Ch 19 Exam 4 Flashcards
immune (broad definition)
being resistant to infection/subsequent diseases
give an example of an individual that’s passively resistant resulting in immunity
dogs immune to HIV since they lack the required cell surface receptors
immune (immunological definition)
the ability of one’s body to detect microbes and prevent it from causing disease
sterile immunity
non-sterile immunity
an immune response that results in the complete removal of a pathogen
an immune response that prevents an infection from causing a disease, but does not clear it
Give an example of non-sterile and sterile immunity
NON-sterile = Mycobacterium tuberculosis
Sterile = Influenza
innate immunity
adaptive immunity
first line of immune defense (non-discriminatory)
immune defense acquired after exposure to foreign invader (remembers foreign invaders to prevent disease
why is the skin important relative to the immune system?
a barrier that prevents microbial invasion within the body
typically acidic pH of about 5.0
covered in stratum corneum (cell armor)
skin oil inhibits a lot of microbes
sweat glands deposit NaCl/lysozyme; degrades bacterial cell wall peptidoglycan
epithelial cells with tight cell junctions are under
desquamination (shedding) rids skin of pathogens
(competitive expulsion) microbes on our skin compete for space making it difficult for pathogens to come in
mucosal membranes
body’s internal surfaces lined with epithelium (mucus coated)
mucus
reduces contact microbes and epithelium by coating membrane surface
mucociliary clearance
What is the intestinal version of this (since in is not lined with ciliary epithelium)
the process of unique ciliated epithelial cells beating cilia to physically move trapped particles/mucus out of passages
peristalsis
antimicrobial peptides
secreted by epithelial cells, disrupt microbial membranes, which result in gaps/pores
True or False: Competitive exclusion does not occur on mucosal surfaces
False
What may limiting the availability of FREE iron do to the body
cause a bacteriostatic effect (stop/ inhibit bacterial growth)
Why do cells keep iron in chemically bound form (like hemoglobin, Ferrin, transferrin, and lactoferrin) than free?
free iron may influence the synthesis of dangerous free radicals/ susceptibility to infection
inflammation
immune response to harmful stimuli
results in the activation of cells that repair/defend damaged/infected site
proinflammatory molecules
What types are secreted during infection
elicit inflammation and attract cells to the site of damage/ infection
cytokines
give examples of cytokines
“tumor necrosis factor-alpha (TNF-α), and interferons (IFNs)”
what are the processes involved in the start of an inflammatory response
1.) inc. cell permeability
2.)vasodilation (inc. in diameter of blood vessels
3. extravasation (the movement of cells/molecules from blood vessels to tissues)
What do phagocytes do and release to attract more cells to the area?
specialized leukocytes that swallow and destroy microbes (like interleukin 8 (IL-8))
How does a fever occur? Why does this happen?
“cytokines IL-1, IL-6, and TNF-α” work on the hypothalamus to cause this
restricts the growth of many pathogens to allow the immune system to clear them
in what case does inflammation work in favor of the body
when it is localized to the infection site
systemic inflammatory response
how may it occur
what does it result in
when inflammation is widespread rather than one particular area (chemical signals that are excessively released)
body shock; a huge drop in blood pressure and excessive circulatory system fluid leak (results in vital organ damage, and death in many cases)
if microbe escapes initial inflammatory site and goes to other places in body (like bloodstream
septic shock
toxic shock
systemic inflammatory response caused by widespread presence of bacteria in the body
systemic inflammatory response caused by exotoxins that trigger the immune system
“Injection of large amounts of either of which cytokines in animal models have shown they can induce clinical signs of septic shock in the absence of infection”
“IL-1 and TNF-α”
PAMPs
give examples
how are PAMPs recognized
(pathogen-associated molecular patterns) unusual molecules on microbes that a host recognizes as foreign
(not usually found in host cells)
lipid A section of gram-negative LPS
PRRs (pattern recognition receptors)
lipoteichoic acid of gram-positive cell walls
mannose of bacterial/yeast cell walls
TLRs
(Toll-like receptors) involved in initiation of immune responses in both invertebrates and vertebrates
signal the immune system about the nature of the pathogen
What does TLR9 recognize
CpG dinucleotides (unmethylated pairs of adjacent cytosine and guanine nucleotides) (these are usually found in bactr=erial and some viral DNA
nuclear factor kappa B (NF-KB)
transcription factor recruited when TLRs bind to PAMP
induce gene transcription of proteins that protect the host depending on the recognized pathogen
Type I interferons (IFNs)
induced by NF-KB; have antiviral activities and proinflammatory cytokines
when it comes to cytokines TNF-α and IL-1 produced by macrophages/ neutrophils, what causes:
1. fever production
phagocyte proliferation
extravasation of leukocytes
vascular permeability increase
C reactive protein production
T cell activation
IL-8 and IL-6 induction (adaptive immunity)
“TNF-α and IL-1”
“TNF-α only”
“TNF-α and IL-1”
“TNF-α and IL-1”
“TNF-α and IL-1”
“TNF-α and IL-1”
“TNF-α and IL-1”
adjuvant
enhances immune response to vaccination through stimulation of innate immune system
Ribi.259
adjuvant that activates TLR4 like bacterial LPS does.
