Surfactant Protein D Augments Bacterial Association but Attenuates Major Histocompatibility Complex Class II Presentation of Bacterial Antigens

Hansen, Søren; Lo, Bernice; Evans, Kathy S.; Neophytou, Pavlos; Holmskov, Uffe; Wright, Jo Rae

doi:10.1165/rcmb.2006-0195oc

Cited by 39 publications

(35 citation statements)

References 51 publications

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“…35,37 SP-D, however, inhibited antigen presentation when dendritic cells were isolated from the lung. 36 Based on these results, we hypothesized here that TNF-α and SP-D serve as antagonists in the regulation of antigenpresenting cells in the lung.…”

Section: Tnf; Sp-d; Dendritic Cell; Mouse Model; Airway Inflammationmentioning

confidence: 92%

“…34 Only a few studies described the effects of SP-A and SP-D on dendritic cell function. [35][36][37] In these studies the authors found that SP-A inhibited and SP-D augmented the antigen-presenting function of bone marrow-derived dendritic cells. 35,37 SP-D, however, inhibited antigen presentation when dendritic cells were isolated from the lung.…”

Section: Tnf; Sp-d; Dendritic Cell; Mouse Model; Airway Inflammationmentioning

confidence: 98%

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Surfactant protein D inhibits TNF-α production by macrophages and dendritic cells in mice

Hortobagyi

Kierstein

Krytska

et al. 2008

Journal of Allergy and Clinical Immunology

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Section: Tnf; Sp-d; Dendritic Cell; Mouse Model; Airway Inflammationmentioning

confidence: 92%

Section: Tnf; Sp-d; Dendritic Cell; Mouse Model; Airway Inflammationmentioning

confidence: 98%

Surfactant protein D inhibits TNF-α production by macrophages and dendritic cells in mice

Hortobagyi

Kierstein

Krytska

et al. 2008

Journal of Allergy and Clinical Immunology

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“…These authors demonstrated that disruption of triglyceride and cholesteryl ester metabolism in alveolar macrophages, as a result of lysosomal acid lipase deficiency, results in respiratory inflammation, tissue remodeling, and emphysema (11,12). Together, these results indicate that factors governing surfactant composition and neutral lipid metabolism in alveolar cells might be associated with chronic pulmonary inflammation resulting in asthma, allergy, chronic obstructive pulmonary disease (COPD), 3 or lung cancer. ABCG1 is a member of the ATP-binding cassette (ABC) family of transmembrane transporters (reviewed in Ref.…”

mentioning

confidence: 97%

Loss of ABCG1 Results in Chronic Pulmonary Inflammation

Baldán

Gomes²,

Ping³

et al. 2008

The Journal of Immunology

116

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ABCG1, a member of the ATP-binding cassette transporter superfamily, is highly expressed in multiple cells of the lung. Loss of ABCG1 results in severe pulmonary lipidosis in mice, with massive deposition of cholesterol in both alveolar macrophages and type 2 cells and the accumulation of excessive surfactant phospholipids. These observations are consistent with ABCG1 controlling cellular sterol metabolism. Herein, we report on the progressive and chronic inflammatory process that accompanies the lipidosis in the lungs of Abcg1−/− mice. Compared with wild-type animals, the lungs of aged chow-fed mice deficient in ABCG1 show distinctive signs of inflammation that include macrophage accumulation, lymphocytic infiltration, hemorrhage, eosinophilic crystals, and elevated levels of numerous cytokines and cytokine receptors. Analysis of bronchoalveolar lavages obtained from Abcg1−/− mice revealed elevated numbers of foamy macrophages and leukocytes and the presence of multiple markers of inflammation including crystals of chitinase-3-like proteins. These data suggest that cholesterol and/or cholesterol metabolites that accumulate in Abcg1−/− lungs can trigger inflammatory signaling pathways. Consistent with this hypothesis, the expression of a number of cytokines was found to be significantly increased following increased cholesterol delivery to either primary peritoneal macrophages or Raw264.7 cells. Finally, cholesterol loading of primary mouse macrophages induced cytokine mRNAs to higher levels in Abcg1−/−, as compared with wild-type cells. These results demonstrate that ABCG1 plays critical roles in pulmonary homeostasis, balancing both lipid/cholesterol metabolism and inflammatory responses.

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“…The collectins are established members of the innate immune system but modulate also the adaptive immune response. SP-D dampens in vitro the T cell activation induced by anti-CD3 Abs or plant lectins as well as through presentation of bacterial Ags on MHC class II by dendritic cells (19,20). Naturally occurring collectin deficiencies among humans or in genetically manipulated mice lead to increased susceptibility to viral and bacterial infections and, in some cases, to unregulated inflammation, activated T cells, and production of autoreactive Abs.…”

mentioning

confidence: 99%

Collectin 11 (CL-11, CL-K1) Is a MASP-1/3–Associated Plasma Collectin with Microbial-Binding Activity

Hansen

Selman

Palaniyar

et al. 2010

The Journal of Immunology

Self Cite

178

233

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Collectins play important roles in the innate immune defense against microorganisms. Recently, a new collectin, collectin 11 (CL-11 or CL-K1), was identified via database searches. In present work, we characterize the structural and functional properties of CL-11. Under nonreducing conditions, in gel permeation chromatography recombinant CL-11 forms disulfide-linked oligomers of 100 and 200 kDa. A mAb-based ELISA estimates the concentration of CL-11 in plasma to be 2.1 μg/ml, and the presence of CL-11 in plasma was further verified by Western blotting and mass spectrometry. Mannan-binding lectin-associated serine protease 1 (MASP-1) copurified with CL-11 and the interaction in plasma with MASP-1 and/or MASP-3 was further demonstrated using ELISA. We identified the adrenal glands, the kidneys, and the liver as primary sites of expression. CL-11 lectin activity was demonstrated by ELISA and showed that CL-11 has preference for l-fucose and d-mannose. We finally show that CL-11 binds to intact bacteria, fungi, and viruses and that CL-11 decreases influenza A virus infectivity and forms complexes with DNA. On the basis of the significant concentration of CL-11 in circulation and CL-11’s interaction with various microorganisms and MASP-1 and/or MASP-3, it is conceivable that CL-11 plays a role in activation of the complement system and in the defense against invading microorganisms.

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Surfactant Protein D Augments Bacterial Association but Attenuates Major Histocompatibility Complex Class II Presentation of Bacterial Antigens

Abstract: Surfactant protein D (SP-D

Cited by 39 publications

References 51 publications

Surfactant protein D inhibits TNF-α production by macrophages and dendritic cells in mice

Surfactant protein D inhibits TNF-α production by macrophages and dendritic cells in mice

Loss of ABCG1 Results in Chronic Pulmonary Inflammation

Collectin 11 (CL-11, CL-K1) Is a MASP-1/3–Associated Plasma Collectin with Microbial-Binding Activity

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