[DISCUSSION] MODULE 2 UNIT 1 Flashcards by Arriane Camacho

Innate immunity

NATURAL IMMUNITY

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Ability of the individual to resist infection

NATURAL IMMUNITY

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Normally present body functions

Ability of the individual to resist infection

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NATURAL IMMUNITY is Considered:

• Non adaptive
• Nonspecific

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Same for all pathogens or foreign substances

NATURAL IMMUNITY

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• No prior exposure is required

NATURAL IMMUNITY

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• No prior exposure is required
• Response does not change = same magnitude every time

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NATURAL IMMUNITY CHARACTERISTICS:

Components are preformed
Standardized
Without memory
Nonspecific

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NATURAL DEFENSE SYSTEM
• TWO PARTS:

• External defense system
• Internal defense system

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EXTERNAL DEFENSE SYSTEM
• Composed of:

Anatomic barriers
Physiologic barriers

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• Prevent most infectious agents from entering the body

Anatomic barriers

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Anatomic barriers Examples:

• Intact skin
• Mucous membranes

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Physiologic barriers

• Temperature
• Low pH
• Physiologic functions → coughing, sneezing, vomiting, diarrhea,
shedding of cells
• Oxygen tension
• Age
• Hormonal balance
• Chemical mediators → lysozyme, interferon, complement, toll-like
receptors, collectins

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Physiologic functions

coughing, sneezing, vomiting, diarrhea,
shedding of cells

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Chemical mediators

lysozyme, interferon, complement, toll-like
receptors, collectins

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• Cleaves bacterial cell wall

• Lysozyme

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• Induces antiviral state in uninfected cells

• Interferon

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• Lyses microorganisms or facilitates phagocytosis

• Complement

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• Recognize microbial molecules

• Toll-like receptors

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• Signal cell to secrete immunostimulatory cytokines

• Toll-like receptors

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→ disrupt cell wall of pathogen

• Collectins

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• Second line of defense

INTERNAL DEFENSE SYSTEM

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• Cells and soluble factors

INTERNAL DEFENSE SYSTEM

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• Designed to recognize molecules that are unique to
infectious organisms

INTERNAL DEFENSE SYSTEM

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• Phagocytosis

INTERNAL DEFENSE SYSTEM: Second line of defense

INTERNAL DEFENSE SYSTEM Designed to recognize molecules that are unique to infectious organisms

mannose found in microorganisms

enhanced by soluble factors called acute phase reactants

Phagocytosis

• Ability to recognize a given class of molecules

PATTERN RECOGNITION

• Ability to immediately recognize and combat invaders displaying such molecules is a strong feature of innate immunity

PATTERN RECOGNITION

Molecules with pattern recognition

PATTERN RECOGNITION

bind PAMPs

PRRs

• Molecules with pattern recognition • May be soluble

complement, lysozyme

• Molecules with pattern recognition • Cell-associated receptors

toll-like receptors (TLR’s)

• normal serum constituents

ACUTE PHASE REACTANTS

• increase rapidly by at least 25% due to infection, injury, or trauma to the tissues

ACUTE PHASE REACTANTS

• produced primarily by hepatocytes (liver parenchymal cells)

ACUTE PHASE REACTANTS

• within 12 to 24 hours

ACUTE PHASE REACTANTS

• within 12 to 24 hours • in response to an increase in certain intercellular signaling polypeptides called

cytokines

IL-1β, IL-6, TNF-α

• most abundant of the coagulation factors in plasma

Fibrinogen

• forms the fibrin clot

Fibrinogen

• dimer with a molecular weight of 340,000 daltons

Fibrinogen

Fibrinogen Normal levels range from

100 to 400 mg/dL

• Promote healing process

Fibrinogen

• Prevents spread of microorganisms

Fibrinogen

• alpha2 -globulin with a molecular weight of 100,000 daltons

Haptoglobin

• bind irreversibly to free hemoglobin released by intravascular hemolysis

Haptoglobin

Preventing loss of free hemoglobin

Haptoglobin bind irreversibly to free hemoglobin released by intravascular hemolysis

Haptoglobin • Normal plasma concentrations range from

40 to 290 mg/dL

Haptoglobin plays an important role in:

