Week 1: Innate Immunity Flashcards
What is a pathogen? Give 5 examples.
A microorganism that can cause disease
Virus Fungus Bacteria Protozoa Helminths
What is an antigen? Give 3 examples.
any substance that elicits an immune response (exogenous- coming from external environment or endogenous-coming within our own body)
Proteins
Carbohydrates
Nucleic acids
3 Noninfectious environmental agents (antigens)
Pollens
Foods
Bee venom
Clinical products that are antigens
Drugs
vaccines
Transplanted tissues
Immune system functions (4)
1) Prevent infection and cell injury
2) Distinguish self from non-self
3) Destroy infected and malignant cells
4) Initiates repair
Normal immune response
Pruritus: itching
Malaise: general feeling of unwellness
Anorexia: loss of appetite
Limited collateral damage of normal tissue
Abnormal immune responses
Immune deficiencies
Hypersensitivities - allergies
Autoimmune disorders
Describe Innate Immunity
- Present at birth
- Immediate
- Non-specific
- Activates inflammation and the adaptive immune response
- First line of defense
- What babies use the majority of the time
What is the bridge between specific and non-specific immune response?
Inflammation
First line of defense
prevent injury/infection
Examples: tears, blinking
Third line of defense
adaptive immunity response
Physical borders of innate immunity
-Prevent entry
Tight junctions (epithelial tissue throughout GI)
Temperature (cool skin limits bacteria growth)
Epithelium (cornea turnover in 7 days)
Examples of mechanical barriers in Innate Immunity
Blinking Coughing/sneezing Mucociliary escalator Swallowing GI tract peristalsis Vomiting Defecation Urination Ejaculation
7 biochemical barriers and their functions
Tears: antibacterial Gastric juices: pH Mucus: antibacterial Sweat: pH, antibacterial Sebum: antibacterial Earwax: antibacterial Saliva: digestive enzymes
Normal bacterial flora makes up _____ of the human body mass. What kind of barrier is this?
1-3%
Biochemical barrier
What is the second line of defense?
Inflammation
What are the goals of inflammation?
Limit infection and further damage Control bleeding Interact with adaptive immune system Prepare the area of injury for healing Limit and control the inflammatory process
Signs of inflammation
Heat Redness Swelling Pain Loss of function
True or False: Inflammation is part of the innate immune system.
True
Does inflammation respond quickly or slowly? Is it specific or non-specific? Is it repeatable or nonrepeatable?
Inflammation responds quickly
It is non-specific
It is repeatable
What 3 things causes inflammation?
Activation of immune system components
Mast cell degranulation
Cellular injury
suffix “itis” means
inflammation
5 Cardinal signs of inflammation
1) Heat - calor
2) Redness - rubor
3) Swelling - tumor
4) Pain - dolor
5) Loss of function - functio laeso
Signs throughout the whole body (Systemic) when immune system is activated
Fever Increased Pulse Increased blood pressure Leukocytosis- white blood cells increase Increase Plasma protein synthesis Cytokine Effects (TNF-a, IL-1)
Why does temperature increase when immune system activated?
Pyrogens act on the hypothalamus to increase the temp.
Vascular response when immune system activated
Send WBC and other immune components to area.
Dilute the bacteria at injury site.
Provide nutrients and oxygen for immune cells and wound repair
What happens to vasculature when immune system is activated?
Brief vasoconstriction Mast cells release histamine Vasodilation Increased capillary permeability Exudation- leakage/buildup of fluid and cells (emigration)
a mass of cells and fluid that has seeped out of blood vessels or an organ, especially in inflammation.
exudate
watery exudate that indicates early inflammation
serous exudate
thick, clotted exudate that indicates more advanced inflammation. Can lead to dysfunctional wound healing
Fibrinous exudate
Exudate that contains pus and indicates bacterial infection
Purulent Exudate
Exudate that contains blood; indicates vascular disease
Hemorrhagic exudate
What type of exudate is central serous chorioretinopathy?
Serous exudate
What type of exudate is pseudomembrane?
Fibrinous exudate
What type of exudate is bacterial conjunctivitis?
Purulent conjunctivitis
What type of exudate is diabetic retinopathy?
Hemorrhagic exudate
Examples of inflammation in the eye
Hordeolum Dry eye syndrome Conjunctivitis Trauma Ocular Rosacea Thermal and Chemical burns Scleritis Vitritis/ retinitis/ chorioretinitis
7 Cellular mediators of inflammation
Mast cells Natural Killer Cells Platelets Granulocytes Monocytes Dendritic cells Lymphocytes
What are the cellular mediators activated by?
