Immunity--Innate Flashcards
1
Q
how do BACTERIA ATTACK?
A
- have to GAIN ACCESS TO HOST CELLS
- have to PENETRATE + EVADE IMMUNE RESPONSES
- cause DAMAGE to the HOST CELLS + TISSUE
- have to EXIT
2
Q
describe INNATE IMMUNITY
A
- present at BIRTH
- ALWAYS AVAILABLE
- its a type of RAPID RESPONSE (immediate or WITHIN HOURS)
- NOT SPECIFIC (no recog. of specific microbe)
- has NO MEMORY
3
Q
describe ADAPTIVE IMMUNITY
A
- is a SPECIFIC RESPONSE to a SPECIFIC ORGANISM
- ACQUIRED OVER TIME
- has SLOWER RESPONSE
- has MEMORY; has a more STRONGER + RAPID RESPONSE to the same microbe at a LATER DATE
4
Q
what does the INNATE IMMUNITY CONSIST of?
A
has our FIRST AND SECOND LINE OF DEFENSES
5
Q
what are our FIRST LINE OF DEFENSES?
A
PHYSICAL FACTORS
- typical BARRIERS TO ENTRY
- processes that REMOVE BACTERIA FROM SURFACES
CHEMICAL FACTORS
6
Q
what are our SECOND LINE OF DEFENSES (4)?
A
- PHAGOCYTIC CELLS
- INFLAMMATION
- FEVER
- ANTI-MICROBIAL SUBSTANCES
7
Q
what are our PHYSICAL BARRIERS (6)?
A
- SKIN
- MUCOUS MEMBRANES
- LACRIMAL APPARATUS
- SALIVA
- NASAL MEMBRANES
- URINE/VAGINAL SECRETIONS
8
Q
describe the SKIN
A
- consists of TWO LAYERS; DERMIS + EPIDERMIS
9
Q
describe the DERMIS
A
- a THICK LAYER of CONNECTIVE TISSUE below the EPIDERMIS
- has the CAPILLARIES, NERVE ENDINGS, SWEAT GLANDS, and HAIR FOLLICLES
10
Q
describe the EPIDERMIS
A
- the PART OF THE SKIN WE SEE
- the OUTER THINNER PORTION that is in DIRECT CONTACT with the EXTERNAL ENVIRONMENT
- has many layers of TIGHTLY PACKED EPITHELIAL CELLS
- top layer always has DEAD AND DRY SHEDDING CELLS
- important and MICROBES CAN RARELY PENETRATE THE SKIN (has other microbiome on skin–leads to COMPETITION for NUTRIENTS + SPACE)
11
Q
describe MUCUS MEMBRANES
A
- LINES the ENTIRE GI, RESPIRATORY, GENITOURINARY TRACTS
- consists of an EPITHELIAL LAYER that secretes MUCUS
- has VISCOUS GLYCOPROTEINS–prevents DRYING OUT
- is PROTECTIVE
12
Q
describe the LACRIMAL APPARATUS
A
- mechanism that PROTECTS THE EYE
- has its own GLANDS + DUCTS + CANALS to drain tears
- is always CONT. WASHING EYE
- drains into NASAL PASSAGES
13
Q
describe SALIVA
A
- helps to DILUTE # of MICROORGANISMS
- washes off TEETH SURFACEs + ORAL SURFACES
14
Q
describe NASAL MEMBRANES
A
- has MUCUS COATED HAIR
- FILTERS AND TRAPS MICROBES
15
Q
describe EPITHELIAL CELLS
A
- seen in the LOWER RESPIRATORY TRACT and are COVERED BY CILIA
- moves SYNCHRONOUSLY + DIRECTIONALLY PROPELS inhaled microbes + dust particles UPWARDS
16
Q
what are our CHEMICAL FACTORS (4)?