• protecting the kidney from damage • preventing the loss of iron by urinary excretion

Haptoglobin Most important function

to provide protection against oxidative damage mediated by free hemoglobin

• single polypeptide chain with a MW of 132,000 daltons

Ceruloplasmin

• Principal copper transporting protein

Ceruloplasmin

• Essential to collagen formation & the extracellular cross-linking and maturation of collagen and elastin

Ceruloplasmin

• Protect the matrix of healing tissue against superoxide ions

Ceruloplasmin

• Protease inhibitor

Alpha-2-macroglobulin

• Binds to proteolytic enzymes released from damaged tissues and from phagocytic cells

Alpha-2-macroglobulin

• Scavenger protease inhibitor that binds excess molecules that cannot be handled by the intended inhibitor

Alpha-2-macroglobulin

• homogeneous molecule with a MWof 118,000 daltons

C-Reactive protein (CRP)

• increases rapidly within 4 to 6 hours following infection, surgery, or other trauma to the body

C-Reactive protein (CRP)

C-reactive protein (CRP) • Capable of:

1. Opsonization 2. Agglutination 3. Precipitation 4. Activation of complement by the classical pathway

• Apolipoprotein synthesized in the liver (30mg/ml)

Serum amyloid A

• Precursor to amyloid deposition

Serum amyloid A

• Reported to cause adhesion and chemotaxis of phagocytic cells and lymphocytes

Serum amyloid A

• Bind to lysosomal enzymes released during inflammation

Serum amyloid A

• Increased levels found to be a risk factor for heart attack in women

Serum amyloid A

• Can increase almost 1000-fold

Serum amyloid A

• Serum proteins that are normally present

Complement

• Mediation of inflammation

Complement

Complement Major functions:

1. Opsonization 2. Chemotaxis 3. Lysis of cells

Trimer that acts as an opsonin that is Ca-dependent

Mannose-binding protein

Recognize foreign carbohydrates such as mannose and a number of sugars

Mannose-binding protein

Mannose-binding protein Recognize foreign carbohydrates such as mannose and a number of sugars present in:

• Bacteria • Some yeasts • Viruses • Several parasites

• Widely distributed in mucosal surfaces throughout the body

Mannose-binding protein

• Binding activates complement cascade and helps to promote phagocytosis

Mannose-binding protein

• High carbohydrate content and MW 44 kD

Alpha-1 acid glycoprotein

• Exact function not known

Alpha-1 acid glycoprotein

• Binds progesterone and may be important in its transport or metabolism

Alpha-1 acid glycoprotein

• Able to bind drugs such as lidocaine, keeping them in an inactive circulating pool

Alpha-1 acid glycoprotein

CELLULAR DEFENSE MECHANISMS

• Neutrophils • Eosinophils • Basophils • Mast cells • Monocytes • Tissue macrophages • Dendritic cells

• Polymorphonuclear neutrophilic leukocyte (PMN)

NEUTROPHILS

• 50 – 70% of the total peripheral wbcs

NEUTROPHILS

• Diameter: 10 – 15 mm

NEUTROPHILS

• Nucleus: 2-5 segments

NEUTROPHILS

• Large number of neutral staining granules

NEUTROPHILS

NEUTROPHILS granules

• Primary granules • Secondary granules

NEUTROPHILS Primary granules (azurophilic) contain:

• Myeloperoxidase • Lysozyme • Proteinase 3 • Elastase • Cathepsin G • Lysosomal acid hydrolases • Defensins

Small proteins that have antibacterial activity

Defensins

NEUTROPHILS Secondary (specific) granules contain:

• Collagenase • Lysozyme • Lactoferrin • Reduced NADPH oxidase • Alkaline phosphatase

NEUTROPHILS Tertiary granules contain:

gelatinase & plasminogen activators

• Normally, half of the total neutrophil population is found in a marginating pool on the walls of blood vessels

NEUTROPHILS

• The rest circulate freely for approx. 6 – 10 hours

NEUTROPHILS

• Capable of moving from the circulating blood to the tissues

NEUTROPHILS

movement through blood vessel walls

DIAPEDESIS→

• Margination & adherence to the vessel wall

DIAPEDESIS

• Formation of pseudopods, squeeze through junctions of the endothelial cells

DIAPEDESIS

• Wander randomly through the tissue or be attracted to a specific area by chemotactic factors

