exam 4 Flashcards
The nervous system
a) Barriers at the surface of the human brain-Meninges: the three membranes (the dura mater, arachnoid, and pia mater) that line the skull and vertebral canal and enclose the brain and spinal cord.
b) Blood-brain barrier: is a highly selective semipermeable membrane barrier, separates the circulating blood from the brain and extracellular fluid in the central nervous system (CNS).
- is formed by brain endothelial cells and it allows the passage of water, some gases, and lipid-soluble molecules by passive diffusion, as well as the selective transport of molecules such as glucose and amino acids that are crucial to neural function.
-it prevents the entry of lipophilic potential neurotoxins by way of an active transport mechanism
-also has astrocytes which support the epithelial cells in maintaining the blood brain barrier
Microbes can enter the blood brain barrier through endothelial cells, can enter using “Trojan horse” by entering white blood cells
Can enter through the paracellular pathway- squeeze through junction between endothelial cells
Cause inflammatory response to cross blood-brain barrier
c) Blood-cerebrospinal fluid barrier: The blood–cerebrospinal fluid barrier is a pair of barriers that separates peripheral and cerebral blood from the cerebrospinal fluid (CSF); it is made of epithelial cells. The blood–CSF barrier serves the same purpose as the blood–brain barrier, but facilitates the transport of different substances into the brain due to the distinct structural characteristics between the two barrier systems.
The blood-cerebrospinal fluid barrier also modulates the entry of leukocytes from the blood to the central nervous system.
b) Blood-brain barrier:
is a highly selective semipermeable membrane barrier, separates the circulating blood from the brain and extracellular fluid in the central nervous system (CNS).
- is formed by brain endothelial cells and it allows the passage of water, some gases, and lipid-soluble molecules by passive diffusion, as well as the selective transport of molecules such as glucose and amino acids that are crucial to neural function.
-it prevents the entry of lipophilic potential neurotoxins by way of an active transport mechanism
-also has astrocytes which support the epithelial cells in maintaining the blood brain barrier
Microbes can enter the blood brain barrier through endothelial cells, can enter using “Trojan horse” by entering white blood cells
Can enter through the paracellular pathway- squeeze through junction between endothelial cells
Cause inflammatory response to cross blood-brain barrier
Blood-cerebrospinal fluid barrier
: The blood–cerebrospinal fluid barrier is a pair of barriers that separates peripheral and cerebral blood from the cerebrospinal fluid (CSF); it is made of epithelial cells. The blood–CSF barrier serves the same purpose as the blood–brain barrier, but facilitates the transport of different substances into the brain due to the distinct structural characteristics between the two barrier systems.
The blood-cerebrospinal fluid barrier also modulates the entry of leukocytes from the blood to the central nervous system.
- Be able to describe the basic structures and functions of the nervous system that are pertinent to microbial infection.
Nasal cavity: through nose, directly to the brain- the olefactory epithelium cells, to the olfactory bulb in the CNS
Microglia: function as macrophages in the CNS. Pathogens will get into the CNS through “Trojan horse- use paracellular transport (the transfer of substances across an epithelium by passing through the intercellular space between the cells), and cause inflammation-induced damage to the nervous system
Through motor neurons-especially viruses
Infect sensor neurons and travel through peripheral nervous system to central
- What are the unique features of rabies virus infection and disease? What is the route through the human body? How does pre- and post-exposure prophylaxis work?
It’s a negative single stranded RNA genome, enveloped. Has 5 proteins: -Nucleoprotein (N) Phosphoprotein (P) Matrix protein (M) Glycoprotein (G) Large RNA polymerase protein (L)
It enters muscle tissue from a bite, replicates, enters the peripheral motor neurons at neuromuscular synapses, gets transported to the CNS, then spreads to salivary glands from the brain
-enters cell->gets transcribed-> then either gets translated or keeps replicating->then is released
Pre-exposure prophylaxis: control in reservoir: animal vaccination- oral vaccination in wildlife, live attenuated and subunit vaccines
Control in humans: pre-exposure vaccines- receive the inactivated virus
Treatment post-exposure prophylaxis: disease is preventable if treated before symptoms manifest by wound cleaning, rabies immunoglobulin infiltrated into wound and given intramuscularly, post-exposure vaccine which is just a booster if already given pre-exposure vaccine
After symptoms: nothing
Rabies Reservoir Basic biology and contribution of this to disease Mechanism of transmission Major sites of colonization Major sites of disease Main diseases Major virulence factors Main disease symptoms Main treatment and control
Rabies Reservoir: humans, infected animals-canines, carnivores, livestock,
Rabies Basic biology and contribution of this to disease: has a negative single stranded RNA genome, is enveloped. Has 5 proteins named after their dominant function- each has multiple functions: Nucleoprotein(N), Phosphoprotein (P), Matrix protein (M)-forms shell, Glycoprotein (G)-major protein that is antigenic, Large RNA polymerase protein (L).
