Immunity--Innate Flashcards
how do BACTERIA ATTACK?
- have to GAIN ACCESS TO HOST CELLS
- have to PENETRATE + EVADE IMMUNE RESPONSES
- cause DAMAGE to the HOST CELLS + TISSUE
- have to EXIT
describe INNATE IMMUNITY
- 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
describe ADAPTIVE IMMUNITY
- 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
what does the INNATE IMMUNITY CONSIST of?
has our FIRST AND SECOND LINE OF DEFENSES
what are our FIRST LINE OF DEFENSES?
PHYSICAL FACTORS
- typical BARRIERS TO ENTRY
- processes that REMOVE BACTERIA FROM SURFACES
CHEMICAL FACTORS
what are our SECOND LINE OF DEFENSES (4)?
- PHAGOCYTIC CELLS
- INFLAMMATION
- FEVER
- ANTI-MICROBIAL SUBSTANCES
what are our PHYSICAL BARRIERS (6)?
- SKIN
- MUCOUS MEMBRANES
- LACRIMAL APPARATUS
- SALIVA
- NASAL MEMBRANES
- URINE/VAGINAL SECRETIONS
describe the SKIN
- consists of TWO LAYERS; DERMIS + EPIDERMIS
describe the DERMIS
- a THICK LAYER of CONNECTIVE TISSUE below the EPIDERMIS
- has the CAPILLARIES, NERVE ENDINGS, SWEAT GLANDS, and HAIR FOLLICLES
describe the EPIDERMIS
- 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)
describe MUCUS MEMBRANES
- LINES the ENTIRE GI, RESPIRATORY, GENITOURINARY TRACTS
- consists of an EPITHELIAL LAYER that secretes MUCUS
- has VISCOUS GLYCOPROTEINS–prevents DRYING OUT
- is PROTECTIVE
describe the LACRIMAL APPARATUS
- mechanism that PROTECTS THE EYE
- has its own GLANDS + DUCTS + CANALS to drain tears
- is always CONT. WASHING EYE
- drains into NASAL PASSAGES
describe SALIVA
- helps to DILUTE # of MICROORGANISMS
- washes off TEETH SURFACEs + ORAL SURFACES
describe NASAL MEMBRANES
- has MUCUS COATED HAIR
- FILTERS AND TRAPS MICROBES
describe EPITHELIAL CELLS
- seen in the LOWER RESPIRATORY TRACT and are COVERED BY CILIA
- moves SYNCHRONOUSLY + DIRECTIONALLY PROPELS inhaled microbes + dust particles UPWARDS
what are our CHEMICAL FACTORS (4)?
- SEBACEOUS GLANDS
- SWEAT GLANDS
- SALIVA
- GASTRIC JUICES
describe SEBACEOUS GLANDS
- found in the SKIN
- seen SEBUM–secretion of ACIDIC OIL ph 3 -5
- allows for a PROTECTIVE FILM over the SKIN
describe SWEAT GLANDS
- production of SWEAT
- has SALT + ANTIMICOBIAL PEPTIDES + LYSOZYME
describe LYSOZYME
type of ENZYME that attacks the CELL WALL
- found in TEARS, URINE, SALIVA, AND NASAL SECRETIONS
describe SALIVA (chemical factor)
- contains a # of ANTIMICROBIAL SUBSTANCES
- has UREA + LYSOZYME
- is SLIGHTLY ACIDIC
describe GASTRIC JUICES
- has a MIX OF HCl ACID + ENZYMES + MUCUS
- has a LOW pH 1-3
describe our SECOND LINE OF DEFENSE + what are OUR SECOND LINES OF DEFENSE (4)
- where the microbe passes ALL FIRST LINE OF BARRIERS
SECOND LINES OF DEFENSE:
- DEFENSIVE CELLS: PHAGOCYTOTIC CELLS
- INFLAMMATION
- FEVER
- ANTIMICROBIAL SUBSTANCES
How does our IMMUNE SYSTEM know its been BREACHED?
- 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
what happens once a PAMP is recognized?
- DEFENSIVE CELLS release CYTOKINES
- CYTOKINES: chemical messengers that PLAY A NUMBER OF ROLES in IMMUNITY
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
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
describe PLURIPOTENT
- cell that gives rise to ALL CELL TYPES that MAKE UP THE BODY
describe MULTIPOTENT
cells that develop MORE THAN ONE CELL TYPE within a LINEAGE
- much more LIMITED vs. PLURIPOTENT
what are the TYPES OF WBCs?
- GRANULOCYTES–granulated LEUKOCYTES
(contains LARGE GRANULES, stains diff. colors) - AGRANULOCYTES–agranulated LEUKOCYTES
(appears UNIFORM UNDER LIGHT MICROSCOPE)
what are the THREE TYPES OF GRANULOCYTES?
- BASOPHILS (stain BLUE)
- EOSINOPHILS (stain red/orange–eosin)
- NEUTROPHILS/POLYMORPHONUCLEAR (PMNs) (stain lilac)
describe NEUTROPHILS
- they are PHAGOCYTIC
- HIGHLY MOTILE (can leave blood to enter tissue)
- ACTIVE IN INITAL STAGES of INFECTION
describe EOSINOPHILS
- SOMEWHAT PHAGOCYTIC
- MOTILE
- can make TOXIC PROTEINS attack INVADIES (injects H2O2 into HELMINTHES)
describe BASOPHILS
- releases HISTAMINES
- TRIGEERS INFLAMMATION and ALLERGY RESPONSE
what are our types of AGRANULOCYTES?
