The gram negative cell wall Flashcards
1
Q
What is Braun’s lipoprotein
A
Links the outermembrane to peptidoglycan
2
Q
What is the endotoxic response
A
in gram negative cells
-> induces a endotoxic response: inflammatory response which can result in shock and death
3
Q
what is unique to gram negativ ebacteira
A
the outer membrane
4
Q
Does bacteria need to be alive for the outer membrnae to be in effect
A
No
5
Q
Whats the major role of gram negative outer membrane and important biological properties
A
Major role is structurual
importnat properties is toxicity to animals
6
Q
What are the toxic properties in gram negatives associated with
A
lipopolysaccharides (LPS) and specifically lipid
A which is an endotoxin (cell bound)
7
Q
What are symptoms of endoxins
A
fever (due to pyrogens), severe gastrointestinal distress (gas, diarrhea and vomiting)
8
Q
A
8
Q
What are the components of the outer membrane in gram negative. Outer layer, inner layer, whats embedded
A
- outer layer: composed of species-specific lipopolysaccharides (LPs)
- Inner layer: consists of phospholipids, similar to those in the plasma membrnae
- embedded in the outer membrnae:
+ specific and nonspecific proins
+ brauns lipoprotein (connecitng the membrane and the glycoprotein)
+ other otuer membrane proteins (omp)
+ divalent cations essential for structual integrity of outer membrnae
9
Q
What are proins
A
form specific and non-specific aqueous channels through the
hydrophobic outer membrane (OM)
10
Q
outer membrnane of gram negative is
A
hydrophobic
11
Q
What are speicfic proins
A
E.coli LamB which allows passage of
maltose and related sugars (receptor for bacteriophage Lambda)
12
Q
What are nonspecific proisn
A
OmpF (larger than OmpC) and OmpC which limit passage of aqueous substances based on size
13
Q
How is the presence of a particular porin is regulated by the cell’s environment for lamB
A
- LamB present when maltose is present and glucose is absent
14
Q
How is the presence of a particular porin is regulated by the cell’s environment for OmpC and OmpF
A
in high solute environments e.g. the human colon the E.coli outer membrane has more OmpC channels than OmpF channels
15
Q
how does changes in porins contribute to virulence
A
resistance to β-lactam antibiotics can be due to decreased
permeability of β-lactam antibiotics across the o.m.
» can be due to a mutation in a porin gene on the
bacterial chromosome
16
Q
Which component of the outer membrane contributes to the stability of the outer membrane
A
Braun’s lipoprotein
17
Q
What is the braun’s lipoprotein
A
is the most abundant outer membrane (o.m.) protein
N-terminus of the protein is covalently linked to the o.m. inner leaflet phospholipid while the C-terminus is linked to amino acid 3 of peptidyl-muramic acid in the peptidoglycan layer
18
Q
What happens hwen a cell has defective braun’s lpp
A
- continuously lose or shed their o.m.
