The European respiratory journal · 2026
Trimodulin supports antibacterial defence and restricts inflammation in preclinical pneumonia models.
СтатьяНазвание и аннотация: Перевод в очереди
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Nouailles Geraldine, Bischoff Romina, Linke Kerstin, Taylor Alexander, Gutbier Birgitt, Pennitz Peter, Goekeri Cengiz, Kunder Sandra, Voß Anne, Brömel Theresa C, Kershaw Olivia, Milek Miha, Farztdinov Vadim, Mülleder Michael, Weissmüller Sabrina, Heinz Corina C, Visser Mayken, Bohlaender Fabian, Ahrens Katharina, Beule Dieter, Gruber Achim D, Koenig Martin, Witzenrath Martin
Аннотация
BACKGROUND: Severe community-acquired pneumonia remains a global health challenge with high mortality despite advances in antibiotic therapy and supportive care. Immunoglobulin therapies, especially IgM-containing ones, have shown promise in enhancing host defence and reducing inflammation. The CIGMA trial highlighted the potential of trimodulin to lower mortality in patients with severe community-acquired pneumonia with high C-reactive protein and low IgM levels.
METHODS: We investigated the protective effects of trimodulin on clinical status, bacterial burden, lung integrity and inflammatory responses in murine models of lung injury, including both ventilator-induced lung injury and infection-induced models with nonsterile inflammation.
RESULTS: In mice, trimodulin significantly protected against lethal pneumococcal pneumonia by reducing bacterial burden and disease severity while preserving alveolar barrier integrity and limiting lung oedema. The antibacterial action of trimodulin was mediated through opsonophagocytosis, and its anti-inflammatory effects operated independently of the latter. When combined with ampicillin, trimodulin exhibited enhanced suppression of inflammation.
CONCLUSION: Our findings in preclinical pneumonia models suggest that trimodulin could be a promising therapy for severe community-acquired pneumonia. We provide evidence that trimodulin enhances host defence, reduces detrimental pulmonary inflammation and barrier dysfunction, and limits pulmonary oedema, which may explain the beneficial effects observed in patients with severe community-acquired pneumonia.
METHODS: We investigated the protective effects of trimodulin on clinical status, bacterial burden, lung integrity and inflammatory responses in murine models of lung injury, including both ventilator-induced lung injury and infection-induced models with nonsterile inflammation.
RESULTS: In mice, trimodulin significantly protected against lethal pneumococcal pneumonia by reducing bacterial burden and disease severity while preserving alveolar barrier integrity and limiting lung oedema. The antibacterial action of trimodulin was mediated through opsonophagocytosis, and its anti-inflammatory effects operated independently of the latter. When combined with ampicillin, trimodulin exhibited enhanced suppression of inflammation.
CONCLUSION: Our findings in preclinical pneumonia models suggest that trimodulin could be a promising therapy for severe community-acquired pneumonia. We provide evidence that trimodulin enhances host defence, reduces detrimental pulmonary inflammation and barrier dysfunction, and limits pulmonary oedema, which may explain the beneficial effects observed in patients with severe community-acquired pneumonia.