Term
|
Definition
| Takes benefits without hurting nor helping the host |
|
|
Term
|
Definition
| Exposed to outside / external environment such as skin, oral, nasal cavities, lungs, etc. |
|
|
Term
|
Definition
| Internal Organs. If you find a microbe here, it means that there is an infection |
|
|
Term
|
Definition
Prevents microbes from growing due to: 1) acidic low pH 2) low water 3) high salt 4) lysozyme, an antimicrobial enzyme that breaks bacterial walls |
|
|
Term
| What microbes must do to inhibit ORAL/NASAL sites? |
|
Definition
| Adhere to surface of teeth or gums |
|
|
Term
| What bacteria can inhibit oral/nasal cavities? |
|
Definition
Step-TO-coccus. Causes biofilms and the fermentation causes cavities. |
|
|
Term
| What is a danger of oral microbes going to blood? |
|
Definition
| if they enter bloodstream, they can cause bacteremia. |
|
|
Term
| What microbes do lungs or trachea in the respiratory system have? |
|
Definition
| None. The cilia in the epithelial cells traps bacteria and pushs them out. |
|
|
Term
| What bacteria or microbes are in the stomach? |
|
Definition
| None due to low pH, highly acidic. Stomach lining though have slighter higher more basic pH |
|
|
Term
| Bacteria in Stomach lining |
|
Definition
Heli-co-bacter Pylori
Helicobacter pylori |
|
|
Term
| Normal microbes in intestine |
|
Definition
anerobes in majority. some facultative anerobes. Diverse biota microbes can be harmful if they go to nearby tissue.
anerobes of Clostridium and Bacteriodetes species Facultative type of Entero(relating to intestine)bacteriaceae |
|
|
Term
|
Definition
Help restore balance of intestine microbe population. Lacto-bacillus Bi-fido-bacterium |
|
|
Term
|
Definition
Generally has no microbes.
Distal part of uretha has enteric and Staphylococcus types. |
|
|
Term
|
Definition
rich environment Lacto-bacillus most popular -changes with menstrual cycle |
|
|
Term
|
Definition
-make vitamin and digest food -prevent colonization by pathogens -Enhance immune system by immunomodulin proteins -potential as a vaccine delivery vehical |
|
|
Term
|
Definition
| normal benign bacteria become opportunistic and causes disease when host defenses are compromised (such as during medical treatment or disease) |
|
|
Term
| Nonadaptive Innate Immunity |
|
Definition
| Present at birth Physical barriers: skin, mucous membrane, lungs Chemical barrier: pH, lysozyme, antimicrobials Nonspecific cellular barriers: inflammatory response, natural killer cells, inferons, phagocytosis, complement, fever |
|
|
Term
|
Definition
Reaction to specific antigens (foreign protein/sugar/chemical parts)
-Body reacts to antigen when exposed -Retains memory of these antigens and responds faster in the next exposure |
|
|
Term
|
Definition
| Found in the bones, where all blood cells (WBC, RBC, Platelets) come from |
|
|
Term
Lymphoid stem cells in bone/3 types of lymphocytes originate from lymphoid tissue |
|
Definition
gives rise to lymphocytes which differentiate into three kinds:
1) Natural killer cells: innate 2) T cells: adaptive 3) B cells |
|
|
Term
Types of white blood cells (The purpose of WBC is to fight microbes) |
|
Definition
Toxin releasing: Baso-phils and Eosino-phils Engulf via phagocytosis: Mono-cytes, Neuro-phil Act in adaptive immunity: Lymphocytes |
|
|
Term
| What do Monocytes differentiate into? |
|
Definition
Macrophages: phagocyte in both adaptive and innate systems
Dendritic cells: antigen-presenting cells, act as a bridge between the innate and adaptive immune systems |
|
|
Term
|
Definition
Where lymphocytes (T cells / B cells) mature
T cells: Thymus B cells: Bone marrow |
|
|
Term
| Secondary Lymphoid organs |
|
Definition
Where lymphocytes encounter antigens
spleen and lymph.
