Innate Immunity Flashcards
What is innate immunity?
Natural barriers (physical and biochemical) and inflammation
Surface barriers harbour what?
Natural flora (group of microorganisms) that protect against pathogens
What’s the role of the physical and biochemical barrier in innate immunity?
It’s the first line of defence at the body surface, in place at birth to prevent damage by substance from environment and thwart infections by pathogenic microorganisms
What is the second line of defence?
Inflammatory response
What is the role inflammation response?
Inflammatory response is activated to protect against further injury, prevent infection of injured tissues and promote healing
What is adaptive (acquired or specific) immunity?
3rd line of defence
Slower
More specific process
Targets particular invading microorganisms and eradicate them
Body develop memory for rapid response at future exposure to the same organism
What is the timing of the first line of defence!
Constant
What is the specificity of immunity in first line of defence?
Broadly specific
What are the cells involved in first line of defence?
Epithelial cells and microbiome
What type of memory occurs in first line of defence in innate immunity
No memory involved
What are the active molecules in innate immunity first line of defence?
Defensins,
cathelicidins,
collectins,
lactoferins,
bacteria toxins
Protection in the first line of defence in innate immunity involves what?
- Anatomical barriers( skin and mucus membranes
- Cells and secretory molecules ( lysozymes, low pH of stomach and urine)
- Ciliary activity
Inflammatory response occur as what?
Second line defence response to tissue injury or infection
What type of response do we have in 2nd line defence of innate immunity?
Immediate response
What type of specificity of response do we have in 2nd line defence of innate immunity?
Broadly specific
What cells are involved in the 2nd line defence of innate immunity?
Mast cells
Granulocytes- ( neutrophils, eosinophils, basophils)
Monocytes/macrophages
Natural killer cells (NK)
Platelets
Endothelial cells
What is the type of memory in 2nd line of defence in innate immunity?
No memory
What are the active molecules in 2nd line defence of the innate immunity?
Compliments
Clotting factors
Kinnins
Cytokines
What is the process involved in 2nd line defence of innate immunity?
- Vascular response
- Cellular component( mast cells, neutrophils, macrophages)
- Secretory molecules or cytokines
- Activated plasma protein system
What are the 3 lines of human defence from infections and injury
- Innate immunity (natural barrier)
- inflammatory response and
- adaptive(acquired) immunity
What are the physical barriers in innate immunity?
Skin and mucus membranes
List the antibacterial peptide that provide biochemical barriers against pathogens in mucus secretions, perspiration, saliva, tears and other secretions
Cathelicidin
Defensin
Collectins
Mannose binding lectins
What are the functions of commensal and mutualistics organisms that colonize mucus membrane and skin or what are functions of microbiomes
Release chemicals that facilitate immune response
Prevent colonization by pathogens
Facilitate digestion in GI tract
What are the characteristics of inflammatory response
It’s the 2nd line of defence
It’s rapid and non specific
It can only occur in the vascularized tissue
Where does inflammatory response occur?
Vascularized tissues only
What are the macroscopic hall mark of inflammatory response
Redness
Swelling
Heat
Pain
Loss of function of the inflamed tissue
What are the microscopic hallmarks of inflammatory response?
Vasodilation
Increased capillary permeability
Accumulation of fluid and cells at inflammation site
What are the 3 key plasma protein systems involved in inflammation
Complement system
Clotting system
Kinin system
What protein system is bradykinin found
Kinin system
What’s the role of bradykinin in inflammation
Vascular permeability, smooth muscle contractions and pain
What are the types of cells involved in inflammatory process
Mast cells, endothelial cells, platelet, phagocytes(neutrophils, eosinophils, monocytes/macrophages, dendritic cells) natural killer cells and lymphocytes
List the cytokines(biochemical mediators in innate immunity
Chemokines
Interleukins
Interferons
Other molecules
What’s the function of interleukin 10?
To down regulate inflammatory response
What’s the most important activator of inflammatory response is what?
Mast cells
What’s the function of histamine in inflammatory process?
Causes capillary dilation and retraction of endothelial cells lining capillaries causing increased vascular permeability
What is interstitial space?
Free and opened space between tissue endothelial calls and vasculatures
What is tissue endothelial cells
Walls and intercellular space and content e.g nucleus
When mast cells are triggered by damaged endothelial cells or endotoxins what are the immune cytokines released?
