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805 > Lecture 6 (Quiz 3) > Flashcards

Lecture 6 (Quiz 3) Flashcards

Innate Immune Defenses

1
Q

Variolation

A

First form of vaccination where scabs of small pox were ground up and blow into the nose. Began in 10th century China.

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2
Q

Host Defenses

A

Complex network of tissues and effector cells including:

  • Tissue barriers
  • Chemical Defense
  • Lymphatic System
  • Diversity of WBCs: some stationary while others move, non-specific and specific
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3
Q

Nonspecific Innate Immunity

A
  • Immediate or rapid response
  • Broad protection without specificity
  • Lacks “memory”
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4
Q

Specific Adaptive Immunity

A
  • Takes weeks to develop
  • Pathogen-specific
  • “Memory” programmed is faster and stronger in response to subsequent exposures to the same pathogen
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5
Q

Which lines of defense are innate?

A

First and second

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6
Q

Which lines of defense are adaptive?

A

Third line

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7
Q

First Line Defenses (4)

A
  1. Physical Defense
  2. Chemical Defense
  3. Normal Microbiota
  4. Genetics
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8
Q

Physical Defense Include (2)

A

Physical barriers and mechanical defenses

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9
Q

Types of Physical Barriers (3)

A
  1. Skin
  2. Mucous Membranes
  3. Goblet Cells
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10
Q

Skin

A

3 layers of skin act as a barrier made up of epidermis cells that are cemented together by keratin. Surface is salty, acidic, and sloughs off.

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11
Q

Mucous Membranes

A

Line respiratory, intestinal, and genitourinary tracts. Can be ciliated or not to assist with with the removing of pathogens.

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12
Q

Goblet Cells

A

Make sticky mucous that layers organ tracts. Made up of ciliated columnar epithelium for additional protection and can at times trap pathogens to be later removed by cilia in the mucous.

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13
Q

Mechanical Defenses (4)

A
  1. Shedding of skin cells
  2. Mucociliary escalation
  3. Flushing action - tears, sweat, urine, ear wax
  4. Expelling of bacteria - diarrhea, vomiting, defecation
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14
Q

Types of Chemical Defenses (2)

A

Enzymatic and Chemical

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15
Q

Examples of Enzymatic Defense (2)

A
  • Lysozymes in saliva

- Digestive enzymes in gastrointestinal tract

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16
Q

Examples of Chemical Defenses (3)

A
  • Acidic pH of stomach and vagina (increases in the elderly and in those who use antacids)
  • Bile secreted into intestinal tract
  • Endogenous and exogenous chemical mediators
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17
Q

Endogenous Mediator

A

Something that our body makes that is antibacterial or antipathogenic. Ex: Sebaceous gland that makes sebum on the skin.

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18
Q

Exogenous

A

Something not made by our body that fights a pathogen. Ex: Acid made from bacteria that live on our skin and eat the sebum.

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19
Q

Normal Microbiota

A

Microbial life found in and on healthy people usually on the skin or mucous membranes. NOT found in deep tissues. 10^13 “self” cells and about 10x more bacteria in or on us.

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20
Q

Acquisition of Normal Flora (2)

A
  1. Lactobacilli - rapid growth in vagina before birth which becomes the first normal flora for most infants (doesn’t occur if delivered by C-section)
  2. Other flora - from personal contact, breathing, and eating
21
Q

Defense Against Infectious Disease (3)

A
  1. Occupy binding sites
  2. Compete for available nutrients
  3. Produce antimicrobial substances
22
Q

Normal Flora in Female Genitourinary Tract

A

Lactobacilli is the majority of microbiota in most women. Produce lactic acid which lowers the pH and protects the vagina from invading pathogens.

23
Q

Vaginal pH + Age

A
  • Childhood/Menopause - slightly alkaline
  • Child-bearing years - pH = 3.6-4.5 from the estrogen produced causing glycogen to be fed to the normal flora in the vagina which lowers the pH from making lactic acid
  • During menstrual cycle, estrogen levels drop and the pH rises which makes the vagina more susceptible to infection
24
Q

Genetics Affects on Immunity (3)

A
  1. Cell receptors required for infection - interspecies restrictions. Ex: not getting distemper from your pet
  2. Intraspecies restrictions - Ex: innate resistance to HIV and limited spread of the bird flu
  3. Cell Physiology & Resistance - Ex: sickle cell anemics having a natural resistance to malaria (important reason sickle cell anemia is still in population)
25
Q

Second Line Defenses (4)

A
  1. Cellular
  2. Antimicrobial Proteins
  3. Inflammatory Response
  4. Fever
26
Q

Cells involved in Cellular Defense (4)

A
  1. Macrophages
  2. Dendritic Cells
  3. Neutrophils
  4. Natural Killer Cells
27
Q