- Under these conditions: have increased requirement for Mg++ and Ca++ and are sensitive to certain antibiotics e.g. novobiocin and detergents
19
Q
which component of the gram negative induces production of cells needed to make antibodies
A
Braun’s lipoprotein (Lpp)
20
Q
Effect of braun’s lipoprotein on B lymphoctes
A
- the lymphocytes that are involved in humoral (which means circulating in blood and lymph) antibody synthesis
- Lpp causes B lymphocytes to undergo mitosis -> increase the number of B lymphocytes available -> presence of gram negative induces production of cells needed to make antibodies
21
Q
What are the functions of lipoprtoeins (including Braun’s lipoprotein. when refer to lipoprotein, it can refer to other stuff rather than
A
- Cell division
- Stress response
- Virulence
- Outer membrnae biogenesis
- Peptidoglycan syntheis and remodelling
22
Q
What are lipopolysacchardies (LPs) and lipooligosaccharides (LOs)
A
the lipids in the outer leaflet of the
gram negative o.m. consists of
LPs or LOs
23
Q
Structure of LPs and LOs
A
3 regions in the same direction: O-antigens, Core, Lipid A
24
Whats the O-antigens
Sugar (polysachcaride) side chain
- Side chains extend and are highly immunogenic
- induce the sysntheiss of antibodies in a host aminal
25
How are species or strains identified using O antigens
antibodies made to O-antigens are often used in identifying specific
species or strains
26
O-antigens consist of
chains of a variety of sugars
the number of sugars and type of sugar in the side chain depends
on the bacterial species or strain
27
Compositon of the O antigens can vary
can also vary with the physiological state of the
bacterial cell or due to mutations
28
What are changesin O antigens lead to
small changes in O antigens can result in lack of recognition by
antibodies made to other side chains
29
How do bacteria evade the host immune system
- switching of O-antigens is one of the mechanisms employed by bacteria for evading the host immune system
- this is transient evasion since antibodies will eventually
(several days later) be made to the new variants Brunt 2025
30
colonies of cells with long chain O antigens are (physical appearance)
smooth, glistening, mucoid
31
What is samolla responsible for
outbreaks of salmonellosis which is the second
most common gastroenteritis (nausea, vomiting, diarrhea,
sometimes fever)
considered a food infection, usually resolves itself but can be life threatening to the
elderly
32
The different serotypes of salmonella is due to
small variations in O antigens (LPS)
and H antigens (flagella)
33
common O antigens in Salmonella include
mannose,
abelose, rhamnose and galactose
34
LPs
(lipopolysaccharide) are when
when the o.m. outer leaflet polymer contains long chains of sugars of 30-40 sugars long, common in gram negative rods such as
E.coli and Salmonella
35
called a LOs (lipo-oligosaccharide).
when the o.m. contains short chains of sugars of 10 -20 sugars long
LOs is
common in gram negative cocci [e.g. Neiserria: N.gonorrheae is
causative agent of gonorrhoea and N. meningitidus is the
causative agent of meningitis
36
common in gram negative rods such as
E.coli and Salmonella
lipopolysaccharide
37
common in gram negative cocci [e.g. Neiserria: N.gonorrheae is
causative agent of gonorrhoea and N. meningitidus is the
causative agent of meningitis
when the o.m. contains short chains of sugars of 10 -20
sugars long it is called a LOs
38
Is absence of O antigens lethal
no
39
absence/or differences in O antigens can alter
- adherence and interaction with other cell types or tissues
➢ability to be phagocytized
▪ cells with short O antigens are easier to engulf
than those with long O antigens
➢ability to be killed by host complement or bile salts
➢colonial morphology
▪ colonies of cells with short chain O-antigens or
no O-antigens are rough/ dry and fall apart
easily
40
cells with short O antigens are _____ to engulf
than those with long O antigens
easier
41
Funciton of diavalent cations
Divalent cations like calcium (Ca2+) and magnesium (Mg2+) bind to lipopolysaccharides (LPS) and other negatively charged components in the cell wall, neutralizing electrostatic repulsion and strengthening the overall structure.
42
What does EDTA do
EDTA binds to divalent cations like Ca²⁺ and Mg²⁺ → removes them from the membrane.
When those cations are removed, the LPS becomes unstable, and the outer membrane falls apart (becomes permeable or disrupted).