Histamine
Leucotrienes
Prostaglandins
Chemotatic factors (positive chemotaxis)
TNF (alpha), interleukins (IL, 4, 5, 6, 13)
What are the 2 major area in mast cell reaction!
Degranulation and synthesis
Degranulation of mast cell produce 3 reactions
- Histamine for vascular effect
- Cytokines- TNF alpha and interleukim 4, 5, 6, 13 for inflammation
- Chemotatic factors to attract neutrophils and eosinophils to start phagocytosis
What is the function of histamine in innate immunity
- Vasodilation, by rapid constriction of smooth muscles, and dilation of post capillary venules causing increase blood flow to micro circulation
- Increase vascular permeability
Increase adherence of leukocytes to endothelium - Affect binding sites H1 and H2 on target cell surface
What’s the function of chemotatic factors in Degranulation of mast cells
Attract neutrophils and eosinophils to start phagocytosis process
What is the function of cytokines in mast cell Degranulation?
Cytokines - TNF alpha and IL 4, 5, 6, 13 Tiggers overall inflammation process. Call for phagocytize cells and plasma to manage pathogen and for healing
Mast cell synthesis involves what?
Damaged epithelial or tissues has phospholipid on surface which need to be broken down for repair by enzyme - phospholypase A2 which into breaks down arachidonic acid and platelet activating factors.
Arachidonic acid is broken down into 2 enzymes Lopo- oxygenase and cyclo oxygenase. Cyclo-oxygenase produce leukotrienes which has vascular effects and lipooxigynase produce prostaglandin which has vascular effect and pain
Arachidonic acid is broke down into 2 enzymes what are they?
Lopo- oxygenase (LPO) and cyclooxygenase (COX1 or COX2)
In mast cell synthesis, Phospholipase A2 breakdown phospholipid to what?
Arachidonic acid and platelet activating factors
What is the role of platelet activating factor in mast cell synthesis?
1 Vascular effects- Increase vascular permeability by relaxing smooth muscles and creating gaps in the cells lining the internal vasculature
2 platelet activation for clotting
Cyclooxygenase breaks arachidonic acid into what? And what’s the function of the product?
Prostaglandin
Function:
Contribute to vascular permeability
Pain
Neutrophil chemotaxis
Lipooxygenase breakdown arachidonic acid into what? And what is the function of the product?
Leukotrienes
Function
Vascular effect- leukotrienes impact smooth muscles, and increase vascular permeability by contracting the endothelial cells in similar way to platelet activating factors and histamines
Corticosteroids work by what?
Inhibiting phospholipase
NSAIDs mechanism of action is what?
Inhibits COX from producing prostaglandin
Mast cell histamines attach to what receptors!
H1 rectepor or H2 receptor
What is inflammation?
Reaction to tissue damage or invasion by microorganisms
What is the function of inflammation?
To manage invading organisms, clean up debris and initiate healing
What are the 4 characteristics of inflammation?
- It occur in tissues with good blood supply
- Vascular response(humoral response)
- Activated rapidly within seconds of cellular damage
- Include cellular and chemical reactions at vascular and interstitial levels.
It is non specific and antibodies are not involved at the onset
H1 rector activate what?
Smooth muscles cells and epithelial cells
What is the effect of Binding of Histamine to H1 receptor on smooth muscles and endothelial cells?
Contraction or vasodilation
Contraction ( retraction at endothelial junctions)
What is the effect of Histamine binding to H1 receptors on neutrophil/mast cells?
Neutrophils = Increase chemotaxis Mast cells = prostaglandin synthesis
Binding of Histamine to H1 receptor causes what
Cell activation of target cells - smooth muscle cell endothelial cell, neutrophil and mast cell.
Binding of Histamine to H2 receptor causes what?
Cell deactivation resulting in decrease leukocytes, eosinophil, neutrophil and mast cell
What is the effect of histamine binding to H2
Decrease lymphocyte and eosinophils activity
Decrease neutrophil chemotaxis
Decreased mast cell Degranulation
H1 receptor blockers/antagonist are?
Antihistamines used for allergic immune reactions
H2 receptor blockers/antagonist examples are
Famotidine (Pepcid)
Ranitidine (Zantac)
They plug H2 receptor causing decrease in gastric acid in stomach lining.
They are used to treat acid reflux and peptic ulcer
What we the plasma protein systems in inflammatory response
Complement system
Clotting system
Kinin system
True or false: mast cell reactions takes place same time as plasma protein system reactions
True
What’s the other name for Factor XII
Hageman factor
In the Kinin system, vascular endothelial damage activate what?
