Surfactant protein A (SP-A) inhibits agglomeration and macrophage uptake of toxic amine modified nanoparticles

The current study examined whether long-term culture of macrophages affects their metabolism of surfactant components. Compared with freshly isolated resting macrophages in culture for 1 h, macrophages attached to plastic dishes for 24 h showed evidence of conversion to a “primed” state with 1) an altered morphology characterized by a larger size, ruffled membranes, lamellipodia, and a “foamy” appearance after attachment to glass and 2) a fivefold greater respiratory burst in response to phorbol 12-myristate 13-acetate stimulation. On incubation with iodinated surfactant protein A (SP-A), the 24-h alveolar or tissue macrophages showed a 5- or a 23-fold greater increase in SP-A degradation, respectively, than macrophages cultured for 1 h. Conditioned media experiments demonstrated that the elevated rate of SP-A degradation after prolonged culture was not a result of proteases secreted by the macrophages. Incubation of cells with NH4Cl reduced the degradation of SP-A to a similar extent (to 33% of control values) in resting and primed tissue macrophages. On the other hand, length of time of cell culture did not affect macrophage uptake and degradation of [3H]dipalmitoylphosphatidylcholine in mixed unilamellar liposomes. Thus freshly isolated resting tissue and alveolar macrophages can be primed to specifically increase their rate of SP-A degradation. Activation of macrophages associated with lung disease may be important for SP-A metabolism and surfactant function.

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A comparison of lung surfactant protein A (SP-A) from human bronchoalveolar lavage fluid and synovial fluid

Immunology Letters ◽

10.1016/s0165-2478(97)87286-0 ◽

1997 ◽

Vol 56 (1-3) ◽

pp. 112-113

Author(s):

T Hickling

Keyword(s):

Synovial Fluid ◽

Bronchoalveolar Lavage ◽

Bronchoalveolar Lavage Fluid ◽

Lung Surfactant ◽

Protein A ◽

Lavage Fluid ◽

Surfactant Protein ◽

Surfactant Protein A ◽

Lung Surfactant Protein

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Surfactant protein a (sp-a) reduces human rhinoviruses (hrvs)-induced inflammatory responses and inhibits viral replication in human airways epithelial cells

10.26226/morressier.5afd6e2ed64f25002cfc368e ◽

2018 ◽

Author(s):

Sasipa - Tanyaratsrisakul

Keyword(s):

Epithelial Cells ◽

Viral Replication ◽

Inflammatory Responses ◽

Protein A ◽

Surfactant Protein ◽

Surfactant Protein A ◽

Human Airways

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Faculty Opinions recommendation of Interaction of surfactant protein A with peroxiredoxin 6 regulates phospholipase A2 activity.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1050437.502345 ◽

2007 ◽

Author(s):

Maurizio Luisetti

Keyword(s):

Phospholipase A2 ◽

Protein A ◽

Surfactant Protein ◽

Surfactant Protein A ◽

Peroxiredoxin 6 ◽

Phospholipase A2 Activity

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Faculty Opinions recommendation of Surfactant protein-A inhibits mycoplasma-induced dendritic cell maturation through regulation of HMGB-1 cytokine activity.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.5172956.5134062 ◽

2010 ◽

Author(s):

Andrea Tenner ◽

Marie Bonhomme - Benoit

Keyword(s):

Dendritic Cell ◽

Protein A ◽

Surfactant Protein ◽

Dendritic Cell Maturation ◽

Cell Maturation ◽

Surfactant Protein A

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Screening and Identification of Aptamers Aganinst Pulmonary Surfactant Protein A

CHINESE JOURNAL OF ANALYTICAL CHEMISTRY (CHINESE VERSION) ◽

10.3724/sp.j.1096.2013.30461 ◽

2013 ◽

Vol 41 (11) ◽

pp. 1659

Author(s):

Li-Juan LIU ◽

Yi CHEN ◽

Wei WANG ◽

Chao CHEN ◽

Ming-Hao GAO ◽

...

Keyword(s):

Pulmonary Surfactant ◽

Protein A ◽

Surfactant Protein ◽

Surfactant Protein A ◽

Screening And Identification ◽

Pulmonary Surfactant Protein

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Surfactant protein A reduces TLR4 and inflammatory cytokine mRNA levels in neonatal mouse ileum

Scientific Reports ◽

10.1038/s41598-021-82219-y ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Lidan Liu ◽

Chaim Z. Aron ◽

Cullen M. Grable ◽

Adrian Robles ◽

Xiangli Liu ◽

...

Keyword(s):

Proinflammatory Cytokine ◽

Inflammatory Cytokine ◽

Protein A ◽

Surfactant Protein ◽

Surfactant Protein A ◽

Mrna Levels ◽

Wild Type ◽

Cytokine Mrna ◽

Protein Levels ◽

Cytokine Levels

AbstractLevels of intestinal toll-like receptor 4 (TLR4) impact inflammation in the neonatal gastrointestinal tract. While surfactant protein A (SP-A) is known to regulate TLR4 in the lung, it also reduces intestinal damage, TLR4 and inflammation in an experimental model of necrotizing enterocolitis (NEC) in neonatal rats. We hypothesized that SP-A-deficient (SP-A−/−) mice have increased ileal TLR4 and inflammatory cytokine levels compared to wild type mice, impacting intestinal physiology. We found that ileal TLR4 and proinflammatory cytokine levels were significantly higher in infant SP-A−/− mice compared to wild type mice. Gavage of neonatal SP-A−/− mice with purified SP-A reduced ileal TLR4 protein levels. SP-A reduced expression of TLR4 and proinflammatory cytokines in normal human intestinal epithelial cells (FHs74int), suggesting a direct effect. However, incubation of gastrointestinal cell lines with proteasome inhibitors did not abrogate the effect of SP-A on TLR4 protein levels, suggesting that proteasomal degradation is not involved. In a mouse model of experimental NEC, SP-A−/− mice were more susceptible to intestinal stress resembling NEC, while gavage with SP-A significantly decreased ileal damage, TLR4 and proinflammatory cytokine mRNA levels. Our data suggests that SP-A has an extrapulmonary role in the intestinal health of neonatal mice by modulating TLR4 and proinflammatory cytokines mRNA expression in intestinal epithelium.

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