43
What does adding CaCl2 to the cell do
can weakened the
o.m. and mask the negative charges in phospholipids in the inner leaflet (useful in cloning foreign DNA into E.coli since treatment allows passage of large molecules such as plasmid DNA into the periplasm and cytoplasm)
44
Are core region of LPs and LOs toxic
do not appear to be as toxic to mammals
as lipid A (faces interior)
45
What is the core region of LPs and LOs
ontains a variety of sugars e.g. glucose,
galactose, N-acetylglucosamine and the unusual substance KDO ( 2 keto- 3-deoxyoctonate) linked by phosphates to
ethanolamide
46
ROle of core region
- maintaining the integrity of
the o.m. in conjunction with OmpA and Lpp (peptidoglycan lipoprotein)
- it contains calcium and magnesium and is affected be agents that chelate these cations (EDTA): causes o.m. to fall apart at
high concentrations (.50mM) of Calcium chloride or other divalent cations salts
47
What is lipid A
is a component of LPs and LOs that extend toward the inner leaflet of the outer membrane
48
Is lipid A essential to the bacterial cell
Yes
49
changes in lipid composition are
lethal
50
What is lipid A? What does it contain
- lipid A is a component of LPs and LOs that extend toward the inner leaflet of the outer membrane
- Lipid A contains a number of fatty acids, such as lauric, palmitic, myristic acids as well as other lipids
- the fatty acids are attached to a disaccharide sugar glucosaminephosphate
51
Effect of lipid A on mammalian cell membrnaes
lipid A directly damages mammalian cell membranes and is the component of LPs (or LOs) that is responsible for the highly toxic
effects (endotoxic) induced by gram negative cell walls, o.m. only or isolated LPS in humans and other animals
52
Bacterial endotoxin refer to
gram-negative lipopolysaccharides
53
Whats an exotoxin
not a structural component of a bacterial cell (i.e. not LPs) but rather a bacterial toxin that is synthesized and released from the
bacterial cell (i.e. secreted)- the bacterial cell does not lyse when it releases an exotoxin
54
Whats an endotoxin
a bacterial toxin that is a structural part of the bacterial cell and is only released when all or part of the bacterial cell falls apart. The
only bacterial endotoxin is LPs
55
When are 2 major physiological responses induced by endotoxins?
REMEMBER, ITS THE CELL WALL, ITS THE POLYLIPOSACCHARIDE
if LPs or gram negative cell
walls or gram negative cells find
their way into an animal blood
stream or tissue (i.e. in locations
other than the lumen of the
gastro-intestinal tract which is a
normal environment)
56
What is the endotoxic response also known as
Innate Immune Response
or inflammatory
response
57
What are the 2 major physiological responses induced by endotoxins? who is responsible
1. Innate Immune Response
(endotoxic or inflammatory
response): component of
LPs primarily responsible;
lipid A
-part of first line of defence
2. Acquired Immune response
(specific immune response)
component of LPs primarily
responsible is O antigens
-requires expose to antigen
and
development of antibodies
58
Difference between O-antigens, LipidA and exotoxins: heat
heat stable
Heat stable
Heat labile
59
Difference between O-antigens, LipidA and exotoxins compositin
polysaccharide
Lipid and sugar
protein
60
Difference between O-antigens, LipidA and exotoxins dose level
Toxic only in high
doses (rarely toxic)
Toxic only in
high doses
Toxic at very low
doses
61
Difference between O-antigens, LipidA and exotoxins: variability
O: Highly variable: depends on cell type and
physiological state of the bacterial cells
LipidA: Generally similar in all cells
Exotoxin: Many belong to a family of proteins (dimeric exotoxins with similar structure)
62
Difference between O-antigens, LipidA and exotoxins: immunogenitiy
O: highly immunogenic
LipidA: weakly immunogenic
Exotoxins: immunogenic
63
Differences between exotoxins and endotoxins
Fever, location and production
Exotoxins: do not produce fever, usually excreted outisde the living cell, produced by gram positive and gram negative bacteria
Endotoxins: produce fever, part of the cell wall, found only in gram negative bacteria, released on bacterial death and liberated duiring growth
64
When are endotoxins reelased
only when the bacteria dies or when the cell wall partly dies
65
Virulence factors in salmonella
- Enterotoxin
- cytoxin
- Fimbriae (adherance)
- VI capsule antigen: inhibits complement binding
- Flagella (H antigen - motilidty)
- O antigen (inhibits phagocyte killing)
66
How are capsules a virulent factor
- it decreases phagocytosis in S pyogenes by releasing a protease that cleaves a complement factor -> inhibit ability to attract phagocytes to infected area
- Staphylococcus produces leukocidins
67
Whats non specific host defence
innate immunity
68
