In a multicenter cross-sectional study published in the American Journal of Respiratory and Critical Care Medicine, researchers sought to investigate if immunoglobulin A (IgA) autoantibodies target lung-specific proteins and contribute to disease severity.

The researchers examined 147 blood samples, nine lung tissue samples, and 36 bronchoalveolar lavage (BAL) fluid samples from patients treated at three Swiss hospitals and one German tertiary hospital.

The researchers employed enzyme-linked immunosorbent assays on blood samples, immunofluorescence staining on tissue samples and immunoprecipitations, and mass spectrometry on BAL fluid samples to detect IgA autoantibodies and assess their impact on lung surfactant. The researchers also obtained surface tension calculations with medical surfactant.

The results revealed that in patients with severe COVID-19 infection, IgA autoantibodies targeting pulmonary surfactant proteins B and C were elevated, but they were not in patients with influenza or bacterial pneumonia. The authors also indicated that pulmonary surfactant failed to diminish surface tension after incubation with either plasma or purified IgA from patients with severe COVID-19.

The authors wrote, “Our data reveal a potential mechanistic driver of disease, as we show that auto-IgA interferes with the ability of pulmonary surfactant to lower surface tension. This could lead to impaired stabilization of the pulmonary air sacs, thus contributing to alveolar collapse and insufficient oxygen exchange.”

The authors concluded that their findings further reinforce the idea that IgA antibodies against self-antigens in the lung alter crucial components of alveolar gas exchange, thus offering innovative systematic understandings with regard to COVID-19 infection progression.

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