A
- SEBACEOUS GLANDS
- SWEAT GLANDS
- SALIVA
- GASTRIC JUICES
17
Q
describe SEBACEOUS GLANDS
A
- found in the SKIN
- seen SEBUM–secretion of ACIDIC OIL ph 3 -5
- allows for a PROTECTIVE FILM over the SKIN
18
Q
describe SWEAT GLANDS
A
- production of SWEAT
- has SALT + ANTIMICOBIAL PEPTIDES + LYSOZYME
19
Q
describe LYSOZYME
A
type of ENZYME that attacks the CELL WALL
- found in TEARS, URINE, SALIVA, AND NASAL SECRETIONS
20
Q
describe SALIVA (chemical factor)
A
- contains a # of ANTIMICROBIAL SUBSTANCES
- has UREA + LYSOZYME
- is SLIGHTLY ACIDIC
21
Q
describe GASTRIC JUICES
A
- has a MIX OF HCl ACID + ENZYMES + MUCUS
- has a LOW pH 1-3
22
Q
describe our SECOND LINE OF DEFENSE + what are OUR SECOND LINES OF DEFENSE (4)
A
- where the microbe passes ALL FIRST LINE OF BARRIERS
SECOND LINES OF DEFENSE:
- DEFENSIVE CELLS: PHAGOCYTOTIC CELLS
- INFLAMMATION
- FEVER
- ANTIMICROBIAL SUBSTANCES
23
Q
How does our IMMUNE SYSTEM know its been BREACHED?
A
- has specific PROTEIN RECEPTORS in their plasma membranes known as TOLL LIKE RECEPTORS (TLRs)
- TLRs: can recog. and attach to compounds seen on MICROBEs known as PATHOGEN ASSOC. MOLECULAR PATTERNS (PAMPS)
- some PAMPS:
- flagella, peptidoglycan cell wall, bacterial or viral DNA/RNA
24
Q
what happens once a PAMP is recognized?
A
- DEFENSIVE CELLS release CYTOKINES
- CYTOKINES: chemical messengers that PLAY A NUMBER OF ROLES in IMMUNITY
25
describe IMMUNE CELLS IN BLOOD; definition of PLASMA
- blood consists of FLUID known as PLASMA + FORMED ELEMENTS
- PLASMA:
mostly made of WATER that contains ELECTROLYTES, DISSOLVED GASES, NUTRIENTS and PROTEINS
26
what are the FORMED ELEMENTS in the BLOOD
- RBC + WBC + PLATELETS
- have BLOOD CELLS (HEMATOPOIETIC CELLS) made from the RED BONE MARROW --process known as HEMATOPOIESIS
27
describe PLURIPOTENT
- cell that gives rise to ALL CELL TYPES that MAKE UP THE BODY
28
describe MULTIPOTENT
cells that develop MORE THAN ONE CELL TYPE within a LINEAGE
- much more LIMITED vs. PLURIPOTENT
29
what are the TYPES OF WBCs?
- GRANULOCYTES--granulated LEUKOCYTES
(contains LARGE GRANULES, stains diff. colors)
- AGRANULOCYTES--agranulated LEUKOCYTES
(appears UNIFORM UNDER LIGHT MICROSCOPE)
30
what are the THREE TYPES OF GRANULOCYTES?
- BASOPHILS (stain BLUE)
- EOSINOPHILS (stain red/orange--eosin)
- NEUTROPHILS/POLYMORPHONUCLEAR (PMNs) (stain lilac)
31
describe NEUTROPHILS
- they are PHAGOCYTIC
- HIGHLY MOTILE (can leave blood to enter tissue)
- ACTIVE IN INITAL STAGES of INFECTION
32
describe EOSINOPHILS
- SOMEWHAT PHAGOCYTIC
- MOTILE
- can make TOXIC PROTEINS attack INVADIES (injects H2O2 into HELMINTHES)
33
describe BASOPHILS
- releases HISTAMINES
- TRIGEERS INFLAMMATION and ALLERGY RESPONSE
34
what are our types of AGRANULOCYTES?