- MONOCYTES
- DENDRITIC CELLS
- LYMPHOCYTES
describe MONOCYTES
- NOT ACTIVELY PHAGOCYTIC till the LEAVE BLOOD
- matures into MACROPHAGES–they are PHAGOCYTIC
- removes MICROBES FROM BLOOD and LYMPH
describe DENDRITIC CELLS
- is ABUNDANT IN THE SKIN, MUCUS MEM., THYMUS and LYMPH NODES
- is PHAGOCYTIC
- initiates the ADAPTIVE IMMUNE SYSTEM
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
describe contents of a BLOOD HEMATOCRIT
- has normally around 45% (38-48%) of CELLS and 55% PLASMA
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
describe LEUKOPENIA
- condition where we have a DECREASED LEVEL OF WBCs
- can cause;
- AUTO IMMUNE DISORDERS
- CONGENITAL DISEASES
- BONE MARROW CONDITIONS
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
describe the LYMPHATIC SYSTEM
- part of the CIRCULATORY SYSTEM
- plays vital role in IMMUNITY
- TRANSPORTS LYMPH
what is LYMPH?
- the fluid that CIRCULATES throughout the LYMPHATIC SYS
- formed when INTERSTITIAL FLUID is collected through the LYMPH CAPILLARIES
what are the THREE PRIMARY FUNCTIONS of the LYMPHATIC SYSTEM?
- MAINTENANCE OF FLUID BALANCE
- FACILITATION OF ABSORPTION OF DIETARY FATS from GI TRACT to BLOODSTREAM (for metabolism + storage)
- ENHANCEMENT + FACILITATION of the IMMUNE SYSTEM
what does the LYMPHATIC SYSTEM CONSIST OF?
- LYMPHATIC TISSUE
- LYMPHATIC VESSELS
- LYMPHATIC ORGANS
- LYMPH NODES
describe LYMPHATIC TISSUE
- scattered THROUGHOUT THE BODY
- aggregates in PATCHES; seen in TONSILS and PEYERS PATCHES (mostly have B CELLS)
describe our LYMPHATIC ORGANS
- have the SPLEEN;
contains LYMPHOCYTES + MACROPHAGES, helps to MONITOR MICROBES IN BLOOD - have the THYMUS;
site for T CELL MATURATION
describe our LYMPH NODES
- helps to ACTIVATE T AND B CELLS
- TRAPS MICROBES–has DENDRITIC CELLS AND MACROPHAGES TO PHAGOCYTIZE
definition of PHAGOCYTOSIS
- the INGESTION OF MICROORGANISMS BY CELLS
definition of PHAGOCYTES
all types of WBCs that perform PHAGOCYTOSIS
what are the FIVE STAGES OF PHAGOCYTOSIS?
- CHEMOTAXIS
- ADHERENCE
- INGESTION/ENGULFMENT
- DIGESTION
- ELIMINATION
describe CHEMOTAXIS
- PHAGOCYTES are attracted to MICROORGANISMS;
- MICROBIAL BYPRODUCTS
- CYTOKINES
- DAMAGED TISSUE
- PEPTIDES OF COMPLEMENT SYS
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
describe INGESTION/ ENGULFMENT
- membranes begin to FORM PSEUDOPODS + ENGULF MICROORGANISMS
- creation of PHAGOSOME
- H+ PUMPED IN to REDUCE pH to around 4`
describe DIGESTION
- fusing with LYSOMES within CYTOPLASM–formation of a PHAGOLYSOSOME
- digestion of microorganism by ENZYMES;
- LYSOZYMES (hydrolyzes peptidoglycan cell wall)
- LIPASES
- PROTEASES
describe ELIMINATION
RESIDUAL BODY:
- PHAGOLYSOSOME that contains DEGRADED MICROBE
- begins to MOVE TO PM and DISCHARGES WASTE PRODUCTS to the OUTSIDE
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
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
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)
what happens after TISSUE DAAMGE?
- greater INCREASE OF CHEMICALS THAT LEADS TO VASODILATION and INCREASED PERMEABILITY OF BV
- recruits PHAGOCYTES
describe HISTAMINES
- released by IMMUNE CELLS in DIRECT RESPONSE to DAMAGE
- BOOSTS BLOOD FLOW + INCREASES BV PERMEABILITY
describe KININS
- present in BLOOD PLASMA in INACTIVE FORM
- activated; ATTRACTS PHAGOCYTES to SITE
describe PROSTAGLANDINS
- released by DAMAGED CELLS
- intensifies EFFECTS OF HISTAMINE and KININS
describe LEUKOTRIENE
- produced by MAST CELLS (type of GRANULOCYTE–tissues) + BASOPHILS
- ATTRACTS PHAGOCYTES
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
why does the WOUND SWELL?
- due to an INCREASE OF BLOOD FLOW
- VASODILATION + MOVEMENT OF PHAGOCYTES into TISSUE
- causes wound to feel WARM + PAINFUL
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
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
what are our ANTIMICROBIAL SUBSTANCES?
- PROTEINS OF THE COMPLEMENT SYSTEM
- INTERFERONS
- IRON BINDING PROTEINS
- ANTIMICROBIAL PEPTIDES
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
is the COMPLEMENT SYSTEM DANGEROUS?
yes!! has the POTENTIAL TO BE EXTREMELY DAMAGING
- is QUICKLY TURNED OFF TO MINIMIZE EFFECTS
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)
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
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
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
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)
describe the TYPES OF IRON BINDING PROTEINS
- TRANSFERRIN
(bloodstream iron transport) - LACTOFERRIN
(found in MILK, SALIVA, and MUCUS) - FERRITIN
(in the LIVER–storage)
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)
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)
what are our HUMAN AMPS
DEFENSINS
- produced by NEUTROPHILS and MACROPHAGES
THROMBOCIDIN:
- produced by PLATELETS
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
