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HISTOLOGICAL STRUCTURE OF THE LUNGS AND PATHOLOGICAL
ALTERATIONS
Akhmedova Lola Abdulkhamidovna
Andijan State Medical Institute,Uzbekistan
Abstract:
The lungs are vital organs responsible for gas exchange, providing oxygen to tissues
and removing carbon dioxide from the bloodstream. Histologically, the lungs are composed of a
branching bronchial tree ending in alveoli, where gas exchange occurs across the alveolar-
capillary barrier. Pathological conditions such as pneumonia, chronic obstructive pulmonary
disease (COPD), and pulmonary fibrosis cause characteristic alterations in lung histology that
directly impair respiratory function. This article reviews the normal histological structure of the
lungs and describes common pathological changes with emphasis on their diagnostic and clinical
relevance.
Keywords:
lung histology, alveoli, pneumonia, COPD, pulmonary fibrosis
Introduction
The lungs are essential organs for respiration and survival, providing the interface between the
external environment and the circulatory system. Each lung is divided into lobes and lobules and
contains a highly specialized histological architecture adapted to optimize gas exchange. The
bronchial tree, composed of bronchi, bronchioles, and terminal bronchioles, progressively
narrows and transitions into respiratory bronchioles and alveolar ducts. At the end of this
branching system are alveoli, the structural and functional units of the lung. The thin alveolar
epithelium, together with the capillary endothelium and fused basement membrane, forms the
alveolar-capillary barrier through which efficient diffusion of oxygen and carbon dioxide occurs.
Normal lung histology ensures the maintenance of adequate ventilation and perfusion. Type I
alveolar epithelial cells cover most of the alveolar surface and facilitate gas exchange, while type
II cells produce surfactant to reduce surface tension and prevent alveolar collapse. Macrophages
within alveoli provide immune defense against inhaled pathogens. Any disruption to this
architecture leads to significant impairment of pulmonary function.
Pathological conditions manifest with distinct histological features. Pneumonia is characterized
by inflammatory exudates filling alveolar spaces, while COPD shows bronchial wall thickening,
goblet cell hyperplasia, and alveolar destruction (emphysema). Pulmonary fibrosis presents with
interstitial collagen deposition and thickening of the alveolar walls, severely limiting gas
exchange. These histological changes correlate with clinical symptoms such as dyspnea,
hypoxemia, and reduced pulmonary compliance.
This article aims to describe normal lung histology and analyze structural alterations observed in
major respiratory diseases, highlighting their diagnostic value and clinical implications.
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The lungs are highly specialized organs that serve as the primary site of gas exchange, providing
oxygen for cellular metabolism and eliminating carbon dioxide, a byproduct of energy
production. They occupy the thoracic cavity and are divided into lobes, lobules, and acini, each
possessing a unique histological organization. This intricate structure ensures that the pulmonary
system can adapt to varying physiological demands, from rest to intense exercise, while
maintaining homeostasis.
Histologically, the respiratory system is organized into conducting and respiratory portions. The
conducting system, which includes the trachea, bronchi, and bronchioles, is lined by
pseudostratified columnar epithelium containing ciliated cells, goblet cells, and basal cells. This
epithelial arrangement not only allows efficient airflow but also provides defense through
mucociliary clearance, removing inhaled particles and pathogens. As the airway branches into
smaller bronchioles, the epithelium transitions into simple cuboidal cells, reflecting the gradual
adaptation from conduction to gas exchange.
The respiratory portion begins with respiratory bronchioles and continues into alveolar ducts and
alveoli, which represent the functional units of gas exchange. The alveolar wall, or interalveolar
septum, is composed of a thin layer of type I pneumocytes, responsible for gas diffusion, and
type II pneumocytes, which secrete pulmonary surfactant to reduce surface tension and prevent
alveolar collapse. In addition, alveolar macrophages provide immune surveillance by
phagocytosing microorganisms and debris. This highly specialized histological design ensures
that the lungs function efficiently under normal conditions.
Pathological processes such as pneumonia, chronic obstructive pulmonary disease (COPD), and
pulmonary fibrosis result in distinct structural alterations that impair respiratory function. In
pneumonia, alveoli are filled with inflammatory exudates, reducing surface area for gas
exchange. COPD is characterized by chronic inflammation, mucus hypersecretion, airway
remodeling, and emphysematous destruction of alveolar walls. Pulmonary fibrosis involves
excessive collagen deposition within alveolar septa, leading to thickening of the alveolar-
capillary barrier and progressive respiratory insufficiency. These changes highlight the
importance of understanding normal histology to recognize and interpret disease-related
alterations.
Therefore, the study of lung histology not only provides essential insight into basic physiology
but also establishes the foundation for diagnosing and managing pulmonary diseases. The
purpose of this article is to review the normal histological organization of the lungs and to
describe characteristic pathological alterations observed in major respiratory disorders,
emphasizing their diagnostic and prognostic significance.
Methods
Histological study of lung tissue is performed on biopsy, surgical, or autopsy specimens.
Samples are fixed in 10% formalin, embedded in paraffin, and cut into 4–6 μm sections.
Hematoxylin and eosin (H&E) staining provides a general overview of the bronchial epithelium,
alveolar spaces, and vascular structures. Special stains such as Periodic Acid–Schiff (PAS) for
mucus, Masson’s trichrome for collagen, and Gram or Ziehl–Neelsen stains for microorganisms
are frequently applied. Immunohistochemistry is used to identify specific inflammatory markers,
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fibrosis-related proteins, or tumor antigens in cases of neoplasia. Electron microscopy provides
ultrastructural details of alveolar epithelial and endothelial cells.