- MONOCYTES
- DENDRITIC CELLS
- LYMPHOCYTES
35
describe MONOCYTES
- NOT ACTIVELY PHAGOCYTIC till the LEAVE BLOOD
- matures into MACROPHAGES--they are PHAGOCYTIC
- removes MICROBES FROM BLOOD and LYMPH
36
describe DENDRITIC CELLS
- is ABUNDANT IN THE SKIN, MUCUS MEM., THYMUS and LYMPH NODES
- is PHAGOCYTIC
- initiates the ADAPTIVE IMMUNE SYSTEM
37
describe LYMPHOCYTES
- contains NATURAL KILLER CELLS
- kills a WIDE RANGE OF TUMOR + INFECTED CELLS
- attacks them if they display ABNORMAL PLASMA MEM. PROTEINS
- BINDS TO INFECTED CELLS
- releases VESICLES CONTAINING TOXIC SUBS (PERFORINS + GRANZYMES) into the INFECTED CELL
- has T AND B CELLS
38
describe contents of a BLOOD HEMATOCRIT
- has normally around 45% (38-48%) of CELLS and 55% PLASMA
39
what happens DURING INFECTION; WBC?
- TOTAL NUMBER OF WBC - INCREASES to COMBAT MICROBES; process known as LEUKOCYTOSIS
- around 2x-4x depending on severity of infection
40
describe LEUKOPENIA
- condition where we have a DECREASED LEVEL OF WBCs
- can cause;
- AUTO IMMUNE DISORDERS
- CONGENITAL DISEASES
- BONE MARROW CONDITIONS
41
what is a CBC?
- a COMPLETE BLOOD COUNT
- helps to give an examination of OVERALL HOMEOSTASIS; looks for INFECTIONS, ANEMIAS, MONITORS TREATMENTS etc..
- evaluates OVERALL HEALTH
MEASURES:
- RBCs
- WBCs
- HEMOGLOBIN
- HEMATOCRIT
- PLATELETS
42
describe the LYMPHATIC SYSTEM
- part of the CIRCULATORY SYSTEM
- plays vital role in IMMUNITY
- TRANSPORTS LYMPH
43
what is LYMPH?
- the fluid that CIRCULATES throughout the LYMPHATIC SYS
- formed when INTERSTITIAL FLUID is collected through the LYMPH CAPILLARIES
44
what are the THREE PRIMARY FUNCTIONS of the LYMPHATIC SYSTEM?
1. MAINTENANCE OF FLUID BALANCE
2. FACILITATION OF ABSORPTION OF DIETARY FATS from GI TRACT to BLOODSTREAM (for metabolism + storage)
3. ENHANCEMENT + FACILITATION of the IMMUNE SYSTEM
45
what does the LYMPHATIC SYSTEM CONSIST OF?
- LYMPHATIC TISSUE
- LYMPHATIC VESSELS
- LYMPHATIC ORGANS
- LYMPH NODES
46
describe LYMPHATIC TISSUE
- scattered THROUGHOUT THE BODY
- aggregates in PATCHES; seen in TONSILS and PEYERS PATCHES (mostly have B CELLS)
47
describe our LYMPHATIC ORGANS
- have the SPLEEN;
contains LYMPHOCYTES + MACROPHAGES, helps to MONITOR MICROBES IN BLOOD
- have the THYMUS;
site for T CELL MATURATION
48
describe our LYMPH NODES
- helps to ACTIVATE T AND B CELLS
- TRAPS MICROBES--has DENDRITIC CELLS AND MACROPHAGES TO PHAGOCYTIZE
49
definition of PHAGOCYTOSIS
- the INGESTION OF MICROORGANISMS BY CELLS
50
definition of PHAGOCYTES
all types of WBCs that perform PHAGOCYTOSIS
51
what are the FIVE STAGES OF PHAGOCYTOSIS?
1. CHEMOTAXIS
2. ADHERENCE
3. INGESTION/ENGULFMENT
4. DIGESTION
5. ELIMINATION
52
describe CHEMOTAXIS
- PHAGOCYTES are attracted to MICROORGANISMS;
- MICROBIAL BYPRODUCTS
- CYTOKINES
- DAMAGED TISSUE
- PEPTIDES OF COMPLEMENT SYS
53
describe ADHERENCE
- the ATTACHMENT OF PHAGOCYTES to the PLASMA MEMBRANE of MICROORGANISMS
- PAMPS bind to the TLRs
- initiation of PHAGOCYTOSIS
- release of CYTOKINES to attract MORE PHAGOCYTIC CELLS
54
describe INGESTION/ ENGULFMENT
- membranes begin to FORM PSEUDOPODS + ENGULF MICROORGANISMS
- creation of PHAGOSOME
- H+ PUMPED IN to REDUCE pH to around 4`
55
describe DIGESTION
- fusing with LYSOMES within CYTOPLASM--formation of a PHAGOLYSOSOME
- digestion of microorganism by ENZYMES;
- LYSOZYMES (hydrolyzes peptidoglycan cell wall)
- LIPASES
- PROTEASES
56
describe ELIMINATION
RESIDUAL BODY:
- PHAGOLYSOSOME that contains DEGRADED MICROBE
- begins to MOVE TO PM and DISCHARGES WASTE PRODUCTS to the OUTSIDE
57
how do BACTERIA EVADE PHAGOCYTOSIS?
