Tuberculosis, Lung Infections, and Respiratory Care

Immunology of Tuberculosis and Respiratory Infections

The immunology of tuberculosis (TB) and other respiratory infections is fundamental to understanding how the body defends itself against airborne pathogens and how these microbes evade immune control. When *Mycobacterium tuberculosis* is inhaled, it is engulfed by alveolar macrophages, which trigger an innate immune response involving cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-12 (IL-12), and interferon-gamma (IFN-γ). These signals recruit immune cells to form granulomas—structured clusters that aim to contain the infection. While this process helps control bacterial spread, *M. tuberculosis* can survive within macrophages, leading to a latent infection that may later reactivate if immune defenses weaken. The balance between protective and pathological immune responses determines whether the infection remains dormant or progresses to active disease.

In other respiratory infections, including viral and bacterial diseases like influenza, pneumonia, and COVID-19, the immune system responds through both innate and adaptive mechanisms. The airway’s epithelial cells, macrophages, and dendritic cells recognize invading pathogens using pattern recognition receptors, initiating inflammation and antiviral defenses. Adaptive immunity follows, with T cells targeting infected cells and B cells producing antibodies that neutralize pathogens and provide long-term protection. However, excessive immune activation can lead to tissue injury and respiratory failure, as seen in cytokine storm syndromes during severe viral infections. Balancing effective pathogen clearance with controlled inflammation is therefore crucial for recovery and lung health.