What are the non-specific host deferndces in skin
skin-associated lymphoid
tissue: keratinocytes that
represent major component of
epidermis that secret cytokines:
inflammatory response
69
What are the non-specific host deferndces in our body
- Lysozyme
- mucus, cilia,
- mucus, phagocytes
- blood and lymph proteins
- rpaid pH change
- flushing of uinary tract
70
What are the 4 charactersistics of acute inflmmation
heat, redness, swelling, pain, --> closs of function
71
Why are defences non specific
because they act against any type of
invading microbe
72
The cascade of responses that occur in the endotoxic (inflammatory) response is
one type of non-specific host defense. immunity that is with you from birth
non-specific defenses are present and/or go into action before specific
host defense mechanisms (acquired immune response) are activated
73
Non specific host defenses: physical barriers
-the skin and mucous membranes
-thick keratinocytes on outer layer
(secrete cytokines)
-key point is the shedding of outer skin
layer that removes microorganisms
74
Non specific host defenses: chemicals barriers
-antimicrobial substances (lysozyme)
in body fluids such as saliva,
mucus, gastric juices (HCl), acid pH of
stomach (pH 1-2) and skin (3-5)
-anti-bacterial fatty acids on skin
-bacteriocins (toxins) produced by
normal bacterial flora that kill other
related species
-iron limitation mechanisms (mucousmembrnaes)
75
Other non specific host defences
- surveillance by phagocytes:
neutrophils, macrophages
skin associated lymphoid tissue ,
e.g. Langerhans (myeloid cell) prevent
access to blood stream
- inflmamation: heat, redness, swelling, pain
- pyrogenitiy (dever): -kills or inhibits invading microbes may also inhibit exotoxins or
enzymes produced by invading agent
- molecular defenses: interferons and complement proteins produced by certain cell
types that inhibit or destroy invading
microbes
-molecules secreted by non-phagocytic
basophils
76
What is inflammatory repsose
innate respons
77
What is an endotoxic response
is an inflammatory response induced by the
presence of gram-negative cells, gram-negative cell walls or LPs (bacterial endotoxin: lipopolysaccharide)
- primarily the tissue damage caused by lipid A that is responsible Inflammatory
78
Responses similar to endotoxic response can be induced by
- infection with other microbes
* mechanical damage (abrasions, cuts, burns)
* chemical damage (phenols, strong acids and alkali) to tissues
79
inflammation involves a cascade of interrelated responses including:
- pyrogenesis (fever)
* inflammation
* shock: ( at higher levels of inflammation)
* death: massive organ failure: insufficient oxygen to brain
80
Whats septic shock
Septic shock occurs when a bacterial infection causes low blood pressure.
if induced primarily by the
presence of microbes
81
Whats a toxic shock
if induced primarily by a toxin
82
What are cytokines
Associated cell products involved in the endotoxic response. ALl are secreted:
– interleukins (1-17)
– interferons (multiple types)
– Chemokines (direct chemotaxis therefore also called chemokines)
– colony-stimulating factors,
- tumor necrosis factors
83
Defensive cells include
- circulating : i.e. found in the blood but can move into tissue in
response to microbes e.g. WBC such as monocytes (mature into macrophages and dendritic cells), granulocytes
(neutrophils) cells
- fixed (e.g. macrophages) cells: they are located in specifictypes of tissues
84
What are the types of blood cells
lymphocytes and leukocytes
85
What are lymphocytes
WBC from lymphoid line involved in the acquired immune response
86
What are leukocytes
WBC from the myeloid cell line
but not RBC’s andplatelets are involved primarily in the
innate immune respons
87
origins of blood cells
pluripotent stem cells in the bone
marrow produce two major cell lines
88
lymphocytes include and come from
lymphocytes: b cells, t cells and natural killer cells
come from lymhoid stem cells
89
Whats the myeloid cell line give rise to
- erythrocytes (RBC),
- thrombocytes (platelets)
- certain WBC:
- granulocytes: basophils, neutrophils
- agranulocytes: monocytes
- mast cell
90
What are basophils
are non-phagocytic (cannot migrate from
bloodstream) that release compounds needed for response: e.g vasoactive mediators and play a role in allergic response along with mast cells
help the phagocytes
91
What are neutrophils
- phagocytic , produce antimicrobial substances to kill ingested microorganisms and like macrophages have
receptors for antibodies and complement proteins
- but unlike
macrophages do not reside in healthy tissue but circulate in blood
so they can rapidly migrate to the site of tissue damage and
infection,
92
What are monocytes
agranular leukocytes, circulate and then migrate to tissue and mature into macrophages or dendritic cells.