Histological evaluation of lung tissue is performed on specimens obtained from surgical
resection, bronchoscopy-guided biopsy, or autopsy. Proper fixation and preparation are essential
to preserve delicate pulmonary structures. Samples are typically fixed in 10% neutral buffered
formalin, followed by dehydration, paraffin embedding, and sectioning at 4–6 micrometers.
Routine staining with hematoxylin and eosin (H&E) is the primary method for evaluating
general tissue architecture, including the bronchial epithelium, alveolar spaces, vascular
structures, and interstitial tissue. This staining allows visualization of cellular morphology,
inflammatory infiltration, and gross pathological alterations.
To obtain more detailed information, additional histological and histochemical stains are applied.
Periodic Acid–Schiff (PAS) highlights mucus and basement membranes, useful in evaluating
goblet cell hyperplasia and epithelial thickening in chronic bronchitis. Masson’s trichrome stain
is employed to demonstrate collagen deposition, which is crucial in assessing interstitial fibrosis.
Gram and Ziehl–Neelsen stains aid in the identification of bacterial and mycobacterial organisms
in infectious pneumonia. Congo red is used when amyloidosis is suspected.
Immunohistochemistry provides further diagnostic accuracy by identifying cell-specific markers
and inflammatory mediators. For instance, antibodies against surfactant proteins can confirm
type II pneumocyte activity, while markers for CD68 highlight macrophage infiltration. Fibrotic
activity can be studied using α-smooth muscle actin and collagen-specific antibodies.
Electron microscopy serves as a valuable adjunct in selected cases, offering ultrastructural details
of alveolar epithelial cells, endothelial junctions, and surfactant lamellar bodies. It is particularly
useful in the evaluation of diffuse interstitial lung diseases and rare congenital disorders of
surfactant metabolism.
In addition, morphometric analysis and digital image processing are increasingly used to
quantify structural changes such as alveolar wall thickness, fibrotic deposition, and capillary
density. These advanced methods provide objective data that can be correlated with clinical and
functional outcomes, enhancing the translational value of histological research.
Altogether, a combination of routine histology, special staining, immunohistochemistry, and
ultrastructural analysis provides a comprehensive understanding of pulmonary histology under
both normal and pathological conditions.
Results
In normal histology, the lungs display a well-organized bronchial tree lined by pseudostratified
columnar epithelium with ciliated cells and goblet cells. Bronchioles lack cartilage and glands,
while terminal bronchioles lead into respiratory bronchioles and alveolar ducts. Alveoli are lined
predominantly by thin type I pneumocytes, supported by type II pneumocytes, which secrete
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surfactant. Capillaries closely appose alveolar walls, forming the thin alveolar-capillary barrier
critical for gas exchange.
In pneumonia, alveoli are filled with neutrophilic infiltrates and proteinaceous exudates, leading
to consolidation of lung tissue. In COPD, histological changes include hypertrophy of
submucosal glands, goblet cell hyperplasia, chronic inflammation of airway walls, and
emphysematous destruction of alveolar septa. Pulmonary fibrosis shows thickened alveolar septa
with extensive collagen deposition, fibroblast proliferation, and distortion of alveolar architecture,
resulting in honeycomb-like lung tissue.
Discussion
Histological analysis of lung tissue provides essential information for diagnosing and
characterizing respiratory diseases. Each pathological entity has unique structural alterations that
correlate with functional impairment. Pneumonia demonstrates acute inflammatory processes
that explain impaired gas exchange and hypoxemia. COPD reflects chronic injury associated
with environmental exposures such as smoking, and histology explains symptoms like airway
obstruction and loss of elastic recoil. Pulmonary fibrosis illustrates the progressive replacement
of functional parenchyma with fibrotic tissue, which accounts for restrictive physiology and
reduced lung compliance.
While radiological imaging and pulmonary function tests are important in clinical practice, they
cannot fully substitute for histological evaluation in identifying specific cellular and structural
changes. Moreover, histology provides insight into disease mechanisms, guides treatment
strategies, and assists in prognostic evaluation. Modern techniques such as
immunohistochemistry and molecular histopathology further enhance diagnostic accuracy by
detecting specific markers of inflammation, fibrosis, or neoplasia.
Conclusion
Lung histology illustrates the delicate structural arrangement necessary for efficient gas
exchange. The integrity of alveoli, bronchioles, and the alveolar-capillary barrier is critical for
maintaining adequate respiration. Pathological processes such as pneumonia, COPD, and
pulmonary fibrosis disrupt this architecture in different ways, producing characteristic
histological patterns that directly explain clinical manifestations. Histological analysis therefore
remains indispensable for the diagnosis, staging, and management of pulmonary diseases.
Although imaging and functional tests are valuable in monitoring respiratory disorders, histology
provides the most direct and detailed evaluation of structural pathology. Advances in molecular
pathology and immunohistochemistry continue to expand the diagnostic potential of histology,
making it an even more powerful tool in respiratory medicine. A deeper understanding of
structural alterations in the lung not only improves diagnostic precision but also facilitates the
development of targeted therapies to reduce the burden of pulmonary diseases.
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