Innate Immunity and Inflammation Flashcards
Examples of antigens that are non infectious environmental agents and clinical products
Environment:
Bee venom
Food
Pollen
Clinical:
Drugs
Vaccines
Transplant
Normal immune responses
Puritis: Itching
Mailaise
Anorexia
Limited collateral damage
Two examples of an overactive immune system
Hypersensitivites
Autoimmune disorders
First line of defense
Physical:
Skin- tight junctions and turn over
Mucous membranes
Temperature (Cool skin limits bacterial growth)
Mechanical: Blinking Coughing Urination Vomitting Cilia
Biochemical: Tears, mucous, sweat, sebum, earwax: Antiviral Gastric juices: pH Saliva: Digestive Normal bacterial flora
What activates inflammation?
Activation of immune system components
Mast cell degranulation
Cellular injury- necrosis
Systemic Manifestations of Inflammation
Fever due to pyrogens that tap hypothalamus
Increased pulse
Increased blood pressure
Leukocytosis (more circulating WBC)
Increased plasma protein synthesis (complement, kinin, coagulation)
Cytokine effects- IL, TNF-a, Interferons
5 steps of vascular response
- Brief vasoconstriction. Causes transudate- movement of fluid out due to constriction.
- Vasodilation due to histamine from mast cells.
- Increased capillary permeability due to histamine.-allows exudation (leakage/build up)
- Diapedesis
- Chemotaxis
Exudative fluids
Serous
- Watery, easily reabsorbed, early inflammatory
- Central serous chorioretinopathy
Fibrinous
- Indicates more advanced inflammation. Thick and clotted. Leads to scars.
- Pseudomembrane. Worst form of pink eye.
Purulent
- Indicates bacterial infection. Pus due to neutrophils
- Bacterial conjunctivitis
Hemorrhagic exudate: Contains blood. Indicates vascular disease.
-Diabetic retinopathy
Trasudate vs exudate
Transudate: Fluid exits vessel due to vasoconstriction.
Exudate: Fluid exits due to inflammatory response. Can cause serous, fibrinous, purulent, or hemorrhagic exudate.
PRR
Pattern recognition receptor found on immune cells that will bind to group of pathogens. PAMPs (pathogen associated molecular patterns). Will also recognize cellular debris.
Non specific. Part of innate immune system.
Phagocytic mobilization 4 steps
- Margination
- Adherence
- Diapedesis
- Chemotaxis
Monocytes
Macrophages in the blood system. Become macrophages after they leave the blood.
What is found in phagolysosome?
ROS, lactoferrin, defensins, lactic acid.
Where are mast cells located?
In loose connective tissue and in high risk areas of the body.
Gi tract, lungs, skin, other mucosal tissues
Mast cells. What is immediate and what is delayed
Immediate: Degranulation of histamine and chemotactic factors for neutrophils and eosinophils
Delayed: Synthesis of prostaglandins (pain with pro and anti inflammatory characteristics) and leukotrienes (arachidonic acid cascade. Similar to histamine)
What role does histamine have?
Vasoactive amine (dilates blood vessels) and causes capillary contraction. Causes increased tear and mucous production CNS stimulant (Which is why anti-histamines make you sleepy)
What 2 things does NK cells release?
Perforin- poke holes
Granzyme- induces apoptosis
Platelets carry what?
pre-formed granules that they release upon activation.
Role of platelets
Contribute to clot formation and wound healing.
3 phagocytic cells
Neutrophils, macrophages, and eosinophils
Eosinophils play what role
Defend against parasites. Cause allergies and asthma. Vasodilator.
How long does it take for macrophages to reach inflammatory site?
3-7 days.
What three checks are in place to control inflammation?
Neutrophil life span is short
Anti-inflammatory cytokines
Inflammatory mediators degrade quickly.
4 outcomes of acute inflammation
- Healed completely
- Scar due to fibrinous exudate
- Abscess formation- pus in confined space due to proteases.
- Chronic inflammation after 2 weeks.
What can cause chronic inflammation?
High lipid and wax content on microorganism.
Ability to survive inside macrophage
ToxinsChemicals
Physical irritants
Signs of chronic inflammation
Granuloma
Fibrosis (thickening and scarring of connective tissue)
Angiogenesis (due to hypoxic tissues releasing VEGF)