- the INHIBITION OF ADHERENCE
- has CAPSULES (s. pneumonia) or M PROTEINS (s. pyogenes)
- AVOIDS DIGESTION
- releases their OWN LYSOZYME (s. auerus) or PORE FORMING TOXINS to LYSE THE ACTUAL PHAGOCYTIC CELL (L. monocytogenes)
- or ESCAPES PHAGOSOME PRIOR TO FUSION with LYSOSOME (Shigella)
- SURVIVE INSIDE PHAGOLYSOSME (C. brunetti) -- not affected
- PREVENTION OF ACIDIFICATION and FUSION OF LYSOSOME
- has BIOFILMS (helps the BACTERIA HIDE FROM PHAGOCYTES
58
describe INFLAMMATION and WHAT TYPES
- a NONSPECIFIC RESPONSE to TISSUE DAAMGE from VARIOUS CAUSES
- characterized by REDNESS, HEAT, SWELLING + PAIN
TYPES:
- ACUTE:
- easy to remove--an INTENSE SHORT TERM RESPONSE
- CHRONIC:
- more LONG LASTING--LESS INTENSE RESPONSE
59
describe EARLY INFLAMMATION
- have MICROBIAL STRUCTURES such as FLAGELLA AND LPS
- stimulation of TLRS of MACROPHAGES -- production of CYTOKINES (TNFalpha)
- TNF(alpha) = RELEASES ACUTE PHASE PROTEINS
- KININS
- BLOOD CLOTTING FACTORS
(all which tells the BODY that there is INFECTION within the BODY)
60
what happens after TISSUE DAAMGE?
- greater INCREASE OF CHEMICALS THAT LEADS TO VASODILATION and INCREASED PERMEABILITY OF BV
- recruits PHAGOCYTES
61
describe HISTAMINES
- released by IMMUNE CELLS in DIRECT RESPONSE to DAMAGE
- BOOSTS BLOOD FLOW + INCREASES BV PERMEABILITY
62
describe KININS
- present in BLOOD PLASMA in INACTIVE FORM
- activated; ATTRACTS PHAGOCYTES to SITE
63
describe PROSTAGLANDINS
- released by DAMAGED CELLS
- intensifies EFFECTS OF HISTAMINE and KININS
64
describe LEUKOTRIENE
- produced by MAST CELLS (type of GRANULOCYTE--tissues) + BASOPHILS
- ATTRACTS PHAGOCYTES
65
describe MARGINIATION + DIAPEDESIS
MARGINATION:
- more BLOOD FLOW into TISSUE
- STICKING OF NEUTROPHILS and MONOCYTES to SITE
DIAPEDESIS:
- begin to SQUEEZE between ENDOTHELIAL CELLS
later killed and destroyed by PHAGOCYTES
66
why does the WOUND SWELL?
- due to an INCREASE OF BLOOD FLOW
- VASODILATION + MOVEMENT OF PHAGOCYTES into TISSUE
- causes wound to feel WARM + PAINFUL
67
describe TISSUE REPAIR
- where NEW TISSUE replaces DEAD and DAMAGED TISSUE
- can only begin during INFLAMMATION ONCE ALL HARMFUL SUBSTANCES ARE GONE
- all depends ON LOCATION
68
describe FEVER
- a SYSTEMIC RESPONSE TO INJURY
- often a COMMON CAUSE from BACTERIAL or VIRAL INFECTION
- HYPOTHALAMUS sets TEMP
- release of TNFalpha and INTERLUEKIN 1 - PROSTAGLANDINS to RESET TEMP HIGHER
- maintained until ALL CYTOKINES are GONE
69
what are our ANTIMICROBIAL SUBSTANCES?
