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Immunology of Interstitial Lung Diseases Flashcards

1
Q

Immunology of Interstitial Lung Diseases

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

•Upper airways and bronchi

A 
–Anatomic barriers
–Cough
–Mucociliary apparatus
–Airway epithelium
–Secretory IgA
–Dendritic cells, lymphocytes, neutrophils
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3
Q

Lung defense can be divided into two locations

•Host defenses in alveolar spaces

A

–Alveolar macrophages
–Immunoglobulins, opsonins, and surfactants
–Lymphocyte-mediated immunity
–Neutrophils and eosinophils

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4
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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5
Q

Diagnostic morphologic changes in BAL fluids

Normal:

A

Primarily alveolar

macrophages

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6
Q

Diagnostic morphologic changes in BAL fluids

Smoker with
interstitial lung
disease

A

many
carbonaceous
macrophages

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7
Q

Diagnostic morphologic changes in BAL fluids

Sarcoidosis:

A

increased numbers
of lymphocytes: CD4
alveolitis

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8
Q

BAL from a Scleroderma Patient

A

Typical bronchoalveolar lavage from a patient with systemic sclerosis illustrating neutrophils and eosinophils

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9
Q

Classification of Idiopathic Interstitial Pneumonias

A

IPF = Idiopathic pulmonary fibrosis, NSIP = Non-specific interstitial pneumonia, COP =
Cryptogenic organizing pneumonia, AIP = Acute interstitial pneumonia, DIP =
Desquamative interstitial pneumonia, LIP = lymphoid interstitial pneumonia, RBILD =
Respiratory bronchiolitis-associated interstitial lung disease

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10
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
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11
Q

•Effectiveness of corticosteroids depends on the disease

A

–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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12
Q

Events in the Development of IPF

A

Vasodilation
Coagulation
Oxidative stress
Vascular remodeling

Increased
expression:
TGF-β
TNF-α
PDGF
Injury, failed repair, fibrosis with activated myofibroblasts and fibroblastic foci
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13
Q

Evidence for the Role of Cellular and Humoral Immunity in IPF

A
  • Involvement of CD4+ T cells (activated phenotype)
  • Biased T cell receptor Vβrepertories (BAL and peripheral)
  • Presence of autoantibodies in some studies with IPF patients
  • Evidence of lymphoid neogenesis without organized structure
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14
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 *MUC5Bpromoter polymorphism and pulmonary fibrosis. N Engl J Med 2011; 364: 1503-12.
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15
Q

Connective Tissue Diseases

A
  • Rheumatoid arthritis (RA)
  • Systemic lupus erythematosus (SLE)
  • Sjögren syndrome
  • Systemic sclerosis (SSc)
  • Pulmonary manifestations include ILD
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16
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
17
Q

Inflammatory Response in Sarcoidosis

Relevant proteins

A

TNF-α
IL-7
MMP-12

18
Q

Persistent Granulomatous Inflammation

A
  • Persistence of antigen

* Failure of the immune system to halt inflammatory processes

19
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
20
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
  • Tx with corticosteroids aids recovery initially, long-term outcome is unaffected
21
Q

Immunology Associated with HP

•Cell-mediated immune process

A

–TGF-β, IL-1, IL-12, TNF-α
–IL-2, IFN-
–IL-6, IL-17, IL-22

22
Q

airway epithelium

A

toll like receptors when activated they secrete cytokines and defensins

23
Q

alveolar macros

A

eat

24
Q

Lymphocyte-mediated immunity

Neutrophils and eosinophils

A

eosiniphilic lung disease when they get out of control

25
Q

BALT and GALT

A

t and b cells are activated in lymph nodes

dendritic cells pick up antigen and go to lymph node and then t and b cells are activated

t and b cells traffic back to where they antigen was found

26
Q

Inflammatory Response in Sarcoidosis

A

predominant th1 response the dendritic cell is presentin the antigen to the cd4 th1 cell on class 2 molecules the th1 cells have cytokines as ifn y and the dendritic ell relase il2 il18, tnf a il7 and mmp 12 and ifny

there is proliferation and activation of the tcells with tnf a and there is persistent inflammation in alveolar space with no resolution so you get alveolitis which leads to ild

27
Q

IL-2, IFN-gamma

A

th1 cd4

28
Q

IL-6, IL-17, IL-22

A

th17

29
Q

th1

A

inflammation

30
Q

th2

A

fibrotic

31
Q

Eosinophilic Lung Diseases

A

predominance of eosinophils

32
Q

Simple Pulmonary Eosinophilia

Etiology -

Duration of symptoms -

Respiratory Failure -

Blood Eosinophls -

BAL findings -

Dehst Radiographic -

Pleural Effusions -

Treament -

Clinical Relapse -

A

Etiology - idiopathic drugs parasites

Duration of symptoms - 1-2 weeks

Respiratory Failure - never

Blood Eosinophls - increased

BAL findings - eosinophils

Dehst Radiographic - transient opacities

Pleural Effusions - rare

Treament - unnecessary

Clinical Relapse - rare

33
Q

Chronic Eosinophilic Pneumonia

Etiology -

Duration of symptoms -

Respiratory Failure -

Blood Eosinophls -

BAL findings -

Dehst Radiographic -

Pleural Effusions -

Treament -

Clinical Relapse -

A

Etiology - idiopathic

Duration of symptoms - several weeks to months

Respiratory Failure - very rare

Blood Eosinophls - increased

BAL findings - eosinophils

Dehst Radiographic - peripheral opacities

Pleural Effusions - rare

Treament - several years

Clinical Relapse - frequent

34
Q

Acute Eosinophilic pneumonia

Etiology -

Duration of symptoms -

Respiratory Failure -

Blood Eosinophls -

BAL findings -

Dehst Radiographic -

Pleural Effusions -

Treament -

Clinical Relapse -

A

Etiology - idiopathic tobacco smoke drugs

Duration of symptoms - 1-5 days

Respiratory Failure - frequent

Blood Eosinophls - normal

BAL findings - eosinophils lymphocytes and neutrophils

Dehst Radiographic - diffuse opacities kerley b lines

Pleural Effusions - frequent

Treament - 2-12 weeks

Clinical Relapse - rare

Resp (11 decks)

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