Macrophages

A
  • Professional phagocytes - some move while others don’t
  • Produce cytokines (chemical signals) that call other defense cells into area and activate them
  • Important in antigen processing and presenting (1st step in activating 3rd line defenses)
28
Q

Dendritic Cells

A
  • Professional phagocytes that also secrete cytokines and process/present antigens
  • More talented than macrophages in activating and directing 3rd line defenses
29
Q

Types of Granulocytes (3)

A
  1. Neutrophils
  2. Eosinophils
  3. Basophils
30
Q

Neutrophils

A
  • Aka PMN - polymorphonuclear leukocytes (phagocytes)
  • Short-lived (only hours)
  • Don’t multiply
  • Do NOT process or present antigens
  • Kill EXTRACELLULAR bacteria
31
Q

Neutrophils + Detecting Infection

A
  • Adult produce 10^11 each day
  • Levels of PMN increase when dealing with bacterial infection
  • Increase of immature band cells (become PMN) cause a “shift to the left” seen with bacterial infection
32
Q

Granulocyte Stimulating Factor

A
  • Aka GSF
  • Mechanism of Action: Glycoprotein that increases neutrophil production and activity
  • Indication: Neutropenia patients from chemotherapy, bone marrow transplants, and other diseases that cause neutropenia
33
Q

Granulocyte-Macrophage Colony Stimulating Face

A
  • Aka GM-CSF
  • Mechanism of action: Also a glycoprotein that increases neutrophil production and activity. Has additional impact on antigen-presenting cells
  • Same indications as GSF but also includes stem cell transplants
34
Q

Two Types of Cell Movement

A
  1. Chemotaxis

2. Diapedesis

35
Q

Chemotaxis

A
  • Movement of cell to site of infection
  • Phagocytes move along a chemokine gradient like a bread crumb trail
  • “Bread crumbs” = bacterial products, cytokines, complement factors
36
Q

Diapedesis

A
  • Migration of cells out of blood
  • Squeeze between loosened endothelial cell junctions
  • Loosened from vasodilation and inflammation
37
Q

Factors Assisting with Pathogen Recognition (3)

A
  1. Toll-like receptor (TLR)
  2. Pathogen-associated molecule pattern (PAMP)
  3. Pattern Recognition Receptors (PRR)
38
Q

Steps of Phagocytosis & Killing (4)

A
  1. Attachment
  2. Ingestion - phagocytosis
  3. Creates phagosome that pumps H+ into the vesicle and drops the pH sometimes down to 4
  4. Phagolysome - adds into enzymes, toxins, or oxygen radicals to break down contents
39
Q

Natural Killer Cells (NK)

A
  • Important Defense against intracellular pathogens
  • Fights against viruses, bacteria
  • Also deals with tumor cell surveillance and destruction
40
Q

NK Action

A
  • Attach and kill STRESSED host cells
  • Not a phagocyte
  • Recognize stress signals on cell’s membrane
  • Attack and release toxic granule while causes cell death via apoptosis
41
Q

Lactoferrin/Transferrin

A
  • Lactoferrin - found in secretions and WBCs
  • Transferrin - found in blood
  • Proteins that bind to iron and limit its availability for pathogen growth (bacteriostatic)
42
Q

Antimicrobial Peptides

A
  • small peptides
  • can be produced by our cells or other pathogens
  • most tend to go after membrane but not the only mechanism they employ
  • attack pathogens that come into body
43
Q

Antiviral Interferons alpha & beta

A

Made by infected cells and released to signal neighboring cells

44
Q

Possible Interferon Responses (3)

A
  1. Signals neighboring, uninfected cells to destroy RNA & decrease protein synthesis
  2. Neighboring, infected cells are influenced to go through apoptosis
  3. Activate immune cells
45
Q

Complement Systems

A
  • 20-30 proteins produced by the liver
  • Innate “complement” to other immune cells
  • Tend to operate via cascade reactions
  • Focus on proteins C3b, C3a, & C5a
46
Q

Defense Mechanisms of Complement (4)

A
  1. Lysis of Bacteria
  2. Phagocyte chemotaxis
  3. Bacteria Opsonization
  4. Membrane Attack Complex
    * *Depends on what complement interacts with**
47
Q

Bacterial Opsonization

A
  • “To get ready for dining”
  • Complement adds on factors like C3b which betters attaches to phagocytes and increases likelihood of it being eaten by said phaogcyte
48
Q

Membrane Attack Complex

A
  • Insert or organize into a large poor that allows water and sodium ions to leave cell and potassium/chloride ions to enter the cell
  • Causes cell to eventually lyse
  • C3a & C5a act through this method and increasing pumping & inflammation response
  • Stimulates vasodilation by binding to mast cells or basophils which makes them release histamine
  • Also can act as bread crumbs for chemotaxis

805 (18 decks)

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