b cells and t cells differentiate here into Memory cells, anti-body producing cells, t-effector--> t-cytotoxic or t-helper cells |
|
|
Term
|
Definition
| trap microbes from non-blood fluid |
|
|
Term
|
Definition
-important in survelling the lumen of the intestine that is open to external environment -contain all kinds of WBCs (B cells, T cells, macrophages, etc). |
|
|
Term
|
Definition
| Dendritic cells of the skin, phagocyte and present antigen on surface |
|
|
Term
| Barriers in Skin to prevent infection |
|
Definition
SALT Langerhans cells (Antigen presenting cells) impermeable keratin structure, oil/sebum secretion |
|
|
Term
| Barriers in Mucous membrane to prevent infection |
|
Definition
microbes get trapped in the mucous, and the mucous chemical destroys them
GALT in Gastrointestine, tonsils, adenoids, |
|
|
Term
| Where are GALT (gut-associated lymphoid tissue) found? |
|
Definition
|
|
Term
|
Definition
| found in the epithelial surface of Peyer's patches or in other mucosa-associated lymphoid tissue, transport microbes from lumen of the intestine to to macrophages /dentric cells, etc. located in the basolateral side |
|
|
Term
| Where are some mucosa-associated lymphoid tissue located? |
|
Definition
| tonsils, intestines (called Peyer's patch), adenoid (lymphoid tissue where the nose blends the throat), GI tract |
|
|
Term
| Chemical barriers to infection |
|
Definition
| acidic pH, lysozyme, superoxide generators which are found in many secretions, defensins |
|
|
Term
| Defensins (innate immunity) |
|
Definition
small antimicrobial (+) cationic peptide made by human cells destroy invader's cell membrane |
|
|
Term
|
Definition
|
|
Term
|
Definition
stored in granules in the cytoplasm of host cells
They degranulate and release defensin extracellularly |
|
|
Term
|
Definition
|
|
Term
|
Definition
| way for body's phagocytic cells to gain access to infected sites |
|
|
Term
|
Definition
leaking of liquid out of its "container"
the movement of white blood cells from the capillaries to the tissues surrounding them |
|
|
Term
| what triggers inflammation? |
|
Definition
| introduction of microbes in the body |
|
|
Term
|
Definition
| released by resident macrophages who phagocytose bacteria |
|
|
Term
|
Definition
increase vascular permability and vasodilation (slows down blood flow and increase blood volume)
allows phagocytes to enter the site |
|
|
Term
|
Definition
| a small protein released by cells that has a specific effect on the interactions between cells or communication btw cells, examples are interleukins and inferons (which trigger inflammation and respond to infection) |
|
|
Term
|
Definition
|
|
Term
|
Definition
promotes extravasation
stimulates mast cells to degranulate and release histamine
stimulates release of prostaglandins |
|
|
Term
|
Definition
stimulates vessels to open further blood plasma, platelets released into the area |
|
|
Term
|
Definition
| stimulate nerve endings, causing pain |
|
|
Term
| cause of inflammation results |
|
Definition
| persistent presence of foreign object, causing permanent tissue damage |
|
|
Term
| Foreign objects that can cause inflammation |
|
Definition
-Pathogens that resist host defenses (Myobacterium Tuberculosis) -Nonliving irritant material (wood splinters (sharp edges), asbestos(builiding material) -autoimmunity(Crohn's disease): body doesn't recognize "self" and attacks it |
|
|
Term
|
Definition
| chronic inflammation; body doesn't recognize its part as "self" and attacks it |
|
|
Term
|
Definition
-collection of macrophages and other lymphocytes, fibrosis
-formed in chronic inflammation, when the immune system tries to wall off a foreign part b.c it can no longer eliminate it
- happen on skin or organs
- |
|
|
Term
|
Definition
| formation of excessive fibrous connective tissue in an organ or tissue in a reactive process |
|
|
Term
| How do phagocytes avoid attacking and engulfing host cells? |
|
Definition
| Through CD47, a surface glycoprotein only host cells have. Bacteria don't have it |
|
|
Term
|
Definition
| -combination of innate and adaptive immune responses |
|
|
Term
| What is one BIG benefit of opsonization and how does it help phagocytes? |
|
Definition
It allows phagocytes to engulf bacteria that is in a huge capsule.