93
What are macrophages
- have the largest collection of receptors
- classed as phagocytic leukocytes
which have receptors that recognize surface components of
pathogens: including toll-like receptors, mannose receptors
and Fc receptors for antibody and receptors for complement
94
What are Dendritic cells
contact, phagocytose and process antigens →
display foreign antigens on their surfaces (antigen presentation)
95
High levels of WBC are indicative of
a systemic bacterial infection)
96
What happens when monocytes leave the blood
they differentiate into macrophages
macrophages may migrate or alternatively become fixed in certain tissues
97
Macrophages and neutrophils are
highly phagocytic cells
98
Where do neutrofils reside
do not reside in healthy tissue (macrophages can) they are found in the
blood but rapidly migrate to site of damage/infection. These cells contain lytic
enzymes and bactericidal substances
99
In a virla infection, the WBC count is lower/higher than normal
lower
100
when microbes invade a tissue
both macrophages and neutrophils migrate to the
site of infection (neutrophils are usually the first to arrive): both are phagocytic
101
cytokines (low molecular weight signalling proteins) are essential for
communication between defensive cells of the innate (myeloid line) and acquired (lymphoid) responses
102
How are cytokines released and how do they work
- are released by the circulating and fixed phagocytes as well as mast cells in
response to bacterial invasion or to presence of endotoxins (LPs)
- interleukins, colony stimulating factors (CSFs) as well as others have several different effects including causing the proliferation of white blood cells
103
a subclass of cytokines are
chemotactins
(chemokines) which attract phagocytes
resulting in the movement of phagocytes
towards the sites of infection and/or tissue
damage
* there is similarities between bacterial and
phagocyte chemotaxis
104
when fixed (immobile) the phagocytes
(macrophage) have
specific names
depending on their location
105
The Monocyte-macrophage system
- fixed macrophages and mast cells are associated with blood vessels and
connective tissue and play a role in the endotoxic inflammatory response
- mast cells, macrophages and neutrophils
release cytokines that are involved in the
inflammatory responses
106
Whats the fever
very important non-specific host
defense
107
What are pyrogens and what do they do
- Agents that cause fever are called pyrogens
- pyrogens act on the hypothalamus of the brain to increase body
temperature
108
What are the 2 classes of pyrogens:
exogenous and endogenous
109
What are exogenous pyrogens
* infectious agents or components of infectious agents (endotoxins)
* can also act as exogenous chemotactins (cytokines) to attract
macrophages
110
What are endogenous cytokines
cytokines released by phagocytes and by damaged
tissues
111
Whats the global regulatory response
heat shock
or stress response
112
What is fever thought to do
slow the metabolism and growth of invading pathogens
113
when invading microbes are subject to an increase in temperature
undergo a heat shock
or stress response (global regulatory response)
114
What are the steps of phagocytosis
Phagocytosis via circulating and fixed macrophages and neutrophils
1. Find
2. Adhere
3. injest
4. digest
115
What are exogenous chemotactins (aka chemokines)
- released by invading microbes
- helps phagocytes find the tissue
116
What are endogenous chemotactins
released by damaged tissue
117
How to phagocytes first find the damaged tissue
exogenous chemotactins (i.e. chemokines) which are released by invading
microbes and endogenous chemotactins released by damaged tissue
mast cells and phagocytes (neutrophils/macrophages) already at the site
recruit phagocytes to the site of infection which allows the phagocytes to find
the invading organisms
118
Where are toll like receptors found
found on phagocytic cell surface
119
Adherance of phagocytic cells can be
can be specific or nonspecific adherence
120
non speicifc adherance of phagocytic cells
can occur by hydrophobic interactions between the
surface of the microbe and the phagocyte
121
Specific adherance of phagocytic cells
Toll like receptors (TLRs): found on phagocytic cell surface has various
receptors that can recognize and adhere to various specific components
of microbial cells
there are receptors for LPs, peptidoglycan, pili, flagellar proteins
(flagellin) bacterial nucleotide sequences as well as other components of bacterial cells)