mannose-binding lectin
What does it bind to?
secreted PRRS that bind to carbohydrates
- N-acetylglucosamine of peptidoglycan
- carbohydrate mannose
opsonization
coating of microbial wall, enhancing phagocytosis
name some secreted PRRs
mannose-binding lectin (MBL)
C reactive protein
LPS-binding protein
Complement factor C3b
What is the most common cause of non-HIV human immunodeficiency?
MBL deficiency
c reactive protein
what does it recognize and bind to
secreted lectin; made by the liver in response to inflammation
” recognizes and binds to phosphatidylcholine of microbial membranes and phosphocholine”
what do MBL and C reactive protein have in common
both secreted PRRs
opsonize microbial cell (enhance phagocytosis)
activate complement cascade
Complement
a group of 30+ proteins involved in binding to microbial surfaces and causing lysis
MAC
(membrane attack complex) result of complement cascade (innate mechanism) leading to lysis of microbes
what pathways activate the complement cascade?
classical pathway
alternative pathway
lectin pathway
What is the difference between the classical pathway and the lectin/alternative pathway?
the latter are activated in an antibody-INdependent manner
what activates the lectin pathway?
The alternative pathway?
MBL attaching to mannose or “N-acetylglucosamine of LPS”
C3b binding to microbial components like LPS
TYPE I Interferons
class of cytokines
can produce an antiviral state to protect unifected neighboring cells from infection
“interferon-alpha (IFN-α) and interferon-beta (IFN-Β) are the major members”
How do TYPE I interferons prevent viral infection?
ribosome binding inhibition
membrane component changes
RNA degradation
cytotoxic T cell division
When it comes to the immune system, what is cellular defense started by?
Why?
phagocytes/natural killer cells
they respond quickly to invasions before adaptive immune system can act
opsonins
molecules that bind to foreign substances, enhancing phagocytosis
respiratory oxidative burst
done by macrophages and neutrophils during phagocytosis
For maximally enhanced phagocytosis, what do macrophages/ neutrophils do?
Need help of cytokines like “interferon-alpha (IFN-α) and interferon-beta (IFN-Β) are the major members” made by the adaptive system
What is the killing action of
lysozymes
proteases
defensins
peptidoglycan hydrolyzation
protein degradation
forms pores in the bacterial membrane
what are the toxic oxygen products of the respiratory burst?
hydrogen peroxide
hypochlorous acid
hydroxyl radical
superoxide anion
nitric oxide
What occurs when pathogens are too big for phagocytosis?
“Eosinophils, basophils, and mast cells release granules that break shit down through degranulation
degranulation
What is usually needed for this to occur?
release of toxic contents onto the target cell (cytotoxic)
the presence of IgE antibodies (made in response to allergens) made by B cells
How does innate immunity deal with immune response to intracellular pathogens?
natural killer cells that target infected cells (cytotoxic not phagocytic)
What are granular components of NK cells?
perforin (pore producer) and granzymes (apoptosis inducer)
how do NK cells target infected cells
they lack the MHC I surface markers
antibody-dependent cell-mediated cytotoxicity
mechanism, where NK cells bind to cell Fc receptors, results in apoptosis of the target cell
hemocytes
strictly for invertebrates; cytokines attract these phagocytic to infected area
