Transregional Collaborative Research Center SFB-TR 84 - “Innate Immunity of the Lung: Mechanisms of Pathogen Attack and Host Defence in Pneumonia“

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Area B

Humoral and cell-based bronchoalveolar defence mechanisms

 

Area B will investigate signalling cascades and mechanisms of cellular responses and cellular malfunctions during lung infection.

The different -and with regard to innate immune activation opposing effects- of the peptidoglycan recognition proteins (PGLYRPs) PGLYRP2 and 4 in S.p.-induced pneumonia will be investigated in project B01 (Aly/Suttorp/Hain). Project B02 (Herold/Pleschka/Wolff) explores the hypothesis that previously undefined inflammatory signalling events in alveolar epithelial cells significantly contribute to structural damage (e.g. oedema formation due to Na/K-ATPase mistargeting) and functional impairment of these cells following IAV infection, and that some of these pathways are simultaneously exploited by IAV to support viral propagation. Project B03 (Hackstein/Bauer/Lohmeyer) will investigate mechanisms that (i) shape the composition of the macrophage and respiratory DC compartment, and determine their role during pneumonia, and (ii) dissect mechanisms of ADAR1-induced lung DC/MP development. Project B05 (Meisel/Meisel) explores how stroke-induced anti-inflammatory cholinergic pathways inhibit protective pulmonary anti-bacterial innate immune responses, and therapeutic intervention strategies will be explored. Mitochondria-related regulation of lung innate immunity (e.g. mtDAMP release) and cell fate decisions will be investigated in B06 (Hocke/Hippenstiel) in human lung tissue.

Abbreviations: B/Gi-M, Berlin/Gießen-Marburg; B, Berlin; Gi-M, Gießen-Marburg; PGLYRP, peptidoglycan recognition protein, S.p., Streptococcus pneumoniae; MØ, macrophage; M1/2, M1/2 macrophage; IAV, influenza A virus; TLR, toll-like receptor; K.p., Klebsiella pneumonia; DC, dendritic cell; ADAR1, adenosine deaminase 1 acting on RNA; mtDAMP, mitochondrial danger-associated molecular pattern; miR, microNRA; nAChR, nicotinic acetylcholine receptor; EC, endothelial cell; AECs, alveolar epithelial cells.