Rabies Mechanism of transmission: bite-saliva of infected animals
Rabies Major sites of colonization: muscle tissue and neurons, has an incubation period. It can replicate in neuron and spread from there
Rabies Major sites of disease: central nervous system, salivary glands
Rabies Main diseases: causes inflammation of the brain and spinal cord that can lead to encephalopathy and, coma and later, death. Also causes paralysis of legs, trouble breathing, Encephalopathy is any type of disease that changes the brain’s function or structure
Rabies Major virulence factors: has Has 5 proteins which affect/inhibit innate immune response, which causes a delay in the adaptive immune response. It slows the innate response long enough for it to get ot the CNS: Nucleoprotein(N), Phosphoprotein (P), Matrix protein (M), Glycoprotein (G), Large RNA polymerase protein (L).
Rabies virus (RABV) inhibits innate immunity until late in infection to delay AMI
-N inhibits RIG-1 activation (which is a pattern recognition receptor)
-P inhibits IFN induction (Interferons are a group of signaling proteins made and released by host cells in response to the presence of several pathogens)
P also prevents nuclear import of STAT1/2 (a transcription factor that activates transcription of interferons etc)
Rabies Main disease symptoms: 2 types: furious and paralytic.
-Furious: behavior: hyperactivity, confusion, and agitation
exposure->first symptoms (1-2 days): fever, pruritus (severe itching) and paresthesia (pins and needles feeling due to damage to nervous system), followed by clinical expression (1-4 days): hydrophobia, hypersalivation, eventually death (1-7 days).
-Paralytic: “calmer” behavior: by drowsiness, lack of energy, coma and then death
Exposure->incubation 20-90 days-> first symptoms- fever, pruritus and paresthesia-> clinical expression: dysphagia, respiratory failure, hypersalivation->coma->death
Rabies Main treatment and control: control in reservoir: animal vaccination- oral vaccination in wildlife, live attenuated and subunit vaccines
Control in humans: pre-exposure vaccines- receive the inactivated virus
Treatment post-exposure: disease is preventable if treated before symptoms manifest by wound cleaning, rabies immunoglobulin infiltrated into wound and given intramuscularly, post-exposure vaccine which is just a booster if already given pre-exposure vaccine
After symptoms: nothing
Rabies Reservoir
Rabies Reservoir: humans, infected animals-canines, carnivores, livestock,
Rabies Basic biology and contribution of this to disease
has a negative single stranded RNA genome, is enveloped. Has 5 proteins named after their dominant function- each has multiple functions: Nucleoprotein(N), Phosphoprotein (P), Matrix protein (M)-forms shell, Glycoprotein (G)-major protein that is antigenic, Large RNA polymerase protein (L).
Rabies Mechanism of transmission
bite-saliva of infected animals
Rabies Major sites of colonization
Rabies Major sites of colonization: muscle tissue and neurons, has an incubation period. It can replicate in neuron and spread from there
Rabies Major sites of disease
Rabies Major sites of disease: central nervous system, salivary glands
Rabies Main diseases
Rabies Main diseases: causes inflammation of the brain and spinal cord that can lead to encephalopathy and, coma and later, death. Also causes paralysis of legs, trouble breathing, Encephalopathy is any type of disease that changes the brain’s function or structure
Rabies Major virulence factors:
has Has 5 proteins which affect/inhibit innate immune response, which causes a delay in the adaptive immune response. It slows the innate response long enough for it to get ot the CNS: Nucleoprotein(N), Phosphoprotein (P), Matrix protein (M), Glycoprotein (G), Large RNA polymerase protein (L).
Rabies virus (RABV) inhibits innate immunity until late in infection to delay AMI
-N inhibits RIG-1 activation (which is a pattern recognition receptor)
-P inhibits IFN induction (Interferons are a group of signaling proteins made and released by host cells in response to the presence of several pathogens)
P also prevents nuclear import of STAT1/2 (a transcription factor that activates transcription of interferons etc)
Rabies Main disease symptoms
: 2 types: furious and paralytic.
