<![CDATA[Non-tuberculous mycobacteria (NTM) refer to all mycobacterial species except those causing tuberculosis and leprosy. These bacteria are acid-fast. The bacteria are environmental bacteria that act opportunistically in humans. The infection can lead to disease, primarily affecting the lungs in susceptible hosts. Risk factors for NTM infection include defects in the body's defence mechanisms (e.g., ciliary defects), changes in lung structure (e.g., bronchiectasis), and immune system abnormalities (e.g., immunosuppressant use), which can be congenital or acquired. The bacteria possess pathogen-associated molecular patterns (PAMPs) and cell wall components that differ from those of Mycobacterium tuberculosis (M. tuberculosis), one of which is the glycopeptidolipid (GPL) component. Different species have distinct cell wall components, enabling them to modulate the immune system in various ways by interacting with multiple pathogen recognition receptors, including toll-like receptors and fibronectin. The cell-mediated immune response plays a role in the response to NTM infection. Alveolar macrophages, as the first line of defence, release interleukin (IL)-12, activating the T-helper-1 (Th1) axis and natural killer (NK) cells, followed by the release of tumour necrosis factor- α (TNF-α), interferon (IFN)-γ, and IL-17. The clinical symptoms of NTM lung disease (NTM-LD) are similar to those of Mycobacterium tuberculosis (M. tuberculosis). Two radiological findings are commonly observed: fibro-cavitary lesions and nodular bronchiectasis. Diagnosis must meet clinical, radiological, and microbiological criteria. The decision to start therapy should consider host factors, clinical conditions, and species type. The treatment approach involves multi-drug therapy and long-term administration, depending on species, disease extent, drug susceptibility testing results, and comorbidities.]]>
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