimental
dermatology. 2008 Dec;17(12):1063-72.
11 HUMAN IMMUNE RESPONSE TOWARDS PATHOGEN
[4] Lopez-Vidriero MT. Mucus as anatural barrier. Respiration. 1989;55(Suppl. 1):28-32.
[5] Smith SA, Travers RJ, Morrissey JH. How itall starts: Initiation of the clotting cascade.
Critical reviews in biochemistry and molecular biology. 2015 Jul 4;50(4):326-36.
[6] Jin NZ, Gopinath SC. Potential blood clotting factors and anticoagulants. Biomedicine &
Pharmacotherapy. 2016 Dec 1;84:356-65.
[7] Gordon S, Martinez-Pomares L. Physiological roles of macrophages. Pfl ügers Archiv-
European Journal of Physiology. 2017 Apr;469(3):365-74.
[8] Elhelu MA. The role of macrophages in immunology. Journal of the National Medical
Association. 1983 Mar;75(3):314.
[9] Keller MA, Stiehm ER. Passive immunity in prevention and treatment of infectious
diseases. Clinical microbiology reviews. 2000 Oct 1;13(4):602-14.
[10] Janeway Jr CA, Travers P, Walport M, Shlomchik MJ. The structure of atypical
antibody molecule. InImmunobiology: The Immune System in Health and Disease. 5th
edition 2001. Garland Science.
[11] Carroll MC. Complement and humoral immunity. Vaccine. 2008 Dec 30;26:I28-33.
[12] Herberman RB, Holden HT. Natural cell-mediated immunity. Advances in cancer
research. 1978 Jan 1;27:305-77.
[13] Parnes OS. The specificity of the clonal selection theory. Nature Immunology. 2003
Feb;4(2):95-.

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