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Pulmonology - OMS 2 > Mucosal Immunity > Flashcards

Mucosal Immunity Flashcards

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?

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?

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?

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?

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?

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?

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?

A

ag presentation

24
Q

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

A
  • upper airways go to cervical nodes
  • lower airways go to mediastinal nodes
25
Q

List the defenses found in the large airways from the trachea to the through the bronchioles.

A
  1. MF
  2. mucous layer
  3. goblet cells
  4. clara cells
26
Q

List the defenses found in the lower respiratory tract, specifically the alveoli.

A
  1. alveolar MF (self-renewing, bad APCs): tolerogenic)
  2. interstitial MFs: inflammation
27
Q

What T cell subtypes are present in the lung and what are their associated pathologies?

A
  1. T regulatory mediated by retinoic acid, IL-10 & TGF-B
  2. TH1: pneumonia
  3. TH17: neutrophilic response
  4. TH2: allergy & asthma
  5. TFH: support B cells
28
Q

What are IELs? What type of cells are they? How do they contribute to host defense?

A
  1. Intraepithelial lymphocytes
  2. CD8
  3. kill infected cells
29
Q

What are AVMs? What are their functions?

A
  • alveolar MFs
  • clear debreise
  • poor APC –> tolerogenic
30
Q

How are AVMs controlled? What cells do the AVMs control?

A
  • 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
Q

What cells are recruited to the mucosa during inflammation?

A
  1. lung-specific lymphocytes
  2. neutrophils
  3. eosinophils
  4. mononuclear cells
32
Q

What are interstitial macrophages? How do they differ from AVMs?

A
  1. at alveoli, but OUTSIDE airway
  2. inflammatory: good APCs
  3. less phagocytic than AVM
33
Q

What molecules mediate lymphocyte homing to the mucosa? Which cell type has each molecule?

A

MadCAM-1 on high endothelial vessles (HEV)

34
Q

How do epithelial cells contribute to oral/nasal tolerance?

A

prevent Ag from crossing

35
Q

What roles do APCs play in maintaining oral/nasal tolerance?

A
  1. Regulatory DCs activate T regs w/IL-10 & TGF-B
  2. Tregs migrate back and inhibit APCs, B cells and T cells –> inhibition of inflammatory response
36
Q

How do the characteristics of an antigen contribute to oral/nasal tolerance?

A

soluble Ag are ignored

37
Q

How is a mucosal vaccine beneficial for a mucosal pathogen?

A

immunity created where the pathogens will be encountered (live-attenuated; not for immune compromised pts)

38
Q

How does FluMist work? What are the steps that lead from vaccine administration to memory responses?

A

live-attenuated influenza vax
dendritis cells take to structured lymphoid tissue (adenoids, tonsils, cervical LN, spleen), memory established, homing back to nasal area

39
Q

What happens in CF that leads to obstruction?

A

dehydration of mucus –> becomes thick –> cilia can’t remove

40
Q

why are CF patients at risk of secondary infection?

A

epithelium breaks down and creates opportunities for microbes

Pulmonology - OMS 2 (28 decks)

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