Hageman factor (factor XIIa which triggers clotting and Kinin system
What’s function of prekallikrein also known as factor XIIa
Activate kinin system
Prekallikrein (Factor XIIa) is used to produce what?
Kallikrien and kininogen
Kininogen is a precursor for what?
Bradykinin
What is the function of bradykinin
- Vasodilation
- Smooth muscle contraction and increase permeability
- Act with prostaglandins to induce pain
Clotting system is triggered by what?
Tissue injury/ infection
Collagen
Proteinase
Kallikrein
Plasmin
Bacterial endotoxins
What is the purpose of clotting cascade
Plug formation and to stop bleeding
Trap microorganisms and prevent spread
Framework to form repair and healing
In the clotting system of inflammatory response the fibrinopeptide do what?
Fibeinopeptides are Chemotatic, migration of neutrophils and
Increase vessel permeability
What is the function of fibrinogen in the inflammatory response?
1 Produce fibrin for blood clot
2. Release fibrinopeptides which cause migration of leukocytes(neutrophils) and increase permeability
Fibrinogen can enhance bradykinin formed from Kinin system, true or false
True
What are the 2 pathways is clotting cascade?
Intrinsic and extrinsic pathways
The extrinsic pathway is triggered by what?
Damage to the endothelial cells in the blood vessels triggers Tissue factor(TF) thromboplastin - extrinsic pathway and trigger factor VIIa
What triggers the intrinsic pathway?
Damage to the full vessel triggers contact activation( intrinsic pathway) and triggers Hageman factor (factor XII to XIIa or prekallikrein)
Both intrinsic and extrinsic pathway trigger what?
Both pathways converge at Factor Xa which is activated in to fibrin that polymerizes into fibrin clot
What does fibrinogen trigger in the clotting cascade
Fibrinogen triggers fibrinopeptide, Chemotatic (neutrophil) and vascular permeability and enhance bradykinin formed from Kinin system
What is the deference between monocytes and macrophages?
They are the same cell.
Inside vasculature it’s called monocytes
When it squeezes through gap and fall into interstitial space, it’s call macrophages
What is margination or pavementing?
When both leukocytes and endothelial cells begin expressing molecules (selectins and intergrins) that increase adhesion or stickiness causing leukocytes to adhere more avidly to the endothelial cells in the walls of the capillaries or venules
What is margination and pavementing?
P selectins encourages and captures plasma cells ( specifically WBC/granulocytes) that is needed in interstitial space for repair and cleanup via phagocytosis
What are the examples of phagocytic cells
Neutrophils, monocytes/macrophages, dendritic cells
What is DIAPIDESIS or emigration?
Squeeze through endothelial gaps via PECAMs(platelet endothelial cell adhesion molecules) and move into the extra vascular space
Chemotaxis or directed migration
Once interstitial space key Chemotactic factors signal to neutrophil/macrophages to move towards the area of injury/pathogen to killing/healing
What’s the process of heat, erythema, edema and pain observed in inflammatory response
- Once mast cell (histamine, leukotrienes, prostaglandins), clotting system, kinin system and complement systems are triggered
- Smooth muscle relax causing vasodilation and increase blood flow to the area causing (erythema and heat).
3.Epithelial gap allow Permeability which allow plasma fluid (fluid, WBC, RBC etc) to leak into interstitial space = edema & joint immobility.
- Increased pressure from fluid in interstitial space applies pressure on the nociceptor (sensory neurons) which activate pain
- Bradykinin (kinin system) and prostaglandin (mast cells) triggers the nociocpetor which activates them to produce pain
What cause erythema and heat in inflammatory response
Relaxation of smooth muscles which results in vasodilation and increase blood flow to the area
What causes edema in inflammatory response
Endothelial gaps allow permeability which allow plasma ( fluids, WBC, RBC) the leak through the interstitial space
What are the 2 ways pain occur in inflammatory response
- Increase pressure from interstitial space apply pressure to nociceptor which activate them to produce pain
 - Bradykinin (Kinin system) and prostaglandin (mast cell) tiggers, the nociceptor which activate them to produce paint
Fever in inflammatory response is caused by what?
