Lecture 7 - Innate Immunity Flashcards
Define and give examples and three lines of defense against infection or cancer.
2 - Local inflammation
Innate Immunity - includes the first 2 lines of defense: Peripheral Barriers and Inflammation
1st = Peripheral Barriers –> Constant and Preventative/ Non specific
A. Physical Barriers include:
- keritanized, stratified squamous epithelium
- mucosal cells of GI tracts with tight junctions
- ciliated pseudostratified columnar epithelium in lungs
B. Mechanical Barriers include:
- cilia sweeping the respiratory tract
- lower temperature of skin
- one way flow of urine
- regular sloughing of skin and GI mucosa
C. Biochemical Barriers include:
- mucous membranes that trap bacteria
- perspiration, saliva, tears (these contain lysozymes and IgA antibodies)
- epithelial cells have cathelicidens and defensins –> insert and disrupt membranes similar to complement
- low pH in vaginal secretions
- sebaceous glands secreting antifungal fatty acids
D. Normal Flora
- secrete chemicals that prevent colonization by pathogenic bacteria in the vagina and intestine
Response is immediate, serves to isolate infection, NONSPECIFIC
Occurs when first line of defense has been breached!!! Activates the acquired immune response.
Vascular response = vasodilation and capillary permeability
Plasma Protein systems =
- platelets from megakaryocytes
- clotting system (+ feedback loop) –> Liver
- complement system (+feedback loop) –> Liver
- Kinin system (+ feedback loop) –> WBC’s
Cellular response =
- Granulocytes: Neutrophils, eosinophils, basophils, and Mast cells
- Leukocytes: Monocytes, macrophages, NK cells
This is VERY SPECIFIC, lag time from primary exposure, MEMORY that is very long lasting
Lymphocytes:
- T lymphocytes - cell mediated (Treg, Tc, and Th cells)
- B lymphocytes - humoral response, antibodies
Define and List examples of:
Innate immunity
1: Peripheral Barriers
Innate immunity is always there and it is nonspecific. It includes the first 2 lines of defense.
They are as follows
A. Physical - keritanized stratified squamous epithelium, mucociliary elevator (ciliated pseudostratified columnar epithelium), mucous membrane with tight junctions in GI tract
B. Mechanical - cilia in the lungs, low temp of the skin, one way flow of urine, sloughing of the skin and GI tract
C. Biochemical - low pH of vagina and stomah, saliva/sweat/tears that contain lysozymes and IgA antibodies, antifungal secretions in sweat, cathelicidens and defensins that insert themselves into bacteria and destroy (these are from macrophages and epithelial cells)
D. Normal Flora - they secrete chemicals which prevent colonization of bacteria in the vagina and the intestine
–> activates the acquired immune response
Vascular response = vasodilation and increased capillary permeability
Protein systems =
- platelets from the megakaryocytes
- complement system from the liver
- kinin system from the WBC’s
- clotting cascade from the liver
Cellular =
Granulocytes - neutrophils, eosinophils, basophils, and mast cells
Leukocytes - macrophages, monocytes, NK
Define and List examples of:
Mechanical Barriers
Mechanical barriers are a part of the first line of defense
They include:
- Cilia sweeping the respiratory tract
- Low temperature of skin
- One way flow of urine.
- Continual sloughing of the skin and GI tract
–> this removes bacteria that are adhering to surfaces
Define and List examples of:
Normal Flora
Normal flora is a part of the first line of defense.
Normal flora secrete chemical that prevent the growth of bacteria. They also occupy receptors so bacteria can’t bind. Prevent infestation of the intestine and vagina.
Define and List examples of:
Peripheral Barriers
Peripheral Barriers are a part of the first line of defense. They include:
A. Physical
- keritanized stratified columnar epithelium
- mucosal lining of the GI tract with tight junctions
- ciliated pseudostratified columnar epithelium
B. Mechanical
- cilia sweeping the respiratory tract
- low temp of skin
- one way flow of urine
- regular sloughing of the skin and GI tract to remove adhering pathogens
C. Biochemical
- mucous membranes that trap bacteria
- tears, saliva, sweat containing lysozymes and IgA antibodies
- antifungal solutions from the sebaceous glands
- low pH of vagina and the stomach
- epithelial cells and macrophages release of cathelicidens and definsins
D. Normal flora
- secrete chemicals which prevent adherence of pathogens
Define and List examples of:
Biochemical Barriers
Biochemical barriers are included within the first line of defense. They include:
a. mucous membranes which trap bacteria
b. saliva, sweat, tears containing lysozymses and IgA antibodies
c. Antifungal secretions from sebaceous glands
d. low ph of stomach and vagina
e. epithelial cells and macrophage release of cathelicidens and defensins
Identify the role of Cathelicidins and defensins as surface barriers
Cathelicidens and Defensins
They are released from epithelial cells and macrophages. They insert themselves into membranes much like complement and cause severe damage.