DIAPEDESIS

chemical messengers that cause migration of cells in a particular direction

Chemotaxins

5 days

Once in tissues, neutrophils’ life span: about

5 days

Once in tissues, neutrophils’ life span: about 5 days

12 to 16 mm

EOSINOPHILS

1 – 3%

EOSINOPHILS

EOSINOPHILS Numbers increased during:

• Allergic reaction • Response to many parasitic infections

Eosinophils Nucleus

• Bilobed or ellipsoidal • Eccentrically located

• Take up the acid eosin dye

EOSINOPHILS

Cytoplasm is filled with large orange to reddish-orange granules

EOSINOPHILS

EOSINOPHILS granules

• Acid phosphatase • b-glucuronidase • Arylsulfatase • Phospholipase • Peroxidase • Histaminase • Aminopeptidase • Ribonuclease

Capable of phagocytosis but much less efficient than neutrophils

EOSINOPHILS

EOSINOPHIL phagocytosis

• Smaller numbers • Lack of digestive enzymes

EOSINOPHILS MOST IMPORTANT ROLE:

• Neutralizing basophil and mast cell products • Killing of certain parasites

ADCC

Eosinophils

• Less than 1% of all circulating wbcs

BASOPHILS

• Smallest of the granulocytes

BASOPHILS

• 10 to 14 mm in diameter

BASOPHILS

• Contain coarse densely staining deep bluish purple granules that often obscure the nucleus

BASOPHILS

• Constituents of granules: histamine, eosinophil chemotactic factor of anaphylaxis (ECF-A), and a small amount of heparin

BASOPHILS

• Induce and maintain immediate hypersensitivity reactions

BASOPHILS

BASOPHILS vasoactive amine that contracts smooth muscle

HISTAMINE

BASOPHILS anticoagulant

HEPARIN

stream• Granules: lack hydrolytic enzymes although peroxidase is present

BASOPHILS

• Capable of phagocytosis

BASOPHILS

• Only present for a few hours in the blood

BASOPHILS

• Resemble basophils

MAST CELLS

• May share a common stem cell precursor

MAST CELLS

• Larger with a small round nucleus and more granules than the basophil

MAST CELLS

• Found in connective tissue, especially around blood and lymphatic vessels

MAST CELLS

• Long life span

MAST CELLS

• May be capable of proliferation in the tissues

MAST CELLS

• The enzyme content of the granules distinguish them from basophils because they contain acid phosphatase, alkaline phosphatase, protease & serotonin

MAST CELLS

• Play a role in hypersensitivity reactions

MAST CELLS

• Largest cells in the peripheral blood

MONOCYTES

• Diameter: 12 to 22 mm, ave. 18 mm

MONOCYTES

• Irregularly folded or horseshoe-shaped nucleus occupying almost ½ of the entire cell’s volume

MONOCYTES

• Abundant cytoplasm stains a dull grayish-blue with a ground glass appearance (fine granules)

MONOCYTES

One type of granules contain peroxidase, ACP, arylsulfatase (similar to neutrophils)

MONOCYTES

• Other type of granules contain b-glucuronidase, lysozyme, lipase, but NO alkaline phosphatase

MONOCYTES

• Make up 4 to 10% of total circulating wbc

MONOCYTES

• Stay in the peripheral blood for up to 70 hours then migrate to the tissue and become macrophages

MONOCYTES

• All tissue macrophages arise from monocytes

TISSUE MACROPHAGES

• Transition from monocyte to macrophage is characterized by progressive cellular enlargement to between 25 and 50 mm

TISSUE MACROPHAGES

• Increase in ER, lysosomes, & mitochondria

TISSUE MACROPHAGES

• Unlike monocytes, macrophages contain NO PEROXIDASE AT ALL

TISSUE MACROPHAGES

Lung

Alveolar macrophages

Liver

Kupffer cells

Brain

Microglial cells

Connective tissue

Histiocytes

Kidney

Mesangial cells

Bone

Osteoclast

Spleen

Littoral cells

Joints

Synovial A cells

• Life span: months

TISSUE MACROPHAGES

TISSUE MACROPHAGES Role →

initiating and regulating IR

TISSUE MACROPHAGES Functions:

1. Microbial killing 2. Tumoricidal activity 3. Killing of intracellular parasites 4. Phagocytosis 5. Secretion of cell mediators 6. Antigen presentation

• Covered with long membranous extensions making them resemble nerve cell dendrites

DENDRITIC CELLS

DENDRITIC CELLS Main function:

• Phagocytose antigen and present it to helper T lymphocytes • Believed to be descendants of the myeloid line • Classified according to tissue location • E.g., Langerhans’ cells → skin and mucous

DENDRITIC CELLS skin and mucous membranes

Langerhans’ cells

▪Interstitial dendritic cells

heart, lungs, kidney, GIT

Toxins released via phagocytosis

Leukocidin Listeriolysin Streptolysin

M. bacterium leptae and MBT contains this material that does not fuse with lysosome

Pristiophorus vacuole

Catalase

Staphylococcus aureus

▪Interdigitating dendritic cells

T lymphocyte areas of the secondary lymphoid tissue and the thymus

▪After capturing Ag in the tissue by phagocytosis or endocytosis,

they migrate to the blood or the lymphoid organs & present Ag

▪Most potent phagocytic cell in the tissue

DENDRITIC CELLS

also known as large granular lymphocytes (LGL)

NK (Natural Killer) Cells

identified by the presence of CD56 and CD16 and a lack of CD3 cell surface markers

NK (Natural Killer) Cells

capable of killing virus-infected and malignant target cells

NK (Natural Killer) Cells

upon exposure to IL-2 and IFN-gamma, NK cells become lymphokine-activated killer (LAK) cells

NK (Natural Killer) Cells

capable of killing malignant cells

lymphokine-activated killer (LAK) cells

not a morphologically distinct type of cell

K (Killer cells)

• any cell that mediates antibody-dependent cellular cytotoxicity (ADCC)

K (Killer cells)

• have on their surface an Fc receptor for antibody and thus they can recognize, bind and kill target cells coated with antibody

K (Killer cells)

Killer cells which have Fc receptors include (?) which have an Fc receptor for IgG antibodies and eosinophils which have an Fc receptor for IgE antibodies

NK, LAK, and macrophages

Additional mechanism recently discovered on certain cells, enhancing natural immunity

TOLL-LIKE RECEPTORS (TLRs)

→ a protein originally discovered in the fruit fly

Toll

Highest concentration occurs on monocytes, macrophages and neutrophils

TOLL-LIKE RECEPTORS (TLRs)

→ recognizes techoic acid and peptidoglycan in g+ bacteria

TLR2

→ recognizes LPS

TLR4

Monocytes, macrophages, endothelial cells, epithelial cells

Interleukin 1 (IL-1)

Vasculature (inflammation); hypothalamus (fever); liver (induction of acute phase proteins)

Interleukin 1 (IL-1)

Macrophages

Tumor Necrosis Factor-alpha (TNF-alpha) & Interferon alpha (IFN-alpha)

Vasculature (inflammation); liver (induction of acute phase proteins); loss of muscle, body fat (cachexia); induction of death in many cell types; neutrophil activation

Tumor Necrosis Factor-alpha (TNF-alpha)

Macrophages, dendritic cells

Interleukin 12 (IL-12)

NK cells; influences adaptive inmmunity (promotes TH1 subset)

Interleukin 12 (IL-12)

Macrophages, endothelial cells

Interleukin 6 (IL-6)

Liver (induces acute phase proteins); influences adaptive immunity (proliferation and antibody secretion of B cell lineage

Interleukin 6 (IL-6)

This is a family of molecules

Interferon alpha (IFN-alpha)

Induces an antiviral state in most nucleated cells; increases MHC class I expression; activates NK cells

Interferon alpha (IFN-alpha) & Interferon beta (IFN-beta)

Fibroblasts

Interferon beta (IFN-beta)

Involves engulfment and destruction of pathogens and particulate matter by cells of the mononuclear phagocyte system

PHAGOCYTOSIS

Macrophages release monokines like (?)