Cytokines IL1, IL6, TNF alpha, prostaglandin, endogenous pyrogens acts on hypothalamus which produce prostaglandin E2 (PGE2) increase the body temperature to kill pathogens and increase metabolism
What the function of Prostaglandin E2 (PGE2)
Increase body temperature to kill pathogens and increase metabolism to increase healing
Leukocytosis
Increase in WBC and left shift ratio of immature neutrophils are more than mature neutrophils due to demand on bone marrow to produce more
Systemic manifestation of inflammation - liver
Plasma protein synthesis- increased synthesis of plasma protein IL1 and induction of IL6 stimulate the liver cell production of active phase reactant
Active phase reactants are what?
The are pro/anti inflammatory.
They are produced in the liver by increase synthesis of plasma protein IL1 and induction of IL 6
C reactive protein (CRP) is specific for what?
Inflammation
CRP is produced in the liver
Systemic manifestation of inflammatory response - fibrinogen
Fibrinogen is associated with adhesion among erythrocytes and increased sedimentation rate ESR.
ERS is indication for inflammation but non specific for inflammation
What are the 2 biggest phagocytes
Neutrophils and macrophages
Difference between neutrophils and macrophages
Neutrophils are members of the WBC (granulocyte)
They arrive early 6-12hrs after initial injury
They are sensitive to acidic environment-short life
Mature cell is unable to divide
Found in purulent exudates
They do not activate the adaptive immune system
Macrophage are antigen presenting cells
True or false
True
Macrophage characteristic in inflammatory response
They a monocytes, when they migrate into tissue for inflammation, they are called macrophages
They appear 24hrs to 3-7 days after neutrophils
They are able to divide
They are attracted by macrophage Chemotatic factors released by neutrophils
They play key role in activation of adaptive immunity- they are antigen presenting cells
Which are the antigen presenting cells
Macrophages and dendritic cells
What is left shift?
Ratio of immature form of neutrophils such as band cells, metamyelocytes and occasionally myelocytes are present on relatively greater then normal propoetion
One of the major link between the innate and acquired immunity is what?
Dendritic cells
What is the location of dendritic cells
Peripheral organs and skin
Dendritic cells migrate through lymphatic vessels to where
Lymphoid tissues (lymph nodes)
Dentritic cells interact with T lymphocytes to generate what?
Acquired immunity
Function of dendritic cells
Primary phagocytize cells - antigen presenting cell
Eosinophils function
- Primary defence against parasites.
Occurs in collaboration with specific antibodies produced by acquired immune system - Help regulate vascular mediators released from mast cells
- They are seen in hypersensitivity
Basophils
Important sources of the cytokine IL4 which is key regulator of adaptive immune system
What are the 5 steps to phagocytosis?
- Recognition and adhesion to target
2 pseudopods engulfment ( ingestion or endocytosis) - Formation of phagosome
- Fusion of a phagosome with lysosomal hydrolytic enzymes
- Destruction occur through O2 dependent or independent mechanism
What are the hydrolytic enzymes for phagocytosis
Protease
Nuclease
Lipase
Glucosidase
Recognition and adherence to target in phagocytosis occurs by what process
- Pathogens- pattens recognition receptor
- Opsonization - tight glue for affinity adherence through antibodies and C3b produced by complement system
Complement is activated by which 3 pathways?
Classic pathway
Alternate pathway
Lectin pathway
What’s the complement classic pathway
Antibody binds to C1 and activates C3 and C5
Alternate pathway
Triggered by Substance in surface is bacteria and fungi then use complexes to trigger complement system.
No need for antibodies
Lectin pathway triggered by plasma proteins that recognize carbohydrate patterns on the surface of pathogens (bacteria, virus, protozoa, and fungi,) bind to these polysaccharides to activate the complement system.
Pathogen nothing nothing but alternate pathway, can be identified by Lectin pathway
Lectin pathway
What is the function of complement C3b
Opsionin(C3b) - coat bacteria to increase phagocytosis, neutrophils and macrophages
What is the function of C5a
Chemotatic C5a- chemotaxis/directional migration
What is the function of anaphylotoxin- C3a, C5a?
Rapid degranulation of mast cells, vasodilation, and capillary permeability
Cell lysis(C5b, C6-9, MAC) activation of these complements components that create pores in the outer membrane of cells/ bacteria, permit, water and cause cell death
Classical pathway is activated by what!