❖ if the bacterial cell is covered with antibodies and/or opsonized
(covered with serum protein complement C3b) the adherence can
also be via another surface receptor and ingestion will be enhanced
122
What happens if bacteria start to lyse
can recognize the components inside the bacteria
123
What happens when a component of the bacterial cell activates a toll like receptor
a signal is transmitted to the nucleus of host to alter gene expression of certain genes: -> produce more cytokines -> recruit more marcrophages (not exactly making more macrophages)
e.g. LPs
triggers monocytes and macrophages to produce chemokine (a cytokine) that attracts
additional phagocytes to the site (i.e. recruitment)
124
Injestion of the bacteria by phagocyte
- adherence of the pathogen to the phagocyte induces ingestion
* pseudopodia surround the bacteria, fuse and form a cytoplasmic vacuole called a
phagosome that contains the bacteria
125
Digestion of the bacteria
once inside the phagosome the invading organism is bombarded with antimicrobial substances
all of the antimicrobial substances cause significant damage to the bacterial cell (if not killed immediately, bacterial cell may in fact mount heat shock response)
- lysosomes (low pH) fuse with the phagosome to form a phagolysosome: continue to attack
the microbe with antimicrobial agents
- the pH drops and lysosomal enzymes are activated, leading to the digestion of bacterial
cells by several enzymes (lysozyme, β-glucoronidase, proteases etc)
- the pH drops and lysosomal enzymes are activated, leading to the digestion of bacterial
cells by several enzymes (lysozyme, β-glucoronidase, proteases etc)
- material in the residual body is either digested completely or the residual body fuses with the
plasma membrane and the debris is removed by exocytosis
126
What are some antimicrobial substances inside the phagosoem
- defensins: cationic proteins that can punch holes in the bacterial plasma membrane
– reactive oxygen intermediates (ROIs) e.g. superoxides and peroxides: toxic oxygen kill
invading microorganisms
– reactive nitrogen intermediates (RNIs) e.g. nitric oxide, nitrites and nitrates that block
bacterial respiration by complexing with iron in electron transport chain
127
What happens if bacteria isnt killed immediately
they mount heat shock respons
128
many bacteria have evolved mechanisms to avoid detection, adherence, ingestion. previous exampe
Fc binding proteins of group A strep:
129
How do phagocytes which are already at the site recruit more
recognition of exogenous chemotactins -> they bind through toll like receptors
-> effect the nucleus, increase transcription of cytokines -> recruit more phagocytes
130
What are chemokines/chemotactins
infectious agents or individual components of infectious agents (microbes) can act as
chemokines which are specific substances that attract phagocytes
131
examples of chemotactins
- gram negative cells and cell walls
– LPs (lipopolysaccharides)
– gram positive cells and cell walls
– peptidoglycan
– teichoic acids
– f-met peptides
since these are bacterial substances and therefore are not normally found in
the animal they are referred to as exogenous chemotactins
most of the above substances can also be recognized by Toll-like receptors
on the surface of phagocytes
132
Additional chemokines/cytokiens are release dwhen
when basophils, mast cells in
connective tissue macrophages and neutrophils come in (exogenous cytokines) or
come in contact with signaling molecules that are produced from damaged tissue
(endogenous cytokines)
133
Are chemkines like cytokines
Chemokines are a subclass of cytokines. they can be exogenous or endogenous
134
What are endogenous cytokines
made and
secreted by host to aid in response
135
Examples of endogenous cytokines
- Interleukins
- interferons
- Hematopeitins
- Tumor necrosis factor (TNF)
- other cytokines including those that function as chemokines (cytokines that are chemtactic for leukocytes: stimulate migration)
136
What are interleukins
induce differentiation of phagocytes : many involved in inducing B cells to increase antibody production
137
What are interferons
induce differentiation of phagocytes : many involved in inducing B
cells to increase antibody production
138
what are Hematopeitins
stimulate blood cell formation (cytokine)
139
What are mast cells
in connective tisuse
140
Are all substances released by mast cells and phagocytes cytokines/chemokines
no
141
What are some substances released by basophils
histamines => release in response to stimulation