Delineate the role of inflammation and describe the mechanisms of actions of the THREE major contributing components and their roles.
Vascular Response
3 plasma protein systems
Cellular response
Inflammation is IMMEDIATE and NONSPECIFIC. It serves to contain the infection once the 1st system of defense has been breached. It also serves to activate the acquired immune response.
Vascular response = vasodilation and increased capillary permeability (this helps with getting leukocytes to infection site and increasing blood flow to the infected area)
3 plasma protein systems
- Complement system - MOST IMPORTANT, it increases adheerance of phagocytes (opsonization), it induces degranulization of mast cells, helps with chemotaxis, lysis the foreign cells
- Kinin system - Bradykinin is the primary kinin and causes dilation of blood vessels, pain, endothelial cell retraction (increased permeability), smooth mm. contraction
- Clotting system - contains the infection (acts to prevent its spread), traps bacteria and pathogens facilitating its removal, keeps phagocytes in area of infection, stops bleeding and provides framework for healing
There is redundancy in these systems to guarantee survival and also because each component is lethal and needs to remain in site of infection only
Delineate the cellular participants or components of the Adaptive Immune system and how if differs from the Innate Immune system.
Adaptive immune response differs from the innate immune response because it is SPECIFIC, it has lag time, and it HAS MEMORY which is very long lasting.
Components:
a) T lymphocytes - cell mediated (T reg, Tc, and Th)
b) B lymphocytes - humoral (antibodies)
Delineate the steps and mechanisms of the acute inflammatory response.
Steps of acute inflammation
- Occurs in response to cell injury or death
- Arterioles initially and temporarily constrict
- General vasodilation
- Increased blood flow (redness)
- Arteriole Dilation (Increases capillary hydrostatic pressure)
- Retraction of capillary endothelial cells
- Exudation of plasma serum and proteins
- Occasional spillage of RBC’s and platelets
- Margination of WBC to capillary endothelial wall
- Diapedesis - migration of WBC to site of infection by chemotaxis
- one in the tissues, cells and plasma proteins work together to prevent further inflammation
Explain the role of Mast Cells in the initiation and perpetuation the inflammatory response, detailing the following:
A. Mechanisms triggering degranulation
B. Degranulation phase & chemicals involved vs Secretory Phase & chemicals involve
General effects of Mast Cell degranulation:
- vasodilation
- increased capillary permeability
- pain
- thrombosis
- cellular infiltration
A. What causes degranulation?
- Chemical Injury
- Mechanical Injury
- . IgE mediated **
- Complement activated (C5a) **
B.
Degranulation phase - releases for immediate response
a) Histamine:
- causes contriction of large blood vessels
- it dilates post capillary venules
- retraction of capillary endothelial cell membrane
- exudation
b) Cytokines: IL-4 B lymphocyte activation
TNF alpha to increase vascular
permeability
c) Neutrophil chemotaxic factor: attracts neutrophils to infection site
d) Eosinophil chemotaxic factor: attracts eosinophils infection site; FIRST DEFENSE AGAINST PARASITES, control mediators of inflammation, Prevents more inflammation as needed
Synthesized phase - secreted by mast cell for longer term response
a) Leukotrienes: smooth mm. relaxation, vasodilation, increased capillary permeability, and some chemotaxic properties
b) Prostaglandin E series: increase capillary permeability and some neutrophil chemotaxic properties, PAIN!!! –> aspirin and NSAIDS block synthesis of prostaglandin E inhibiting inflammation and reducing pain
c) Growth factors: VEGF and PDGF these work to grow endothelial cells and simulate fibroblasts to initiate healing
d) Platelet activating factor (PAF) –> activates the clotting cascade. produced by activated monocytes, neutrophils, endothelial cells ,and platelets.
Identify and describe the systemic response to the following signal molecules
Histamine
Histamine is released from mast cells for immediate response.
Histamine cause constriction of large blood vessels, dilation of post capillary venules, increased capillary permeability, and exudation.
Identify and describe the systemic response to the following signal molecules
Leukotrienes
Leukotrienes are released from mast cell for longer term response.
It causes smooth mm. relaxation, dilation, and increased capillary permeability and some chemotaxic properties.
Identify and describe the systemic response to the following signal molecules
Prostaglandin E series
Released from mast cell for longer term response.
It’s biggest role is PAIN
It increases capillary permeability and has some neutrophil chemotaxic properties.
NSAIDS and aspirins block the formation to prevent pain and inflammation.
Identify and describe the systemic response to the following signal molecules
VEGF and PDGF
VEGF and PDGF are released from the mast cell for long term response.
This initiate healing by causing increased growth of endothelial cells and and fibroblasts.