IL-1, IL-6 and TNFa

PHAGOCYTES:

• Fixed • Wandering

• CHARACTERISTICS OF PHAGOCYTIC PROCESS:

1. AMOEBOID MOVEMENT 2. CHEMOTAXIS

• Cell migration occurs in and out of blood vessels, and throughout the tissues

AMOEBOID MOVEMENT

• Movement of cells or organisms toward objects in response to chemical agents called CHEMOTAXINS

CHEMOTAXIS

→ cell emigration from capillaries

Diapedesis

modified a.a. present in the a.a. termini of proteins of most types of bacteria

Microbial/ bacterial products: N-formylmethionine residues

Attractants of phagocytes/chemotactic agents:

• Microbial/ bacterial products: N-formylmethionine residues • Tissue components (leukotriene) • Activated intermediates of the fibrinolysis, kallikrein, and complement systems

Once a particle is close enough to the target, the cells engulf it

PHAGOCYTOSIS

STEPS IN PHAGOCYTOSIS

1. Physical contact between the white cell and the foreign particle 2. Formation of a phagosome 3. Fusion with cytoplasmic granules to form a phagolysosome 4. Digestion and release of debris to the outside

• Digestion of engulfed material inside the phagolysosome

CYTOPEPSIS

• Contents of the lysosome granules are important in breaking down ingested material and in killing microorganisms

CYTOPEPSIS

TWO MECHANISMS FOR DESTROYING FOREIGN PARTICLES

1. Oxygen-independent mechanisms 2. Oxygen-dependent mechanisms

• Proteinases (hydrolytic enzymes) • Cationic proteins • Lysozyme • Lactoferrin

OXYGEN INDEPENDENT MECHANISMS

OXYGEN DEPENDENT MECHANISMS

• Myeloperoxidase • Hydrogen peroxide (H2O2) • Superoxide anion (O2– )

→ toxic peroxidation of microorganisms

Myeloperoxidase

→ oxygen in which one of the electrons has moved to an orbit of higher energy

Singlet oxygen (‘O2 )

→ a highly unstable oxidizing agent that reacts with most organic molecules it encounters

Hydroxyl radical (OH–)

increase in overall oxygen consumption by the neutrophil

RESPIRATORY BURST/ METABOLIC BURST

• METABOLIC EVENTS DURING PHAGOCYTOSIS • Accompanied by respiratory burst that involves the following:

1. Increase in oxygen consumption 2. Stimulation of HMP shunt activity 3. Increase in production of hydrogen peroxide 4. Superoxide anion production and singlet oxygen production

→ extremely toxic to bacteria and tissue; very unstable; quickly converted to H2O2 by SOD → catalase

Superoxide anion

The (?) combine and act synergistically

oxygen-dependent agents

→ Hypochlorite

Myeloperoxidase + H2O2 + Halide (I- or Cl -)

(?) is more antimicrobial than the three components alone

Hypochlorite

LIMITATIONS OF PHAGOCYTOSIS

1. Presence of capsules 2. Opsonization inhibited 3. Release of toxins 4. Phagolysosome formation inhibited 5. Able to escape into cytoplasm by lysing lysosomal membrane 6. Resistance to killing by producing anti-oxidants

PHAGOCYTOSIS • IMPORTANCE:

1. Destroy/ kill microorganisms 2. Disposal of damaged and dying cells 3. Suppression of the growth of spontaneously arising tumors 4. Processing of antigens 5. Removal of cancer cells 6. Removal of debris from repairing wounds 7. Removal of debris as embryonic tissues replace one another

• Process of enhancing phagocytosis via the presence of opsonins

OPSONIZATION

• Substances that promote phagocytosis

OPSONIZATION

• OPSONINS:

1. C3b split product of complement cascade 2. C5a and C5b67 → chemotactic factors that also aid in the clearance of foreign materials 3. Antibodies (phagocytes have a receptor for the Fc portion of IgG)

→ chemotactic factors that also aid in the clearance of foreign materials

C5a and C5b67

Antibodies (phagocytes have a receptor for the Fc portion of IgG)

• IgG1 and IgG3

→ gp that opsonizes & acts like glue to cause neutrophils and their targets to stick together

