Abstract
Lung diseases are among the leading causes of morbidity and mortality. Complement activation may prevent a variety of respiratory infections, but on the other hand, could exacerbate tissue damage or contribute to adverse side effects. In this review, the associations of factors specific for complement activation via the lectin pathway (LP) with infections of the respiratory system, from birth to adulthood, are discussed. The most extensive data concern mannose-binding lectin (MBL) which together with other collectins (collectin-10, collectin-11) and the ficolins (ficolin-1, ficolin-2, ficolin-3) belong to pattern-recognition molecules (PRM) specific for the LP. Those PRM form complexes with MBL-associated serine proteases (MASP-1, MASP-2, MASP-3) and related non-enzymatic factors (MAp19, MAp44). Beside diseases affecting humanity for centuries like tuberculosis or neonatal pneumonia, some recently published data concerning COVID-19 are summarized.
Highlights
Lung diseases are thought to be the 3rd leading cause of morbidity and mortality worldwide
Activation of complement via the lectin pathway is initiated by several pattern-recognition molecules (PRM), complexed with mannose-binding lectin-associated serine proteases (MASP)
As lectin pathway-associated PRM are constitutively present in the respiratory system or are transferred from the bloodstream to the infected sites [mannose-binding lectin (MBL) and ficolin-2 detected in bronchoalveolar lavage fluid (BALF) from patients suffering from pneumonia or invasive aspergillosis, respectively], they may contribute to excessive inflammation and its detrimental effects
Summary
Lung diseases are thought to be the 3rd leading cause of morbidity and mortality worldwide. As well as cross-talk between lectin and alternative pathways and with the coagulation and contact systems, ficolins and MBL were demonstrated to interact with long and/or short pentraxins contributing to the enhancement or regulation of the early immune response [reviewed in [47, 48]]. As lectin pathway-associated PRM are constitutively present in the respiratory system (ficolin-3 synthesized by type II pneumocytes and ciliated bronchial cell, ficolin-1 produced by lung macrophages) or are transferred from the bloodstream to the infected sites [MBL and ficolin-2 detected in bronchoalveolar lavage fluid (BALF) from patients suffering from pneumonia or invasive aspergillosis, respectively], they may contribute to excessive inflammation and its detrimental effects.
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