-Furious: behavior: hyperactivity, confusion, and agitation
exposure->first symptoms (1-2 days): fever, pruritus (severe itching) and paresthesia (pins and needles feeling due to damage to nervous system), followed by clinical expression (1-4 days): hydrophobia, hypersalivation, eventually death (1-7 days).
-Paralytic: “calmer” behavior: by drowsiness, lack of energy, coma and then death
Exposure->incubation 20-90 days-> first symptoms- fever, pruritus and paresthesia-> clinical expression: dysphagia, respiratory failure, hypersalivation->coma->death
Rabies Main treatment and control
control in reservoir: animal vaccination- oral vaccination in wildlife, live attenuated and subunit vaccines
Control in humans: pre-exposure vaccines- receive the inactivated virus
Treatment post-exposure: disease is preventable if treated before symptoms manifest by wound cleaning, rabies immunoglobulin infiltrated into wound and given intramuscularly, post-exposure vaccine which is just a booster if already given pre-exposure vaccine
After symptoms: nothing
Rabies replication cycle
similar to influzenza, measles. Rabies infects neuron and muscles->virus binds receptos and is taken up via endocytosis->transcription of – RNA to + RNA strand which then makes more – RNA->once replication occurs, virus is released from cell
Herpes Reservoir Basic biology and contribution of this to disease Mechanism of transmission Major sites of colonization Major sites of disease Main diseases Major virulence factors Main disease symptoms Main treatment and control
Herpes Reservoir: humans, life long
Herpes Basic biology and contribution of this to disease: enveloped, has a capsid with DS linear DNA viruses- alpha, beta and gamma strains
Genome is about 150,000bp, and encodes about 80 genes, is about 150 nm in diameter- 50% needed for replication, 50% needed to interact with host cells= complex virus
Has a lipid bilayer, envelope glycoproteins, transmembrane proteins, envelope, capsid
Has its own DNA polymerase and nucleotide scavenging enzymes which allows replication in non-growing cells
Alpha: target are epithelial cells, latency occurs in neurons
Beta: immune cells are primary targets, latency in immune cells
Gamme: immune cells primary target, latency in B cells
Herpes Mechanism of transmission: neonatal transmission and disease
Herpes Major sites of colonization: initial infection in mucoepithelial cells,
Herpes Major sites of disease: most infections are limited to site/latency
Lytic infection: direct cytopathological effect and lesion at infection site
-avoidance of immune response by cell-to-cell spread and syncytia formation, establishes latency in neurons=neveous system, reactivated by stress and travels back to the lesion site for eruption
CMI required to control virus, cell-mediated immunopathology also contributes to symptoms
Lytic infection in epithelial cells
It can’t get to the CNS, but stays in PNS
Herpes Main diseases: complications include infections of eye or brain, systemic disease in immunocompromised people, neonatal transmission and disease
Neonatal herpes can affect skin, eyes and mouth, CNS or be disseminated
Herpes Major virulence factors
Herpes Main disease symptoms: complications inc
Herpes Main treatment and control: no vaccine, but antivirals that inhibit viral DNA polymerase can limit replication upon reactivation, but don’t affect latency
Herpes Reservoir
: humans, life long
Herpes Basic biology and contribution of this to disease
enveloped, has a capsid with DS linear DNA viruses- alpha, beta and gamma strains
Genome is about 150,000bp, and encodes about 80 genes, is about 150 nm in diameter- 50% needed for replication, 50% needed to interact with host cells= complex virus
Has a lipid bilayer, envelope glycoproteins, transmembrane proteins, envelope, capsid
Has its own DNA polymerase and nucleotide scavenging enzymes which allows replication in non-growing cells
Alpha: target are epithelial cells, latency occurs in neurons
Beta: immune cells are primary targets, latency in immune cells
Gamme: immune cells primary target, latency in B cells
Herpes Mechanism of transmission
Herpes Mechanism of transmission: neonatal transmission and disease
Herpes Major sites of colonization
Herpes Major sites of colonization: initial infection in mucoepithelial cells,
Alpha – mucoepithelial cells primary target, latency in
neurons
• Beta – immune cells primary target, latency in immune
cells
• Gamma - immune cells primary target, latency in B cells
Herpes Major sites of disease
most infections are limited to site/latency
Lytic infection: direct cytopathological effect and lesion at infection site
-avoidance of immune response by cell-to-cell spread and syncytia formation, establishes latency in neurons=neveous system, reactivated by stress and travels back to the lesion site for eruption
CMI required to control virus, cell-mediated immunopathology also contributes to symptoms
Lytic infection in epithelial cells
It can’t get to the CNS, but stays in PNS
Herpes Main diseases
complications include infections of eye or brain, systemic disease in immunocompromised people, neonatal transmission and disease
Neonatal herpes can affect skin, eyes and mouth, CNS or be disseminated
Herpes Main treatment and control
no vaccine, but antivirals that inhibit viral DNA polymerase can limit replication upon reactivation, but don’t affect latency
HSV-1
3.7 billion people infected, oral herpes, spread by oral secretions, increase in genital herpes
HSV-2
about 400 million people infected, genital herpes, spreads through sexual contact, infections increase susceptibility to HIV infection
- What are the unique features of Human Herpes Simplex virus infection and disease? How and where is latency established?