Antigen antibody
What triggers the classical pathway
C1 activating C3 and C5
What triggers the alternate pathway
Substances on the surface of the bacterial and fungi
Does alternate pathway require antibodies
No
What triggers the lectin pathway
Plasma proteins that recognizes carbohydrates pattern on the pathogens
Pathogens not noted by the alternate pathway can be identified by lectin pathway- true or false
True
What is opsonin
Coat bacteria to increase phagocytosis- neutrophils/macrophages
What complement is responsible for opsonin
C3b
Complement that play a role in chemotaxis/directional migration is what?
C5a
What is anaphylotoxin
Fragmentation of C3a and C5a resulting Rapid Degranulation of mast cells
What is the result of anaphylotoxin
Vasodilation and capillary permeability
What complement is responsible for anaphylotoxin
C3a and C5a
Cell lysis by complement is caused by which complements
C5b, C6-9
Cytokines responsible for vasodilations
Prostaglandin, histamine
Cytokines responsible for vascular permeability
Histamine, bradykinin leukotrienes
Cytokines involved with pain
Prostaglandins and bradykinin
Fever in inflammatory response is caused by
IL1, IL 6 TNF alpha and prostaglandins
Antimicrobial peptides are?
Cathelicidins,
defensins,
collectins
mannose-binding lectin
Chemical barriers in innate immunity are what?
Saliva, tears, earwax, sweat, mucus
Antimicrobial peptide
Perspiration tears and saliva contain which enzyme that help attack cell wall of gram negative bacteria
Lysozyme
Sebaceous gland contain —— that kill bacteria and fungi
Fatty acids and lactic acid
Antimicrobial peptide
Cathelicidins- attack bacteria that have cholesterol free cell membranes
Defensin- kill pathogens in GI, respiratory urinary and skin
Collectins
What are the 4 xtics of inflammatory response
Occur in tissue with blood supply )vascularized)
Activated rapidly within seconds after damage occur
Depend on both cellular and chemical components
Non specific- takes place same way regardless of rule of stimuli
What causes erythema and warmth in inflammation
Vasodilation and increased blood flow
What causes edema in inflammatory response?
Increased vascular permeability with leakage is plasma from vessels lead to edema
What are the major local changes in the inflammatory response?
- Vasodilation and increase blood flow(erythema and warmth)
- Leakage of plasma proteins (edema)
- Leukocyte (neutrophils) move from the vessel into injured site
What is the plasma systems?
Complement
Clotting
Kinin
What are benefits of inflammation?
1 prevent infection and further damage by invading orgs
2. Limit and control inflammation process - plasma proteins, plasma enzymes and cell prevent inflammation from affecting other cell
3 interact with adaptive immune response
4 prepare injured area for healing
Where are dendritic cells located
1 they are primary phagocytes located in peripheral organ and skin
Function of dendritic cells
Migrate through lymph node to interact with T cells to generate acquired immune response
They guide development of Tcell(helper T cells) and co-ordinate development of functional B and T cells
What are the 3 processes of phagocytosis
- Adhesion and dipedesis
- Tissue invasion by chemotaxis
- Phagocytosis
What is the role/ function of inflammation
To manage invading organisms and clean up debris
To initiate repair and healing
What is tissue endothelial cells?
Walls and intercellular space and content e.g nucleus
What is interstitial space?
Free and open space between tissue endothelial cell and vasculature
Vasculature/capillary space are what?
Walls with intravascular space and content e.g plasma, RBC and WBC
What are the 2 most important phagocytes
Neutrophils
Macrophages
In inflammation process what is margination/pavementing
Increase adherence of neutrophils to endothelium leading to accumulation along vessels wall is call margination/pavementing
Increase adherence of neutrophils to endothelium leading to accumulation along vessels wall is call what?
margination/pavementing
When the neutrophil exit the blood at site of endothelial retraction is called what?
Diapedesis
By what means does neutrophil exit blood through site of endothelial retraction?
Diapedesis
Chemotaxis occur when?
Neutrophils detect Chemotatic gradients the rough surface receptors, migrate towards high concentration of the factor and high concentrations of Chemotatic factors at the inflammation site mobilizes the neutrophils
Phagocytes trap and engulf bacteria using what?
PRRs (pattern recognition receptors)
Damaged endothelial cells and:pathogens release what?
Endotoxins
What’s one of the most important cellular activators of inflammation response?
Mast cell activation
Which cell probably function like mast cells
Basophils
Corticosteroids work by what?
Inhibiting phospholipases
NSAID mechanism of action is what?
Inhibit cyclooxygenase from producing prostaglandins
Acetaminophen works by what mechanism?
