Pau Martí-Lliteras

TL;DR: It was shown that alveolar macrophages clear NTHI infections by adhesion, phagocytosis, and phagolysosomal processing of the pathogen, and Mechanistically, the data showed that CSE reduced PI3K signaling activation triggered by NTH I, and treatment of CSE-exposed cells with the glucocorticoid dexamethasone reduced the amount of TNF-α secreted upon NTHi infection.

TL;DR: It is found that NTHi invades the airway epithelium by a distinct mechanism, requiring microtubule assembly, lipid rafts integrity, and activation of phosphatidylinositol 3-kinase (PI3K) signalling, and it is shown that PCho is not responsible for Nthi intracellular location.

TL;DR: A range of pathogenic traits and a repertoire of genetic variants in the context of persistent infection by NTHi are frame.

TL;DR: It is shown that, in spite of a high level of genetic heterogeneity, NTHi clinical isolates display a prevalent molecular feature, which could confer fitness during infectious processes, and was associated with a higher bacterial resistance to serum mediated killing and enhanced adherence to human respiratory epithelial cells.

TL;DR: The challenge of monitoring both the pathogen and the host in longitudinal studies, and of applying comparative genomics to clarify the meaning of the vast NTHi genetic diversity and its translation to virulence phenotypes are highlighted.