replication in non-growing cells
Genome is about 150,000bp, and encodes about 80 genes, is about 150 nm in diameter
Site of latency established are neurons, but reactivated by stress, and travels back to lesion site for eruption
Infected individuals can produced virus without symptoms
Polio Reservoir Basic biology and contribution of this to disease Mechanism of transmission Major sites of colonization Major sites of disease Main diseases Major virulence factors Main disease symptoms Main treatment and control
Polio virus Reservoir: humans (can affect some primates experimentally) so can be eradicated worldwide
Polio virus Basic biology and contribution of this to disease: part of picornaviruses- small naked RNA viruses, single stranded, + strand RNA virus
Viral particles ae about 30nm in diameter, resistant to environment, resilient viral capsule
Polio virus Mechanism of transmission: fecal-oral route- contaminated water, direct oral secretion ingestion
Polio virus Major sites of colonization: mucosal surface
Polio virus Major sites of disease: primarily gastrointestinal virus, but affects nervous system which is accidental. Spreads from mucosal surface to lymph nodes-> causes viremia-> spreads to spinal cord and motor neurons, and motor end plate, also spreads to extraneural tissue
Polio virus Main diseases: affects nervous system
Polio virus Major virulence factors: its receptor is a PVR protein, delivery of genome doesn’t require complete update, LPS promotes virion stability and infection, exit is destructive
Polio virus Main treatment and control: vaccine- live attenuated so don’t need booster
Polio virus Reservoir
humans (can affect some primates experimentally) so can be eradicated worldwide
Polio virus Basic biology and contribution of this to disease
part of picornaviruses- small naked RNA viruses, single stranded, + strand RNA virus
Viral particles ae about 30nm in diameter, resistant to environment, resilient viral capsule
Polio virus Mechanism of transmission
fecal-oral route- contaminated water, direct oral secretion ingestion
Polio virus Major sites of colonization
Polio virus Major sites of colonization: mucosal surface
Polio virus Major sites of disease:
Polio virus Major sites of disease: primarily gastrointestinal virus, but affects nervous system which is accidental. Spreads from mucosal surface to lymph nodes-> causes viremia-> spreads to spinal cord and motor neurons, and motor end plate, also spreads to extraneural tissue
Polio virus Main diseases
Polio virus Main diseases: affects nervous system
Asymptomatic illness >90%
• Abortive poliomyelitis 5%
- Short term febrile illness
• Nonparalytic poliomyelitis/aseptic meningitis 2%
- Short term febrile illness
- Back pain and spasms
• Paralytic polio 0.1 - 2%
- Paralytic poliomyelitis – flaccid paralysis with no sensory loss
> Recovery, residual paralysis or death may result
- Bulbar poliomyelitis
> Death 75% of time – eating or breathing is affected
- Post-polio syndrome – may be decades later
> Deterioration of previously affected muscles
Polio virus Major virulence factors
Polio virus Major virulence factors: its receptor is a PVR protein, delivery of genome doesn’t require complete update, LPS promotes virion stability and infection, exit is destructive
Polio virus Main treatment and control
Polio virus Main treatment and control: vaccine- live attenuated so don’t need booster
- What is the typical route through the body for poliovirus? How is nervous system disease an outcome of this
Spreads from mucosal surface to lymph nodes-> causes viremia-> spreads to spinal cord and motor neurons, and motor end plate, also spreads to extraneural tissue
- What are the advantages and disadvantages of each type of polio vaccine
1) Inactivated polio vaccine: delivers inactivated polio virus
- more expensive
- safe for immunodeficient people
- no risk of vaccine related disease
- boosters needed
- lack of stimulation of secretory IgA
- higher level of vaccination needed for herd immunity
2) live attenuated vaccine
- replicates in GI tract but not capable of entry to CNS
- taken orally
- less expensive
- no booster needed
- more induction of secretory IgA
- virus sheds in feces-spreads to others
- may very rarely rever to virulence
- possible rare generation of circulating vaccine-derived poliovirus (cDPV) that can lead to outbreaks
Neisseria meningitidis Reservoir
Neisseria meningitidis Reservoir: humans
Neisseria meningitidis Basic biology and contribution of this to disease