Blocks a variant of cyclooxygenase
What triggers mast cells
Damaged endothelial/ invading pathogens
Mast cell Degranulation result in what?
Production of
Histamine- vasodilation/contraction of vasculature creating gaps
Cytokines: TNF alpha, IL 4, 5, 6, 13- trigger oval inflammations and call for backup in vasculature
Chemotatic factors- call for neutrophils and eosinophils. Neutrophil start phagocytosis process
Role of histamine in inflammatory response
Increase vascular permeability
Contraction of smooth muscles
Binding of Histamine to H1 receptor results in what?
Promote inflammation
Binding of neutrophils to H1 receptor
Increase neutrophil chemotaxis
Effect of histamine on H1
Contraction
Cont action (retraction at endothelial junction)
Increased chemotaxis
Prostaglandin synthesis
Binding of histamine to H2 cause cell inactivation results in what
Decrease lymphocytes and eosinophil activity
Decrease chemitaxis of neutrophil
Decrease Degranulation
1st and second generation antihistamine block where?
H1 receptors
Antacids (
Famotidine- Pepcid
Ranitidine -Zantac block with receptor
H2- receptor blockers or antagonist
Mast cell synthesis result in what
Damaged epithelial/tissues has phospholipid that need to be broken down
Phospholipase A2 cleave arachidonic acid into cyclooxygenase and 5 lipoxygenase and tigger platelet activating factor for clot formation
5-lipooxigenase breaks down arachidonic acid into
Leukotrienes
Cyclooxygenase breaks arachidonic acid down to form
Prostaglandins
What’s function of protaglandins
Increase vascular permeability
Neutrophils chemotaxis
Pain
Activation of mast cell result in synthesis of what mediators of inflammation?
Leukotrienes
Protaglandins
Platelet activating factor
Acetylsalicylic acid(Asprin) and NSAID inhibit what
COX1 and COX2
But inhibition-of COX1 cause GI toxicity
Célèbrex or celecoxib selectively inhibit COX2
What triggers Kinin system?
Damage to vascular endothelial activate Hageman factor Factor 12 to 12a trigger clotting and Kinin system
What activate Kinin system?
Perikallikinin - factor 12 a
Prekallikrein activation of the Kinin system result in what?
Formation of kallikrien and kininogen
Kininogene activate what?
Bradykinin
Function of bradykinin - similar to histamine - increase vascular permeability
Stimulate nerve ending causing pain
Factor 12 a produced by clotting system activate what
Kinin system
Clotting system activation?
Extrinsic pathway activated by tissue factor and intrinsic (contact activation) pathway lead to factor 10 and thrombin
Thrombin activate proteolytic enzymes activate fibrinogen to fibrin and fibrinopeptide
Fibrin polymerizes to form clot
Fibrinopeptide which are highly chemotactic factors and increase vascular permeability
Extravascular molecule connect to the vascular endothelial trigger granules to create what type of endothelial selectins
P selectin and intergrins
What are p selectin and intergrins
Key receptors on the surface of cells inside the vascular and plasma flow
What is the role of the p selectin
Encourages and captures plasma cells - WBC/ granulocytes that are needed in the interstitial space for repair and clean up by phagocytosis, this process is called margination/pavementing
The process called margination/pavementing
Process where P selectins Encourages and captures plasma cells - WBC/ granulocytes that are needed in the interstitial space for repair and clean up by phagocytosis, this process is called margination/pavementing
What are the phagocytic cells involved in pavementing/margination
Neutrophils, monocytes/marcrophages dendritic cells
Diapedesis or emigration is what?
Squeezing through the endothelial gaps via PECAMs( platelets endothelial cell adhesion molecules) and move into extra vascular space
Chemotaxis or directional migration is what?
Chemotatic signalling to neutrophils/macrophages to move towards area of injury/pathogen to kill/ heal
Mast cell(histamine, leukotrienes, prostaglandin) clotting, Kinin and complement system triggers what?
1 smooth muscle relaxation = vasodilation = increased blood flow to area = erythema and heat
- Endothelial gaps= increased permeability which allows (fluid, WBC, RBC red) to lease into interstitial space = edema, joint immobility
- Increase pressure from interstitial space on nociceptor = pain
- Bradykinin (Kinin system) and postaglandin (mast cell) trigger nociceptor cause pain
Fever in inflammatory reaction is caused by what?
(Cytokines IL 1, IL6 TNF alpha protaglandins) endogenous pyrogens