Plasma protein system products
Inflammatory cell secretions
Microbial molecules
Debris from cellular destruction
What are pattern recognition receptors (PRR’s)? Where are they found?
Recognition pathogen-associated molecular patterns (PAMPs). Is not specific but can identify whether molecule is pathogen or not.
Found on surface of resident and circulating immune cells
Also recognize cellular debris.
4 step process of Pattern recognition receptor when interacting with pathogen/microbe.
Attachment of pattern recognition receptor to pathogen
Pseudopodia forming a phagosome
Granule fusion and killing of pathogen
release of microbial products
Describe phagocytic mobilization when inflammation is occurring.
Neutrophils, eosinophils, and macrophages emigrate toward the source.
They flow to the walls of the blood vessel (Margination)
They attach to the walls of the vessel (Adherence)
They move through the walls of the capillaries (Diapedesis)
They migrate to the injured area in response to concentration gradients of extracellular signals. (Chemotaxis)
Describe process of phagocytosis
Opsonization, recognition, and adherence Engulfment Phagosome formation Fusion with lysosomal granule Destruction of the target
Describe mast cells. Where are they located?
Key initiator of inflammation and immune respone
Located in loose connective tissue in high risk areas of the body (GI tract, lungs, skin, mucosal tissue)
Sensitive and stimulated by multiple stimuli
Immediate degranulation
Delayed synthesis
What can stimulate mast cells? (4)
Pathogens
Allergens
Physical injury
chemical agents
What are 2 products of mast cell degranulation? Describe them.
1) Histamine:
- Increased glandular production
- Vasoactive amine
- has CNS effects
2) Chemotactic factors
- Neutrophil chemotactic factor
- Eosinophil chemotactic factor of anaphylaxis (ECF-A)
What are 2 mast cell synthesis products? Describe them.
1) Leukotrienes
- Product of the arachidonic acid cascade
- Similar effects to histamine in later stages
2) Prostaglandins
- Induce pain
- Pro and anti-inflammatory properties
In atopic individuals (frequent inflammation), describe the mast cells in these individuals.
More numerous mast cells
higher number of antigen receptors
Mast cells more easily activated
What do natural killer cells do?
Cell mediator that recognizes and eliminates virus infected cells and cancer cells.
Release perforin and granzyme
Describe platelets
Contribute to clot formation Have multiple triggers Degranulate upon activation Contribute to wound healing Pro and anti-inflammatory
Describe neutrophils. What is another name? What happens when dysfunction occurs?
AKA polymorphonuclear neutrophils (PMNs)
Early rescindants in inflammation (within hours)
Ingest bacteria, dead cells, and cellular debris
Dysfunction increases risk of bacteria influx
Describe Eosinophils
Mildly phagocytic
Defend against parasites
Implicated in allergies and asthma
Regulate vascular mediators
Describe Monocytes/ Macrophages.
Produced in bone marrow
Mature and replicate at inflammatory site (3 to 7 days)
Ingest bacteria and cellular debris
Contribute to activation of adaptive immune system
Initiate wound healing
What happens at the end of inflammation?
Removal of an offending agent usually ends response
What checks are present to control course of inflammation
Neutrophil life span is short
Inflammatory mediators degrade rapidly
Anti-inflammatory cytokines
Outcomes of acute inflammation
1) Complete resolution - structure and function recoverable
2) Scarring- substantial damage to connective tissue
3) Abscess formation- pus confined in a closed space. Active proteases produce fluid increasing osmotic pressure. Usually have to drain.
4) Progression to chronic inflammation- Body can’t remove offending agent. Persistent bacteria/toxins or autoimmune disease
Describe chronic inflammation
Lasts longer than 2 weeks
Related to unsuccessful acute inflammation response
Caused by high lipid and wax content of microorganism, ability to survive inside the macrophage, toxins, chemicals, particulate matter, physical irritants
thickening and scarring of connective tissue (fibrin)
fibrosis
Production of new blood vessels
Angiogenesis
walling off of offending agents
Granuloma formation
Possible outcomes of chronic inflammation
Dense infiltration of lymphocyte and macrophages
Fibrosis
Angiogenesis
Granuloma formation
What biochemical immune response does the eye use?
Lysosome enzyme