: gram neg, aerobic and anaerobic respiration, fastidious and fragile, called memingococcus
Has lots of genetic diversity- 13 serogroups based on cell surface molecules, some clonal complexes associated with invasive infection, others not
Has no core pathogenome
Neisseria meningitidis Mechanism of transmission:
large droplets with close contact (not aerosols)
Neisseria meningitidis Major sites of colonization:
nasopharynx of URT- excellent colonists of URT, epithelia
Neisseria meningitidis Major sites of disease
URT from where it spreads to bloodstream and then brain- CNS
Can get from epithelia to epithelial space/past barrier
Mostly stays in nasal passages
If it gets past the epithelia, it can get into the blood and to the brain from the blood, and once in the bloodstream its virulence factors help it survive
Neisseria meningitidis Main diseases:
meningitis- headache, stiff neck, fever are initial symptoms
meningococcal septicemia- thrombosis of small blood vessels and multi-organ involvement
meningococcal diseases are accompanied by disseminated vascular coagulation and skin lesions, also pneumonia, arthritis and urethritis
can be 70-90% fatal if untreated
Neisseria meningitidis Major virulence factors:
: capsule, pili for attachment, LOP (LPS without long O-antigen) binds receptors and triggers release of inflammatory cytokines leading to endothelial damage, may be sialyated
Has outer membrance vesicles, IgA protease
Has antigenic variation in outer membrane proteins
Bacteria has to survive in nasopharynx, bloodstream and CNS
Neisseria meningitidis Main disease symptoms
headache, stiff neck, fever are initial symptoms
Neisseria meningitidis Main treatment and control:
vaccines, prompt antibiotic treatment, antibiotic prophylaxis for close contacts of infected individuals. Risk for neurological complications following recovery and also paralysis, deafness, mental impairment, amputations, and seizures
Neisseria meningitidisReservoir Basic biology and contribution of this to disease Mechanism of transmission Major sites of colonization Major sites of disease Main diseases Major virulence factors Main disease symptoms Main treatment and control
Neisseria meningitidis Reservoir: humans
Neisseria meningitidis Basic biology and contribution of this to disease: gram neg, aerobic and anaerobic respiration, fastidious and fragile, called memingococcus
Has lots of genetic diversity- 13 serogroups based on cell surface molecules, some clonal complexes associated with invasive infection, others not
Has no core pathogenome
Neisseria meningitidis Mechanism of transmission: large droplets with close contact (not aerosols)
Neisseria meningitidis Major sites of colonization: nasopharynx of URT- excellent colonists of URT, epithelia
Neisseria meningitidis Major sites of disease: URT from where it spreads to bloodstream and then brain- CNS
Can get from epithelia to epithelial space/past barrier
Mostly stays in nasal passages
If it gets past the epithelia, it can get into the blood and to the brain from the blood, and once in the bloodstream its virulence factors help it survive
Neisseria meningitidis Main diseases:
meningitis- headache, stiff neck, fever are initial symptoms
meningococcal septicemia- thrombosis of small blood vessels and multi-organ involvement
meningococcal diseases are accompanied by disseminated vascular coagulation and skin lesions, also pneumonia, arthritis and urethritis
can be 70-90% fatal if untreated
Neisseria meningitidis Major virulence factors: capsule, pili for attachment, LOP (LPS without long O-antigen) binds receptors and triggers release of inflammatory cytokines leading to endothelial damage, may be sialyated
Has outer membrance vesicles, IgA protease
Has antigenic variation in outer membrane proteins
Bacteria has to survive in nasopharynx, bloodstream and CNS
Neisseria meningitidis Main disease symptoms: headache, stiff neck, fever are initial symptoms
Neisseria meningitidis Main treatment and control: vaccines, prompt antibiotic treatment, antibiotic prophylaxis for close contacts of infected individuals. Risk for neurological complications following recovery and also paralysis, deafness, mental impairment, amputations, and seizures
- What is the typical route through the body for Neisseria meningitidis? What are colonization features that allow it to survive in other parts of the body? What are the challenges in development of some of the meningococcal vaccines?
