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Respiratory II > Immunology of Interstitial Lung Diseases > Flashcards

Immunology of Interstitial Lung Diseases Flashcards

1
Q

Pulmonary Defense Mechanisms

A
  • The lung is continuously exposed to the outside environment
  • Defense mechanisms are necessary to ensure efficient gas exchange and prevent infection
  • Removal mechanisms are aimed at minimizing inflammation
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2
Q

Lung defense can be divided into two locations

A
  • Upper airways and bronchi
  • Host defenses in alveolar spaces
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3
Q

Lung defense can be divided into two locations

Upper airways and bronchi

A

•Upper airways and bronchi

–Anatomic barriers

–Cough

–Mucociliary apparatus

–Airway epithelium

–Secretory IgA

–Dendritic cells, lymphocytes, neutrophils

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4
Q

Lung defense can be divided into two locations

Host defenses in alveolar spaces

A

•Host defenses in alveolar spaces

–Alveolar macrophages

–Immunoglobulins, opsonins, and surfactants

–Lymphocyte-mediated immunity

–Neutrophils and eosinophils

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5
Q

Scanning Electron Micrograph of Cilia

A
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6
Q

Overview of the Immune Cells in the Pulmonary Immune System

A
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7
Q

BALT and GALT

A
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8
Q

Immunology of Interstitial Lung Disease- Objectives

A
  1. Given a case presentation, identify the specific ILD.
  2. For each ILD listed in this presentation describe the associated immune response when known.
  3. Contrast the characteristic immune responses for IPF, sarcoidosis, and HP.
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9
Q

Interstitial and Inflammatory Lung Diseases (ILD)

A
  • Idiopathic interstitial pneumonias
  • Connective tissue diseases
  • Systemic sarcoidosis
  • Hypersensitivity pneumonitis
  • Eosinophilic lung disease
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10
Q

BAL Apparatus

A
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11
Q

Pulmonary Diseases

A
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12
Q

BAL from a Scleroderma Patient

A
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13
Q

Classification of Idiopathic Interstitial Pneumonias

A
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14
Q

Idiopathic Interstitial Pneumonias

A
  • Heterogeneous group with similar clinical findings and fibrosing in nature
  • BAL findings are used to exclude infection, tumor, asbestosis, or other specific diseases
  • Effectiveness of corticosteroids depends on the disease

–In idiopathic pulmonary fibrosis (IPF) use of corticosteroids is not indicated

–Nonspecific interstitial pneumonia (NSIP) has a more favorable response to corticosteroids

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15
Q

SEM of Transection of Pulmonary Capillary

A

Alv: alveolus

EP: alveolar epithelium

IN: interstitial space

BM: basement membrane

EN: capillary endothelial cell

C: capillary

FB: fibroblast

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16
Q

Events in the Development of IPF

A

TGF-β: normal action is cell-type and context-dependent and includes anti-inflammatory and tissue repair promotion. TGF-β is also anti-proliferative and thought to promote epithelial-mesenchymal transition. Chronic expression of TGF-β has been shown to play a role in tissue fibrosis. In IPF the origin of TGF-β is postulated to be alveolar macrophages.

Source of myofibroblasts: epithelial-mesenchymal transition, mesothelial-mesenchymal transition, local mesenchymal cells, and circulating progenitor cells- all are considered to be a potential source but more research is needed to definitely show the source of increased myofibroblasts in the lungs of IPF patients

Mediators of Fibrosis: Inulin-like growth factor binding protein (IGFBP)5 has been shown to be associated with increased fibrosis. Additionally increased expression of the vasoconstrictors endothelin 1 (ET-1 and angiotensin II has been associated with increased fibroblast activation. Research literature indicates ACE inhibitors are protective against radiation-induced lung fibrosis.

17
Q

Evidence for the Role of Cellular and Humoral Immunity in IPF

A
  • Involvement of CD4+ T cells (activated phenotype)
  • Biased T cell receptor Vβ repertories (BAL and peripheral)
  • Presence of autoantibodies in some studies with IPF patients
  • Evidence of lymphoid neogenesis without organized structure
18
Q

Connective Tissue Diseases

A
  • Rheumatoid arthritis (RA)
  • Systemic lupus erythematosus (SLE)
  • Sjögren syndrome
  • Systemic sclerosis (SSc)
  • Pulmonary manifestations include ILD
  • Mechanism?
19
Q

Genetic Contribution to IPF

A
  1. Wang Y, Kuan PJ, Xing C, et. al. Genetic defects in surfactant protein A2 are associated with pulmonary fibrosis and lung caner. Am J Hum Genet 2009; 84: 52-9.
  2. Nogee LM, Dunbar AE III, Wert SE, Askin F, Hamvas A, Whitsett JA. A mutation in the surfactant protein C gene associated with familial interstitial lung disease. N Engl J Med 2001; 344: 573-9.
  3. Armanios MY, Chen JJ, Cogan JD, et al. Telomerase mutations in families with idiopathic pulmonary fibrosis. N Engl J Med 2007; 356: 1317-26.
  4. Seibold MA, Wise AL, Speer MC, et. al. A common MUC5B promoter polymorphism and pulmonary fibrosis. N Engl J Med 2011; 364: 1503-12.
20
Q

Percentage of Subjects with ILD and RA- Correlation to Smoking

A
21
Q

Systemic Sarcoidosis

A
  • Multisystem granulomatous
  • Noncaseating epithelioid granulomas
  • Depression of DTH responses
  • Interstitial pneumonitis and granulomatous formation can progress to fibrosis with loss of alveolar and bronchial tissue and vascular surface area
22
Q

Inflammatory Response in Sarcoidosis

A
23
Q

Persistent Granulomatous Inflammation

A
  • Persistence of antigen
  • Failure of the immune system to halt inflammatory processes
24
Q

Hypersensitivity Pneumonitis (HP)

A
  • Group of lung diseases caused by inhalation of exogenous antigenic molecules (usually organic)
  • Transient fever, hypoxemia, myalgias, arthralgias, dyspnea, cough 2-9 hr after exposure
  • Symptoms resolve without treatment provided there is no re-exposure to antigen
25
Q

Acute Episode of Pigeon Breeder’s Disease

A
26
Q

Immunology Associated with HP

A
  • Prior sensitization is necessary
  • Not associated with IgE or eosinophils
  • Higher prevalence in non-smokers (80-95%)
  • >40% lymphocytes suggestive of HP; higher percentage of neutrophils and degranulated macrophages
  • Cell-mediated immune process

–TGF-β, IL-1, IL-12, TNF-α

–IL-2, IFN-g

–IL-6, IL-17, IL-22

•Tx with corticosteroids aids recovery initially, long-term outcome is unaffected

27
Q

Proposed Mechanism for the Pathogenesis of HP

A
28
Q

HP Flow Chart

A
29
Q

Eosinophilic Lung Diseases

A
30
Q

Eosinophilic Lung Disease

Chart

A
  • Pulmonary infiltrates with eosinophilia (PIE)
  • Eosinophilic infiltration into airways, alveoli, or interstitium

Respiratory II (14 decks)

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