What pathophysiology of pulmonary host defense against viral pneumonia?

Updated: Mar 24, 2021
  • Author: Zab Mosenifar, MD, FACP, FCCP; Chief Editor: John J Oppenheimer, MD  more...
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The pulmonary host defense is complex and includes the following components:

  • Mechanical barriers

  • Humoral immunity

  • Phagocytic cells

  • Cell-mediated immunity

Mechanical barriers are hairs from the nostrils that filter particles larger than 10 microns, mucociliary clearance, and sharp-angle branching of the central airways that helps the 5- to 10-micron particles to become impacted in the mucosa.

Humoral immunity is represented by mucosal immunoglobulin A (IgA), alveolar immunoglobulin M (IgM), and immunoglobulin G (IgG) present in transudates from the blood.

Phagocytic cells consist of polymorphonuclear (PMN) cells; alveolar, interstitial, and intravascular macrophages; and respiratory dendritic cells. Alveolar macrophages provide the first defense involved in internalizing and degrading the viral pathogens. They act as antigen-presenting and opsonin-producing cells.

Respiratory dendritic cells undergo maturation, activation, and early migration into the regional lymph nodes after the viral exposure. They act as antigen-presenting cells and are involved in the activation and differentiation of CD8+ T cells.

Cell-mediated immunity is the most important defense mechanism against the intracellular viral pathogens. This immunity is involved in antibody production, cytotoxic activity, and cytokine production. CD8+ memory or effector T cells tend to dominate the lymphocyte component of the virus-induced inflammatory component.

Experimental models demonstrated that 30-90% of CD8+ T cells recovered from bronchoalveolar lavage (BAL) are virus specific at the peak of the primary response. Studies in transgenic mice infected with influenza viruses documented that the CD8+ T cells are not recruited in the lung during the viral infection. They are resting memory cells formed after a previous encounter with the antigen, or they are acutely activated T cells after a nonrespiratory infection that undergo early migration in the lung and that are maintained there by specific ligands.

A substantial number of peripheral CD8+ memory T cells reside in the lung after a viral infection.

A secondary infection induces extensive renewal of CD8+ T cells in both lymphoid nodes and lungs. This replacement takes place in the absence of substantial inflammation or a substantial effector-cell population in the lungs. Respiratory infection allows numerous T cells to enter the airways and may permanently alter the permeability of the lung and mediastinal lymph nodes to lymphocytes.

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