Abstract
Exhaled breath condensate acidification reflects the presence of airway acidification. Mycobacterium tuberculosis is an organism particularly sensitive to acidity. We aimed to determine if there is evidence of airway acidification in a cross section of patients with active tuberculosis.We enrolled 51 subjects with active tuberculosis in Ghana and Thailand, and compared them to control subjects. We collected exhaled breath condensate, and assayed for pH after gas standardization.Exhaled breath condensate pH from the control group revealed a median of 7.9 (7.7 - 8.0, n = 21), significantly higher than the active pulmonary tuberculosis patients who had a median pH of 7.4 (7.0 - 7.7; n = 51; p=0.002). Presence or absence of antibiotic therapy did not affect EBC pH values.These exhaled breath condensate data support the theory that airways become acidic in active tuberculosis infection. This may be a mechanism of immune response and pathology not previously considered.
Highlights
Acidification of exhaled breath condensate (EBC) has been identified in multiple respiratory illnesses(J. Hunt, 2007), and is caused by acidification of the airway lining fluid at some level
Our data reveal that patients with active pulmonary tuberculosis in Ghana and Thailand have a higher incidence of EBC acidification than controls enrolled in the same area
The median EBC in active pulmonary TB is substantially lower than all published historical controls as summarized in reference 12 (Paget-Brown et al, 2006)
Summary
Acidification of exhaled breath condensate (EBC) has been identified in multiple respiratory illnesses(J. Hunt, 2007), and is caused by acidification of the airway lining fluid at some level. The degree and precise location of airway acidification is uncertain, invasive measures with pH probe in bronchi correlate well with EBC pH in a bovine lung model(Bunyan et al, 2005). Despite acid-induced stress responses, survival of Mycobacterium tuberculosis is inhibited by an acidic environment(Piddington, Kashkouli, & Buchmeier, 2000). Acidification of phagosomes is an important innate immune mechanism(Krause, 2000), but with the recent recognition that the extracellular airway fluids can acidify in association with inflammatory and infectious diseases, the possibility arose that intrinsic airway acidification might serve as a host response against Mycobacteria. Airway pH may be a therapeutic target, and its measurement serve as a biomarker of responses to active mycobacterial disease
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