The Surfactant System

Kingma, Paul S.; Jobe, Alan H.

doi:10.1016/b978-0-323-44887-1.00005-5

Cited by 4 publications

(2 citation statements)

References 80 publications

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“…Mannose-binding lectin binds to phospholipids, carbohydrates (mannose, Nacetylglucosamine), and non-glycosylated proteins [75]. Surfactant protein A binds N-acetyl mannosamine, bacterial phospholipids [76]. Collectins/ficolins bind to carbohydrate moieties displayed on bacterial surfaces through their carbohydrate-recognition (lectin) domains [70].…”

Section: Nanoparticles and Many Different Viruses Can Acquire Biocoro...mentioning

confidence: 99%

Could a Non-Cellular Molecular Interactome in the Blood Circulation Influence Pathogens’ Infectivity?

Hardy¹,

Sarker²,

Fernández-Patrón³

2023

Preprint

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We advance the notion that much, like artificial nanoparticles, relatively more complex biological entities with nanometric dimensions such as pathogens (viruses, bacteria and other microorganisms) may also acquire a biomolecular corona, upon entering the blood circulation of an organism. We view this biomolecular corona as a component of a much broader non-cellular blood interactome that can be highly specific to the organism, akin to components of the innate immune response to an invading pathogen. We review published supporting data and generalize these notions from artificial nanoparticles to viruses and bacteria. Characterization of the non-cellular blood interactome of an organism may help explain apparent differences in the susceptibility to pathogens among individuals. The non-cellular blood interactome is a candidate therapeutic target to treat infectious and non-infectious conditions.

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Section: Nanoparticles and Many Different Viruses Can Acquire Biocoro...mentioning

confidence: 99%

Could a Non-Cellular Molecular Interactome in the Blood Circulation Influence Pathogens’ Infectivity?

Hardy¹,

Sarker²,

Fernández-Patrón³

2023

Preprint

View full text Add to dashboard Cite

show abstract

“…Mannose-binding lectin binds to phospholipids, carbohydrates (mannose, N-acetylglucosamine), and non-glycosylated proteins [ 99 ]. Surfactant protein A binds N-acetyl mannosamine and bacterial phospholipids [ 100 ]. Collectins/ficolins bind to carbohydrate moieties displayed on bacterial surfaces through their carbohydrate-recognition (lectin) domains [ 94 ].…”

Section: Introductionmentioning

confidence: 99%

Could a Non-Cellular Molecular Interactome in the Blood Circulation Influence Pathogens’ Infectivity?

Hardy

Sarker

Fernández-Patrón

2023

Cells

View full text Add to dashboard Cite

We advance the notion that much like artificial nanoparticles, relatively more complex biological entities with nanometric dimensions such as pathogens (viruses, bacteria, and other microorganisms) may also acquire a biomolecular corona upon entering the blood circulation of an organism. We view this biomolecular corona as a component of a much broader non-cellular blood interactome that can be highly specific to the organism, akin to components of the innate immune response to an invading pathogen. We review published supporting data and generalize these notions from artificial nanoparticles to viruses and bacteria. Characterization of the non-cellular blood interactome of an organism may help explain apparent differences in the susceptibility to pathogens among individuals. The non-cellular blood interactome is a candidate therapeutic target to treat infectious and non-infectious conditions.

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Alveolar macrophage metabolic programming via a C-type lectin receptor protects against lipo-toxicity and cell death

et al. 2022

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Alveolar macrophages (AM) hold lung homeostasis intact. In addition to the defense against inhaled pathogens and deleterious inflammation, AM also maintain pulmonary surfactant homeostasis, a vital lung function that prevents pulmonary alveolar proteinosis. Signals transmitted between AM and pneumocytes of the pulmonary niche coordinate these specialized functions. However, the mechanisms that guide the metabolic homeostasis of AM remain largely elusive. We show that the NK cell-associated receptor, NKR-P1B, is expressed by AM and is essential for metabolic programming. Nkrp1b−/− mice are vulnerable to pneumococcal infection due to an age-dependent collapse in the number of AM and the formation of lipid-laden AM. The AM of Nkrp1b−/− mice show increased uptake but defective metabolism of surfactant lipids. We identify a physical relay between AM and alveolar type-II pneumocytes that is dependent on pneumocyte Clr-g expression. These findings implicate the NKR-P1B:Clr-g signaling axis in AM-pneumocyte communication as being important for maintaining metabolism in AM.

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The Surfactant System

Cited by 4 publications

References 80 publications

Could a Non-Cellular Molecular Interactome in the Blood Circulation Influence Pathogens’ Infectivity?

Could a Non-Cellular Molecular Interactome in the Blood Circulation Influence Pathogens’ Infectivity?

Could a Non-Cellular Molecular Interactome in the Blood Circulation Influence Pathogens’ Infectivity?

Alveolar macrophage metabolic programming via a C-type lectin receptor protects against lipo-toxicity and cell death

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