Fibronectin

→ derivatives of arachidonic acid

Leukotrienes

• Several kinds, not all act as opsonins

Leukotrienes

• LTBy is chemotactic

Leukotrienes

→ tetrapeptide split product of IgG that stimulates chemotactic and phagocytic activities

Tuftsin

• Complex series of non-specific soluble and cellular events

INFLAMMATION

• Promotes elimination of the foreign entity

INFLAMMATION

• Initiated by chemical mediators whenever phagocytosis alone fails to prevent infection or when tissues are injured

INFLAMMATION

INFLAMMATION Induced by:

pathogen attack, inert tissue injury, products of complement activation, or by cytokines released by innate or adaptive leukocytes that were activated elsewhere

Five cardinal signs/clinical symptoms: (Celsus)

1. Redness (rubor) 2. Swelling (tumor) 3. Heat (calor) 4. Pain (dolor) 5. Loss of function (functio laesa)(Galen)

• Major Events associated with inflammation:

1. Increased blood supply to the infected area 2. Increased capillary permeability caused by retraction of endothelial cells lining the vessels 3. Migration of white blood cells (mainly neutrophils) from the capillaries to the surrounding tissue 4. Migration of macrophages to the injured area

EVENTS OF INFLAMMATION

- Histamine released from mast cells - Inreased permeability of the vessels - Soluble mediators - Amplification - Coagulation system and fibrinolytic system

SIGNS OF INFLAMMATION

- Redness and heat - Swelling and pain

→ Cause dilation of the blood vessels & additional flow to affected area

Histamine released from mast cells

→Fluids to leak out to the tissues

Inreased permeability of the vessels

→Stimulation of the pain receptors (skin) by peptide mediators

Inreased permeability of the vessels

initiate and control the response

Soluble mediators

occurs through formation of clots

Amplification

involvement

Coagulation system and fibrinolytic system

→ vasodilation, increased vascular permeability, smooth muscle contraction, pain

Kinins (e.g., bradykinin)

→ activates macrophages (from NK cells)

IFNg

→ perpetuate the inflammatory response

TNF, IL-1, IL-6

→ from hepatocytes responding to TNF and IL-6; initiates complement cascade via C1 activation

CRP

MEDIATORS OF INFLAMMATION

1. Kinins (e.g., bradykinin) 2. IFNg 3. TNF, IL-1, IL-6 4. CRP 5. C3a & C5a → anaphylatoxin 6. C3b 7. Leukotrienes and prostaglandins 8. Serotonin (5-hydroxytryptamine)

→ provokes mast cell degranulation and consequent release of heparin and vasoactive amines (HISTAMINE) that induce Vasodilation increases vascular permeability

C3a & C5a → anaphylatoxin

opsonin

C3b

→ increase vasodilation and promote neutrophil chemotaxis

Leukotrienes and prostaglandins

→ vasodilation

Serotonin (5-hydroxytryptamine)

• Neutrophils • Macrophages

ACUTE INFLAMMATION

• Mobilized within 30 to 60 minutes after the injury

Neutrophils

• Neutrophil emigration lasts (?) hours

24 to 48

• Proportional to the chemotactic factors present in the area

Neutrophils

• Attempt to clear the area through phagocytosis

Macrophages

• Most cases: healing process is completed with a return of normal tissue structure

Macrophages

Migration occurs several hours later and peaks at (?) hours

16 to 48

• Prolonged inflammatory response

CHRONIC INFLAMMATION

• Tissue damage and loss of function may result

CHRONIC INFLAMMATION

• Often follows acute inflammation but can be the only inflammatory response in certain viral infections and hypersensitivity reactions

CHRONIC INFLAMMATION

• Characterized by infiltration of tissue with macrophages, lymphocytes and plasma cells, or eosinophils

CHRONIC INFLAMMATION

Infection: neutrophils. Macrophages Allergy: eosinophils, mast cells

ACUTE

Macrophages, lymphocytes

CHRONIC

Complement, kinins, prostaglandins, leukotrienes, acute phase cytokines, chemokines

ACUTE

Cytokines from macrophages and T cells

CHRONIC

Rash, pus, abscess

ACUTE

Rash, fibrosis, granuloma

CHRONIC

Response to infection, hypersensitivity response

ACUTE

Autoimmunity, response to intracellular bacterial infection

CHRONIC