Adaptive immunity: anticapsular antibodies coat the bacteria and Fc portion of the Antibody finds to receptors on the macrophage site
This allows for phagocytes to engulf the bacteria |
|
|
Term
| What is the next step that happens after the phagocyte engulfs the bacteria? |
|
Definition
| phagosome fuses with the lysosome |
|
|
Term
|
Definition
| a protein that has anti-microbial activity, binds to bacterial walls |
|
|
Term
| When does oxygen-independant killing pathways happen? |
|
Definition
| after bacteria has been engulfed and phagosome-lysosome fusion has happened |
|
|
Term
| What do oxygen-independant killing pathways utilize? |
|
Definition
lysozyme (enzyme that breaks bacterial walls) lactoferrin defensins (small + peptide, destroys invader's cell membrane). |
|
|
Term
| oxygen-dependant killing pathways utilize? |
|
Definition
| use production of oxygen radicals: superoxide anion (O2-), Hydrogen peroxide (H2O2), hydroxy radicals (OH-1). |
|
|
Term
|
Definition
-small cytokines (small molecules that serve as messengers) -low MW - interfere with viral replication -produce to warn host cells of a nearby infection -action is host specific, not virus specific (innate immunity!) |
|
|
Term
| how many kinds of interferons? |
|
Definition
|
|
Term
|
Definition
| -high anti-viral potency: binds to host cell receptors and makes them resistant to viral infection |
|
|
Term
|
Definition
modulates the immune system.
activates various white blood cells to increase MHC antigens on their surface |
|
|
Term
MHC antigens
(Major Histocompatibility Complex) antigens |
|
Definition
--have the antigen binded to them -are located on the cell surface -due to them, T-cells recognize the antigen |
|
|
Term
|
Definition
- they do not require activation in order to kill cells that are missing "self" markers of major histocompatibility complex (MHC) class I.
Destroy host cells that are infected and cancerous, b.c these cells lack MHC I surface proteins
-release perforins protein into target cell that creates pores in the membrane of the host cell, and lysis it nonspecifically |
|
|
Term
|
Definition
-located on various host cells -recognize pathogen-associated molecular patterns (PAMPs), located on microbes which are unique to them (peptidoglycan, flagellin, etc)
-recognize molecules that are constantly associated with threats and not part of self
-once the Toll-like receptors are bound, they trigger an intracellular cascade to regulate.
cause the cells to release cytokines
also bind to immune cells and cause them to engage the invading microbe |
|
|
Term
|
Definition
-it's purpose is to improve the killing of microbes by antibodies
-end results: forms pores in the microbe membrane causing leaking
-also complements help in opsonization by can attract WBC and help facilitate phagocytosis
-has 20 proteins that activate each other by proteolytic cleavage (cutting the AA bonds of proteins) |
|
|
Term
| 3 pathways to activate the complement |
|
Definition
-classical pathway -lectin pathway alternative pathway |
|
|
Term
| Detail of each complement activation pathway |
|
Definition
classical pathway: needs antibody lectin pathway: lectin coats bacteria and activates complement alternative complement pathway: |
|
|
Term
| alternative complement pathway |
|
Definition
Better and more effective for gram-negative bacteria than gram positive
Does not require antibody and attacks bacteria before immune response starts
**Begins with Complement Factor C3. C3 degrades to --> C3a, C3b |
|
|
Term
|
Definition
-used only in alternative complement pathway to activate complement cascade
-stabilized by gram-negative LPS layer -inserts into bacterial outer membrane -C3b+ other factors = form membrane attack complex (MAC), a destructive pore in target cell membrane
-also acts as an opsonin, increasing phagocytosis. Neurophils recognize any C3b bond to microbe targets and phagocytosized them. |
|
|
Term
|
Definition
| responsible for causing fever, a natural rise in body temperature set point |
|
|
Term
|
Definition
| -body's thermostat, regulates body temperature |
|
|
Term
|
Definition
originate outside the body bacteria, virus (LDS, etc) |
|
|
Term
|
Definition
-cytokins -interferons
act directly on hypothalamus to increase temperature set point |
|
|
Term
| Temperature and microbial growth |
|
Definition
-microbial pathogens grow ideally at 37 C -increase temperature slows growth -gives the immune system time to put down the infection |
|
|
Term
| Normal microbes that colonize the skin |
|
Definition
mostly Gram-positive
Staphy-lo-co-ccus
Baci-llus
Yeast (Cand-i-da) |
|
|