prostaglandins => increase vascular permeability
142
What is produced that increases vascular permeability
prostaglandins, produced by basophils
143
What are some other things released by phagocytes and mast cells
lactoferrin and lysozyme and lactoperoxidases
144
purpose of releasing lysozyme and lactoperoxidase
catalyzes superoxide radicals in mucous membranes
145
Purpose of releasing lactoferrin? released by
an iron chelator made by
animals in response to bacterial infections
important because may bacterial genes required for growth of the
bacterial cell require iron for their transcription
-> lead to reduced iron levels bacterial transcription and hence growth reduced
secreted by macrophages
146
Whats the molecular reason for inflmmation
entry of fluids and substances from blood into tissue at an infection site or injury site causes inflammation
147
What are the symtoms of inflammation
1. swelling
2. pain
3. redness (vasodiliation)
4. heat (localized - due to increased blood flow)
5. loss of function
148
Is pyrogenesis different from calor
yes. since feer is systemic and calor is localized at the site of infection
149
How do cytokines released by mast cells, phagocytes and damaged tissue have
effect on blood vessels and blood flow
▪ blood vessels to dilate (vasodilation)
▪ increased blood flow
▪ change capillary permeability
-> allow fluids and white blodo cylles (phagocytes, monocyte/macrophage/neutrophils to leave capilliaries and enter tissue and move to the site of infection
150
What effects the blood vessels and blood flow
cytokines released by mast cells, phagocytes and damaged tissue
151
everything we've discussed about the inflmmatory response doesnt apply to only microorganism infections but also
to trauma or mechanicial injuries.
this elads to endogenous chemical mediators (damanged tisuse)
152
What is the role of inflammation
is to contain the site of damage, localize the response and restore tissue function
153
What is the inflammatory response in a nutshell
coordinated response to microbial invasion or tissue
damage brings phagocytes and other leukocytes to the site:
154
What are the 4 phisological events that occur in inflammation
- Normal blood flow when injury occurs
- Substances released cause dialation of small blood vessels and increased blood flow
- phagocytes attach to endotheilial cells and then sqeeeze between cells into surrounding tissue
- attraction of phagocytes -> site of damage
-> collection of dead tisuse and debris -> pus ->
155
Summarize the physiological events of the acute inflammatory response
at site of injury, chemical messengers are released from the damaged tissue,
mast cells and the blood plasma (e.g. neutrophils, monocytes)
-chemicals stimulate neutrophil/macrophage (phagocyte) migration, chemotaxis and Phagocytosis
156
What should be kept in mind when engulfing a gram negative and killing it there
an endotoxic response resulting in
Fever (pyogenic response) due to
Release of endogenous cytokiner
157
What are the symptoms of inflammation
tumor = swelling
dolor = pain
rubor = redness
calor = heat
158
Does the inflmamtion need to be resolved
yes, by lipoxins, resolvins, protectins
159
What happens if you use anti inflmatory drugs
treat inflammation
but will reduce the protection from infections
160
Why is the inflammatory response essential
it protects the organism from
infection
– once triggered it confers additional transient (for 2-5 days) protection
against subsequence infection by any other microbe
161
certain chronic diseases appear to be the result of an uncontrollable inflammatory response
uncontrollable inflammatory reaction
* inflammatory bowel diseases
treatment may involve massive doses of anti-inflammatory drugs, which is often essential to control the inflammation but will also increase the risk of infections
162
when large amounts of endotoxins, bacterial cells or other inducers
of the inflammatory response are present the response may be
massive and result in
damage to blood vessels and other tissues
163
as long as the damage is not to severe can be treated with
antiinflammatory drugs
164
if not controlled the inflammatory response can cause:
* a dramatic decrease in blood pressure
* tachycardia
* poor pumping of blood leading to anoxia in certain tissues such as
the brain
* change in electrolyte balance
* shock (once entered difficult to reverse leading to the last two steps
* organ failure
* death
165
uncontrolled inflmamatory response was also found in
group A strep
166