Typical route: nasopharyngeal colonization, followed by entry into the bloodstream, and then entry into the CNS
Colonizes the nasopharyngeal by being internalized via host receptor interactions
Gets into the blood, where its capsule and sialyated LOS reduce complement and antibody binding and phagocytosis. The host complement regulators are recruited in the blood->then passes the endothelium to get into the CNS, and inflammation and cytokine damage may increase bacterial transcytosis of all cell barriers->the bacteria interacts with the leptomeninges of the brain, and cytokines are released, leading to meningitis
Has pili for attachment and capsule and sialylated LOS to reduce complement
Challenges with vaccine development: the bacteria has a B serotype which is identical to the sialic acid in human so it is hard to make a vaccine for something humans also make. Another challenge is that vaccines target outer membrane proteins, and not the actual capside
Naegleria fowleri Reservoir
Naegleria fowleri Reservoir: humans, warm freshwater like lakes and rivers
Naegleria fowleri Basic biology and contribution of this to disease
Naegleria fowleri Basic biology and contribution of this to disease: has trophozoite (growing stage), flagellate and cyst
Brain eating bacteria
Naegleria fowleri Mechanism of transmission
Naegleria fowleri Mechanism of transmission: accidental- water up the nose-> straight into brain
Can get it by swimming in infected water
Naegleria fowleri Major sites of colonization
nose
Naegleria fowleri Major sites of disease
Naegleria fowleri Major sites of disease: brain and meninges
Naegleria fowleri Main diseases:
Naegleria fowleri Main diseases: primary and secondary meningoencephalitis
- primary fatal amoebic meningocephalitis: headache, stiff neck, seizures, coma. Strong inglammation in the brain and meninges-primary damage may be due to immunopathology such as excessive cytokine release, olfactory region macrophages recruit intense neutrophil influx
- secondary meningoencephalitis: occurs when an infection starts elsewhere in the body and then travels to your brain, such as due to herpes virus
Naegleria fowleri Major virulence factors
accidental pathogen, has no dedicated tocins, but once it gets to the brain it is very successful. It is also very big which is a challenge for phagocyte
- direct virulence factors: adhesion, ameobastomes degrading enzymes to avoid immune system/phagocytosis, have pore-forming proteins, hydrolytic enzymes
- indirect virulence factors: phenotypic switching, morphology, ubiquity, physiological tolerance, biofilms, chemotaxis, drug resistance, immune evasion, host factors
Naegleria fowleri Main disease symptoms
fever leading to seizures, coma, death, following damage to the brain
Naegleria fowleri Main treatment and control
antiparasitic and anti-inflammatory agents
- How does Naegleria fowleri enter the central nervous system? What is the distinction between primary and secondary amoebic meningoencephalitis?
accidental- water up the nose-> straight into brain
Can get it by swimming in infected water
-primary fatal amoebic meningocephalitis: headache, stiff neck, seizures, coma. Strong inglammation in the brain and meninges-primary damage may be due to immunopathology such as excessive cytokine release, olfactory region macrophages recruit intense neutrophil influx
-secondary meningoencephalitis: occurs when an infection starts elsewhere in the body and then travels to your brain, such as due to herpes virus
- Be able to describe the structures and functions of the gut, including environmental conditions, antimicrobial factors, and metabolic and immune functions.
- Where the most significant interactions with microbes occur
- One cell endothelial layer= prime for pathogens
- Intestinal epithelial cells are a great barrier, coated in mucus
- Mucus is where microbes interact with us, and can also be food for them-they can get their nutrients by degrading it (glycosylating and sulfurylating it)
- Environment in the GI tract: shedding surface- sheds about 2x10^11 cells per day, -flushing action-9L fluid per day enter SI
- IgA, bile, AMO- bile is a mix of cholesterol, phospholipids, bile acids, Ig
- Mucus coated surfaces
- Attachment to mucus or high rate of growth needed to sustain populations
- Has innate and adaptive immunity
