<aside> 💡 a major source of morbidity and mortality in production animals (horses, swine, chicken)

</aside>

Divided into 3 parts:

Conductive system:

• lined by pseudostratified ciliated columnar epithelium
• mucus-secreting cells (Goblet cells)
• from the nares up to the intrapulmonary bronchus

Transitional system:

• gradual disappearance of the ciliated epithelium
• (-) goblet cells but have club (Clara) cells instead / bronchiolar exocrine cells
• larger than epithelial cells, dome-shaped, very short microvilli, found in the cell airways
• produces surfactants
• mainly composed of the bronchioles

Exchange system:

• formed by alveolar ducts and alveoli

Types of epithelial cells:

1. Type I pneumocytes
2. Type II pneumocytes

Alveoli

• Huge surface area (200 m2, dog: 2000 m2, horse)
• Largest capillary bed in the body, where gas exchange occurs

Cells

• Type 1 pneumocyte - squamous and covers 93%
• Type 2 pneumocyte - cuboidal, secretes surfactant
• PAM
• Intravascular macrophages
• Endothelial & stromal cells that lines

• Microorganisms are normally present but usually restricted in the upper respiratory airways - opportunistic infections may occur (Mannheimia haemolytica → pneumonic mannheimiosis or "shipping fever")

Dysfunction / Responses to Injury:

Conductive System - pseudostratified ciliated epithelium is most sensitive to injury

1. Irreversible cellular injury → ciliated cells swell → detach from the BM → with exfoliation comes exudation
2. Exudate of fluid + neutrophils cover the ulcer (exposure of the BM)
3. Basal cells / non-ciliated secretory cells (preciliated cells) → migrate to cover the ulcerated area → undergoes mitosis → differentiate to new ciliated epithelial cells

• Examples of pathogens that target the ciliated epithelium: Infectious bovine rhinotracheitis, feline rhinotracheitis, canine adenovirus, and canine parainfluenza virus

• Chronic damage to mucociliary apparatus (GC & ciliated epithelium)→ goblet cell hyperplasia → excessive mucus production = reduced mucociliary clearance (because the ciliated cells do not multiply)
• Severe cases → squamous metaplasia + scarring (fibrosis) → causes airway obstruction and impediment of mucociliary clearance

Squamous cell carcinoma in lungs

Steps A-E are preneoplastic changes

Transitional system (Brionchioles) - Epithelial lining of the bronchiolar region of the transitional zone is highly susceptible to injury (responds similar with the conductive system)

1. High vulnerability to oxidant and free radicals
2. The presence of Club (Clara) cells → rich in functional oxidases → locally generates toxic metabolites
3. Increased tendency for PAM and leukocytes to accumulate locally

Severe bronchiolar injury → bronchiolitis obliterans (polypoid masses)

1. Severe injury → exudation → exudates attach and cannot be separated from BM of bronchioles, exacerbated by...
2. Exudate infiltrated by fibroblasts → form small nodular masses of fibrovascular tissue → microscopic polyps
3. The external surface is eventually covered by ciliated cells

Repair in Chronic bronchiolar injury

1. Mild but persistent injury → goblet cells proliferate from basal cells → GC metaplasia (altered physicochemical properties of bronchiolar secretions)

• normally GC are absent in bronchioles

2. Mucus from GCs alter bronchiolar fluid released by Club cells
3. Increased viscoelasticity of mucus → secretions cannot be removed by ciliary action (dutay lg ciliated cells sa transition system)→ plugging and obstruction of distal airways → chronic obstructive pulmonary disease (COPD)