- PROTEINS OF THE COMPLEMENT SYSTEM
- INTERFERONS
- IRON BINDING PROTEINS
- ANTIMICROBIAL PEPTIDES
70
describe the COMPLEMENT SYSTEM
- can be activated in THREEWAYS;
- CLASSICAL PATHWAY
- ALTERNATE PATHWAY
- LECTIN PATHWAY
- acts in CASCADES
- can lead to MICRBIAL CLEARING BY;
- CYTOLYSIS
- OPSONIZATION
- INFLAMMATION
71
is the COMPLEMENT SYSTEM DANGEROUS?
yes!! has the POTENTIAL TO BE EXTREMELY DAMAGING
- is QUICKLY TURNED OFF TO MINIMIZE EFFECTS
72
how do microbes EVADE THE COMPLEMENT?
- use of CAPSULES
- the LENGTH OF LPS can prevent MAC FORMATION
- has SIALIC ACID --attached to OUTER MEMBRANE (discourages OPSONIZATION + MAC FORMATION)
73
describe INTERFERONS
- they are ONE OF THE CYTOKINE PROTEINS---communicator that TRIGGERS IMMUNE SYSTEM
- can be ANTI-VIRAL or ANTITUMORIGENIC
- SMALL MOLECULES
- stable at LOW pH
- HEAT RESISTANT
TYPES:
- ALPHA +BETA - EARLY TRIGGERS
- GAMMA - LATE TRIGGERS
74
describe INTERFERON ALPHA/BETA
- often used in EARLY INFECTION (1 - 4 days)
- produced by VIRAL INFECTED HOST CELLS
- they are HOST CELL SPECIFIC / NOT VIRUS SPECIFIC
- TRIGEERS DEFENSES IN NEARBY CELLS
- INDUCES NK CELLS + AVP (ANTI-VIRAL PROTEIN) + PROTEIN KINASE
75
describe INTERFERON- GAMMA
- is a LATE INFECTION (4+ days)
- produced in LYMPHOCYTES
- INDUCES ANTIGEN PRESENTATION + PHAGOCYTIC ACTIVITY of MACROPHAGES
- INDUCES PRODUCTION OF ANTIBODIES from ACTIVATED B CELLS
- causes MACROPHAGES TO PRODUCE NO--KILLS MICROBES + TUMOR CELLS
- promotion of adhesion and binding to leukocytes
76
describe IRON BINDING PROTEINS
- IRON important for GROWTH AND INFECTION for PATHOGENIC BACTERIA
- IRON important for making CYTOCHROMES for the ETC + part of HEMOGLOBIN
- have a FREE CONCENTRATION OF IRON IN BODY (BUT IN LOW CONTENT)
77
describe the TYPES OF IRON BINDING PROTEINS
- TRANSFERRIN
(bloodstream iron transport)
- LACTOFERRIN
(found in MILK, SALIVA, and MUCUS)
- FERRITIN
(in the LIVER--storage)
78
what IRON BINDING PROTEINS does BACTERIA SECRETE?
- SIDEROPHORES
(is a type of BACTERIAL Fe-chelator)
(COMPETES FOR IRON and BINDS IT TIGHTLY)
- HEMOLYSINS
(type of MEMBRANE PORINS)
79
describe ANTIMICROBIAL PEPTIDES
MODE OF ACTION
- INHIBITS ELL WALL SYNTHESIS
- has PORE FORMATION in PM (LYSIS)
- has a BROAD SPECTRUM; affects BACTERIA, FUNIG, VIRUSES
- seen in SYNTHESIS OF AMPS (triggered by SUGARS AND PROTEINS ON MICROBES)
80
what are our HUMAN AMPS
DEFENSINS
- produced by NEUTROPHILS and MACROPHAGES
THROMBOCIDIN:
- produced by PLATELETS
81
what is SPECIAL ABOUT AMPS?
- they WORK SYNERGISTICALLY with other ANTIMICROBIAL AGENTS and SYSTEMS
- have a BROAD SPECTRUM
- stable in wide ranges if pH
- no seen DEVELOPMENT OF RESISTANCE
