Investigation of urinary β2 microglobulin; substitute for interferon-γ as a suppressor of pulmonary fibrosis in a preterm with chronic lung disease following intrauterine infection

We experienced a female infant weighing 866 g at birth after 28 weeks 1 day gestation with apparent intrauterine infection. Bi-level-nasal CPAP was selected for respiratory management as a strategy to minimize the severity of chronic lung disease (CLD). As a result, she survived the acute phase without tracheal intubation and improved without requiring home oxygen therapy. Her urinary β2 microglobulin (u-BMG) in the early neonatal period was less than the cutoff value of 100,000 μg/gCr for the onset of CLD. However, her u-BMG then rose to a markedly high value that peaked at 3 weeks after birth. Her serum KL-6 was markedly high early after birth and increased sharply to a peak of 3016 U/mL on day 9. The increase in KL-6 in the early postnatal period indicated that lung tissue had already been injured by intrauterine inflammation, and although postnatal tracheal intubation was avoided, spontaneous breathing inevitably additionally injured the immature lung. It appears that substantial repair had occurred with fibrosis. It should be noted that the peak of u-BMG was delayed by more than 10 days from the peak of KL-6. This may suggest that the inflammatory cytokine interferon-γ, which increases the production of BMG, had not only an inflammatory effect that exacerbates lung damage, but also a biological self-defense effect that mainly suppresses lung fibrosis.