Chapter 6: Innate Immunity: Inflammation

Question 0

First Line of Defense: biochemical barriers

Answer 0

Synthesized and secreted saliva, tears, earwax, sweat, and sebum
Antimicrobial peptides: cathelicidines, defensins(alpha defensins in neutrophil granules), and collectins(lungs), normal bacterial flora; vaginal:lactobacillus, intestinal:produce ammonia, phenols, indoles, etc. that inhibit colonization by pathogens

Question 1

First Line of Defense: physical and mechanical barriers

Answer 1

Skin
Linings of gastrointestinal, genitourinary, and respiratory tracts: sloughing off if cells, coughing and sneezing, vomiting, mucus and cilia

Question 2

Second line of defense: inflammatory response

Answer 2

Causes: infection, mechanical damage, ischemia, nutrient deprivation, temperature extremes, radiation, etc.
COMPONENTS
Vascular response: blood vessel dilation, increased vascular permeability and leakage, WBC adherence to the inner walls of the vessels and migrations through the vessels

Question 3

Second line of defense: goals

Answer 3

Limit and control the inflammatory process
Prevent and limit infection and further damage
Control bleeding
Interact with components of the adaptive immune system
Prepare the area of injury for healing

Question 4

Plasma Protein Systems

Answer 4

Complement system
Coagulation system
Kinin system
Involve a series of proteolytic cleavages to produce active proteins for each function

Question 5

Complement system

Answer 5

Can destroy pathogens directly
Activates or collaborates with every other component of the inflammatory response
Activated through following pathways: classical, lectin, alternative, leads to generation of a membrane attack complex that inserts into a bacterium to cause lysis

Question 6

Coagulation (clotting) system

Answer 6

Forms a fibrinous meshwork at an injured or inflamed site
Prevents spread of infection
Keeps microorganisms and foreign bodies at the site of greatest inflammatory cell activity
Forms a clot that stops bleeding
Provides a framework for repair and healing
Main substance is an insoluble protein called fibrin

Question 7

Kinin system

Answer 7

Functions to activate and assist inflammatory cells
Primary kinin is bradykinin
Causes dilation of blood vessel, pain, smooth muscle contraction, vascular permeability and leukocyte chemotaxis

Question 8

Cellular mediators of inflammation

Answer 8

Cellular components: granulocytes, platelets, monocytes and lymphocytes
Basic process: infectious particles activate cell surface receptors that recognize microbial molecular patterns, receptor activation leads to cellular activations that results in degranulation and/or phagocytosis

Question 9

Pattern recognition receptors (PRRs)

Answer 9

Recognize molecular “patterns” on infectious agents or their products(pathogen-associated molecular patterns, or PAMPs), or products of cellular damage(necrosis or apoptosis)

Question 10

Toll like receptors (TLRs)

Answer 10

Expressed on the surface of many cells that have direct and early contact with potential pathogenic microorganisms

Question 11

Complement receptors

Answer 11

Found on many cells of the innate and acquired immune responses

Question 12

Scavenger receptors

Answer 12

Primarily expressed on macrophages and facilitate recognition and phagocytosis of bacterial pathogens as well as damaged cells and altered soluble lipoproteins associated with vascular damage

Question 13

Mast cells

Answer 13

Cellular bags of granules located in loose connective tissues close to blood vessels
-skin, digestive lining, respiratory tract
Activation
-physical injury, chemical agents, immunologic processes
-activation of mast cells result in degranulation and secretion of long term mediators

Question 14

Degranulation

Answer 14

Results in release of histamine, cytokines, and chemotactic factors that cause vasodilation and recruitment of other immune cells to affected area
Long term mediators: include prostaglandins, leukotrienes, platelet activating factor and growth factors

Question 15

Phagocytes

Answer 15

Process of phagocytosis:

• Opsonization: recognition, and adherence to the target for phagocytosis
• Engulfment: endocytosis and formation of the phagosome
• Fusion with lysosomes inside the phagocytosis cell to produce a lysophagosome
• Destruction of the target by enzymatic degradation

Question 16

Margination(pavementing)

Answer 16

Process by which leukocytes adhere better to endothelial cells of the capillary walls and venues by the reciprocal change in adhesion molecules on leukocytes

Question 17

Diapedesis

Answer 17

Emigration of the cells through the endothelial junctions that have retracted response to the same mediators

Question 18

Neutrophils

Answer 18

First responders–arrive at inflammatory site within 6-12 hours
Ingest bacteria, dead cells and cellular debris
Cells are short lived and become a component of the purulent exudate

Question 19

Monocytes and macrophages

Answer 19

Monocytes produced in bone marrow, enter circulation and migrate to the inflammatory site where they develop into macrophages
Macrophages typically arrive at inflammatory site 3-7 days after neutrophils
Macrophages are activated by cytokines, activation results in increased size, plasma membrane area, glucose metabolism, number of lysosomes, and secretory products. Activated macrophages secrete factors that help promote healing

Question 20

Eosinophils

Answer 20

Mildly phagocytic

Fight against parasites and are activated by mast cells

Question 21

Basophils

Answer 21

Become active in allergic reactions

Release cytokine IL-4 (interleukin 4) so help to limit inflammation since IL-4 is an anti-inflammatory cytokine

Question 22

Natural killer (NK) cells

Answer 22

Function: recognize and eliminate cells infected with viruses and some function in eliminating cancer cells. More efficient with infected cells in circulatory system vs in tissues

Question 23

Platelets

Answer 23

Activation results in degranulation and interaction with components of the coagulation system to stop bleeding

Question 24

Acute inflammation

Answer 24

2 weeks or less
Local responses: heat, redness, swelling, pain
Systemic responses: fever, leukocytosis, increased levels in circulating plasma proteins

Question 25

Chronic inflammation

Answer 25

More than 2 weeks
Causes: often related to an unsuccessful acute inflammatory response, high lipid and wax content of microorganism ability to survive inside the macrophage toxins, chemicals, particulate matter, or physical irritants

Question 26

Chronic inflammation characteristics

Answer 26

Dense infiltration of lymphocytes and macrophages, granuloma formation, epithelioid cell formation, giant cell formation

Question 27

Wound healing

Answer 27

Regeneration: return of wound to normal structure and function
Resolution: in adults, returning injured tissue to the near normal structure and function
Repair: replacement of destroyed tissue with scar tissue

Question 28

Processes of healing

Answer 28

Filling in the wound
Sealing the wound (epithelialization)
Shrinking the wound (contraction)

Question 29

Primary intention healing

Answer 29

Wounds that heal under conditions of minimal tissue loss

Question 30

Secondary intention healing

Answer 30

Wounds the require a great deal more tissue replacement: open wound

Question 31

Phases of resolution and repair

Answer 31

Reconstructive phase:
Begins 3-4 days after initial injury
Fibroblast proliferation
Collagen synthesis
Epithelialization
Contraction of the wound by myofibriblast
Maturation phase:
Begins several weeks after the injury
Cellular differentiation
Scar formation