Pulmonology - OMS 2 > Mucosal Immunity > Flashcards

Mucosal Immunity Flashcards

(40 cards)

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1
Q

What is lung mucosal immunity?

A
  1. bacterial metabolites = tolerance
  2. immune modulation: mucosal tissues share responses w/other mucosal tissues
  3. coating effect (vaginal birth)
  4. balance between low/high inflammation microbes=homeostasis
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2
Q

What aspects make the lung a unique microbial niche?

A
  1. bidirectional flow of air
  2. low # of nutrients

GI is one way.

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3
Q

How does the microbiota protect the lung?

A

colonization early in life protects from inhaled antigens

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4
Q

What region of the lung has the most mucus? The least?

A

upper airways have more
(trachea and up)

catches what we breath in

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5
Q

What is the mucociliary elevator? Where do the particles go?

A

goblet cells make mucus that traps microbes –> cilia moves up to GI tract

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6
Q

Which cells provide the movement for the mucociliary elevator?

A
  1. goblet cells: mucus to catch microbes
  2. epithelial: cilia
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7
Q

List the antimicrobial molecules located in the lungs (4)

A
  1. lysozyme
  2. lactoferrin
  3. LL37 (cathelicidin)
  4. surfactants (A & D)
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8
Q

What are the most common immune proteins in the lung airway surface interface?

A
  1. lysozyme
  2. lactoferrin
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9
Q

What are surfactants? Which contribute to host defense?

type II epithelium

A
  • lecithins that bind immune cells
  • SP-A & SP-D
SP-B & SP-C not involved in defense
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10
Q

What are the mechanisms of action for the immune-associated
surfactants?

A
  1. Surfactant A (SP-A): ROS, activates MF, opsonization
  2. Surfactant D (SP-D): opsonizes more microbes, counteracts IL-1 & TNF (anti-inflammation)
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11
Q

What is the mucosal antibody isotype?
What is the most abundant subtype in the lungs?

A

IgA1

IgA2 in gut

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12
Q

What are the functions and characteristics of IgA?

A
  • Does NOT cause inflammation or fix complement
  • joined by J-chain tail-to-tail
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13
Q

What molecule moves IgA to the lumen? How does it work?

A

Poly-Ig receptor (pIgR) transfers across epithelial surface

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14
Q

How do IgG and IgE reach the airways?

A

diffusion

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15
Q

List the 6 types of lung epithelial cells
and their role in immune defenses.

A
  1. ciliated
  2. goblet
  3. neuroendocrine (repair)
  4. club cells (secrete mucus at bifurcation)
  5. type II pneumocytes/epithelial (APC action; usually T-reg response)
  6. M cells (found in FAE)
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16
Q

M cells are only found where?

A

where there is structured lymphoid tissue (i.e. nasal FAE)
(sometimes epithelium can differentiate into M cell briefly and return)

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17
Q

What does FAE stand for? Where is it located?

Study These Flashcards
A
  • follicular associated epithelium (contains M cells)
  • upper airways
18
Q

How does the cell composition of the FAE differ
from the rest of the epithelium?

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A
  1. no immune tissues in mucosa
  2. no goblet cells
  3. lymphocytes
  4. APCs
  5. M cells

this is a microbe pit

19
Q

What is the Common Mucosal Immune
System? How do mucosal sites across the
body share activated lymphocytes?

Study These Flashcards
A

induction response in FAE –> spreads to effector sites
(since the lungs don’t have this, they are the EFFECTOR SITE)

20
Q

What is Waldeyer’s Ring and how does it function in immunity?

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A
  • adenoids, tonsils, NALT
  • Ag delivered directly here through epithelial cell surfaces (as opposed to lymph)
  • Prolific IgA production
21
Q

Where is the NALT found? Is it in the same place for each individual?

Study These Flashcards
A

In the nasal passage, underneath FAE
No, it is variable

22
Q

How is the structure of a MALT similar to a Lymph node? What structures do they share?

Study These Flashcards
A

they both have MF, B cells and T cells that interact w/Ag
MALT is associated w/M cells and FAE and has the ability to induce microbes into the lamina propria

in comparison, lymph node is very structured
23
Q

What is the function of the MALT in activating adaptive immune responses?

Study These Flashcards
A

ag presentation

24
Q

Where would an APC go if it were activated in the upper respiratory tract?
In the lower respiratory tract?

Study These Flashcards
A
  • upper airways go to cervical nodes
  • lower airways go to mediastinal nodes
25
List the defenses found in the large airways from the trachea to the through the bronchioles.
1. MF 1. mucous layer 1. goblet cells 1. clara cells
26
List the defenses found in the lower respiratory tract, specifically the alveoli.
1. alveolar MF (self-renewing, bad APCs): tolerogenic) 1. interstitial MFs: inflammation
27
What T cell subtypes are present in the lung and what are their associated pathologies?
1. T regulatory mediated by retinoic acid, IL-10 & TGF-B 1. TH1: pneumonia 1. TH17: neutrophilic response 1. TH2: allergy & asthma 1. TFH: support B cells
28
What are IELs? What type of cells are they? How do they contribute to host defense?
1. Intraepithelial lymphocytes 1. CD8 1. kill infected cells
29
What are AVMs? What are their functions?
* alveolar MFs * clear debreise * poor APC --> tolerogenic
30
How are AVMs controlled? What cells do the AVMs control?
* type II epithelial cells (retinoic acid, IL-10 & TGF-B) * T-regs: tolerance by poor presentation (low co-stim molecules and anti-inflamatory cytockins)
31
What cells are recruited to the mucosa during inflammation?
1. lung-specific lymphocytes 1. neutrophils 1. eosinophils 1. mononuclear cells
32
What are interstitial macrophages? How do they differ from AVMs?
1. at alveoli, but OUTSIDE airway 1. inflammatory: good APCs 1. less phagocytic than AVM
33
What molecules mediate lymphocyte homing to the mucosa? Which cell type has each molecule?
MadCAM-1 on high endothelial vessles (HEV)
34
How do epithelial cells contribute to oral/nasal tolerance?
prevent Ag from crossing
35
What roles do APCs play in maintaining oral/nasal tolerance?
1. Regulatory DCs activate T regs w/IL-10 & TGF-B 1. Tregs migrate back and inhibit APCs, B cells and T cells --> inhibition of inflammatory response
36
How do the characteristics of an antigen contribute to oral/nasal tolerance?
soluble Ag are ignored
37
How is a mucosal vaccine beneficial for a mucosal pathogen?
immunity created where the pathogens will be encountered (live-attenuated; not for immune compromised pts)
38
How does FluMist work? What are the steps that lead from vaccine administration to memory responses?
live-attenuated influenza vax dendritis cells take to structured lymphoid tissue (adenoids, tonsils, cervical LN, spleen), memory established, homing back to nasal area
39
What happens in CF that leads to obstruction?
dehydration of mucus --> becomes thick --> cilia can't remove
40
why are CF patients at risk of secondary infection?
epithelium breaks down and creates opportunities for microbes
Pulmonology - OMS 2
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