Pulmonary Defense Mechanisms Flashcards

1
Q

Airway clearance mechanisms

A
  • Mucous is projected towards the pharynx by the beating of cilia on epithelial cell
  • Cleared by coughing, sneezing and/or swallowing
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2
Q

Ciliary function and causes of reduced clearance

A
  • 10-15 beats per second
  • 200 cilia per cell
  • Coordinated movement
  • Particle movement

–Small airways 0.5-1.0 mm/min

–Large airways 5-20 mm/min

•Examples of reduced clearance

–Air pollution/ozone –Viral infection –Cigarette smoke

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3
Q

Contents of airway epithelial fluid & fxn

A
  • Antimicrobial peptides and proteins
  • Antioxidants
  • Antiproteases
  • IgA
  • Contribute to maintenance of airway structure and function
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4
Q

Innate Immune System function @ lungs

A

–Provides early host defense against virus, fungi, and bacteria

–Relies on recognition of pathogen-associated molecular patterns (PAMPs)

–PAMPs are recognized by secreted, cell surface, or intracellular pattern recognition receptors (PRRs) –Engagement of PRRs results in recruitment of phagocytes, killing of microbes, and inflammation

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5
Q

Adaptive immune system fxn @ lung

A

–B and T cells

–Provides antigen specificity

–Upon re-exposure, immunological memory allows for a more rapid and augmented secondary immune response

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6
Q

Immune system fxn in airway clearance

A
  • Smaller particles (<5 µm) deposit in the lower airways
  • Ingested by resident alveolar macrophages (AM) and/or dendritic cells
  • Bind to lung collectins and surfactant protein A and D (i.e., secreted PRRs) that bind to PAMPs
  • Leads to opsonization and phagocytosis by AM and dendritic cells
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7
Q

Role of macrophages in host defense of lung

A
  • Suppression of adaptive immune responses
  • Clearance of particles, bugs and cell debris
  • Clearance of apoptotic cells
  • Elicit an inflammatory response
  • Transport particles and bugs to lymph nodes
  • Clear alveolar surfactant
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8
Q

Bronchoalveolar lavage procedure & normal cell differential

A
  • bronchoscope into airways ==> fluid squirted into lung ==> fluid collected and analyzed
  • •Normal cell differential
    • 90-95% macrophages
    • < 5% lymphocytes
    • < 1% eosinophils
    • < 1% neutrophils
  • •In smokers, dramatic increase in the number of macrophages
  • •Normal CD4:CD8 ratio-2:1
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9
Q

Consequences of TLR stimulation

A
  • proinflammatory response.
  • •Bridge between innate and adaptive immunity.
  • Activates/enhances oxidative burst from macrophage, neutrophils, eosinophils.
  • Induces cytokines from tissue monocytes & dendritic cells
  • Enhances NK cell activation for killing and IFN-γ production
  • Activation of DCs (Migration to T cell areas of lymphoid tissue)
  • §Induction of type 1 IFN from either infection itself or from TLR stimulation
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10
Q

Summary of lung innate immunity [fxn of resident macrophage, monocytes, and DCs]

A
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11
Q

BAL in sarcoidosis

A
  • Dramatic increase in the number of CD4+ and/or CD8+ T cells in the lungs of patients with granulomatous lung disease
  • Percentage of lymphocytes can range from 5-95% of alveolar cells, depending on the severity of the alveolitis
  • CD4:CD8 ratio > 3-15:1
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12
Q

Activation of adaptive immune response

A
  • The main response occurs in the lymph nodes.
  • Sampling by APCs occurs @ lungs
  • APCs (dendritic cells) take up antigen, processes it, puts proteins in its MHC Class 2, which present to CD4’s
  • It also puts it in MHC 1 which presents to CD8 cells
  • DCs ==> lymph nodes, presents, and activates the adaptive response (activates T cells, proliferation of T cells, etc).
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13
Q

Activation of T Cells @ lungs

A
  • Following presentation of Ag by APCs, T cells are activated and express IL-2R
  • IL-1 and IL-2 attract blood T cells to the site of inflammation
  • T cells in the lung are increased by 2 potential mechanisms:

–Influx of Ag-specific T cells from the blood

–Local T cell proliferation

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