scholarly journals Innate Immune Molecule Surfactant Protein D Attenuates Sepsis-induced Acute Pancreatic Injury through Modulating Apoptosis and NF-κB-mediated Inflammation

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Zhiyong Liu ◽  
Qiao Shi ◽  
Jiao Liu ◽  
Osama Abdel-Razek ◽  
Yongan Xu ◽  
...  
Keyword(s):  
Pancreatic Injury ◽  
Surfactant Protein ◽  
Innate Immune ◽  
Surfactant Protein D ◽  
Immune Molecule

scholarly journals Expression of Surfactant Protein D in the Human Gastric Mucosa and during Helicobacter pylori Infection

2002 ◽  
Vol 70 (3) ◽  
pp. 1481-1487 ◽  
Author(s):  
Emma Murray ◽  
Wafa Khamri ◽  
Marjorie M. Walker ◽  
Paul Eggleton ◽  
Anthony P. Moran ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Surfactant Protein ◽  
Normal Mucosa ◽  
Innate Immune ◽  
Surfactant Protein D ◽  
Human Gastric Mucosa ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Immune Molecule ◽  
H Pylori

ABSTRACT Helicobacter pylori establishes persistent infection of gastric mucosa with diverse clinical outcomes. The innate immune molecule surfactant protein D (SP-D) binds selectively to microorganisms, inducing aggregation and phagocytosis. In this study, we demonstrated the expression of SP-D in gastric mucosa by reverse transcription-PCR and immuohistochemical analysis. SP-D is present at the luminal surface and within the gastric pits, with maximal expression at the surface. Levels of expression are significantly increased in H. pylori-associated gastritis compared to those in the normal mucosa. Immunofluorescence microscopy was used to demonstrate binding and agglutination of H. pylori by SP-D in a lectin-specific manner. These activities resulted in a 50% reduction in the motility of H. pylori, as judged on the basis of curvilinear velocity measured by using a Hobson BacTracker. Lipopolysaccharides extracted from three H. pylori strains were shown to bind SP-D in a concentration-dependent manner, and there was marked variation in the avidity of binding among the strains. SP-D may therefore play a significant role in the innate immune response to H. pylori infection.

scholarly journals Sex and SP-A2 Dependent NAD(H) Redox Alterations in Mouse Alveolar Macrophages in Response to Ozone Exposure: Potential Implications for COVID-19

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 915
Author(s):  
He N. Xu ◽  
Zhenwu Lin ◽  
Chintan K. Gandhi ◽  
Shaili Amatya ◽  
Yunhua Wang ◽  
...  
Keyword(s):  
Alveolar Macrophages ◽  
Imaging Technique ◽  
Redox Balance ◽  
Surfactant Protein ◽  
Redox Status ◽  
Innate Immune ◽  
Ozone Exposure ◽  
Dependent Manner ◽  
Immune Molecule ◽  
Air Control

Co-enzyme nicotinamide adenine dinucleotide (NAD(H)) redox plays a key role in macrophage function. Surfactant protein (SP-) A modulates the functions of alveolar macrophages (AM) and ozone (O3) exposure in the presence or absence of SP-A and reduces mouse survival in a sex-dependent manner. It is unclear whether and how NAD(H) redox status plays a role in the innate immune response in a sex-dependent manner. We investigated the NAD(H) redox status of AM from SP-A2 and SP-A knockout (KO) mice in response to O3 or filtered air (control) exposure using optical redox imaging technique. We found: (i) In SP-A2 mice, the redox alteration of AM in response to O3 showed sex-dependence with AM from males being significantly more oxidized and having a higher level of mitochondrial reactive oxygen species than females; (ii) AM from KO mice were more oxidized after O3 exposure and showed no sex differences; (iii) AM from female KO mice were more oxidized than female SP-A2 mice; and (iv) Two distinct subpopulations characterized by size and redox status were observed in a mouse AM sample. In conclusions, the NAD(H) redox balance in AM responds to O3 in a sex-dependent manner and the innate immune molecule, SP-A2, contributes to this observed sex-specific redox response.

2P-0395 Surfactant protein D of the innate immune defense is negatively associated with obesity

2003 ◽  
Vol 4 (2) ◽  
pp. 125
Author(s):  
U. Holmskov ◽  
G. Lyster ◽  
J. Hjelmborg ◽  
R. Leth-Larsen ◽  
V. Moeller ◽  
...  
Keyword(s):  
Surfactant Protein ◽  
Immune Defense ◽  
Innate Immune ◽  
Surfactant Protein D ◽  
Negatively Associated ◽  
Innate Immune Defense

Circulating Surfactant Protein D Is Decreased in Systemic Lupus Erythematosus

2009 ◽  
Vol 36 (11) ◽  
pp. 2449-2453 ◽  
Author(s):  
SILJE VERMEDAL HOEGH ◽  
ANNE VOSS ◽  
GRITH LYKKE SORENSEN ◽  
ANETTE HØJ ◽  
CHRISTIAN BENDIXEN ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Surfactant Protein ◽  
Innate Immune ◽  
Surfactant Protein D ◽  
Systemic Lupus ◽  
Reactive Protein ◽  
Structural And Functional Properties ◽  
Disease Indicators ◽  
And Function

Objective.Deficiencies of innate immune molecules like mannan binding lectin (MBL) have been implicated in the pathogenesis of systemic lupus erythematosus (SLE). Surfactant protein D (SP-D) and MBL belong to the same family of innate immune molecules — the collectins, which share important structural and functional properties. We aimed to compare concentrations of serum SP-D in patients with SLE and in healthy controls, and to investigate if SP-D is associated with selected disease indicators. We investigated the possible association of the Met11Thr polymorphism with disease, since this polymorphism is an important determinant for serum level, oligomerization pattern, and function of SP-D.Methods.Serum SP-D was measured using a 5-layer ELISA in 70 SLE patients and 1476 healthy subjects. DNA was genotyped for the Met11Thr variant.Results.Median SP-D level in serum was 911 ng/ml (95% CI 776–1118) in patients and 1068 ng/ml (95% CI 901–1246) in controls (p = 0.0004). Circulating SP-D did not differ significantly in patients with high, intermediate, or low SLE disease activity. Similarly, SP-D did not correlate with C-reactive protein, erythrocyte sedimentation rate, and anti-dsDNA seropositivity. Genetic analysis did not support an association of the Met11Thr genotype with SLE.Conclusion.These findings suggest that low SP-D, unrelated to conventional disease indicators, represents an aspect of SLE etiopathogenesis.

scholarly journals Innate Immune Collectin Surfactant Protein D Enhances the Clearance of DNA by Macrophages and Minimizes Anti-DNA Antibody Generation

2005 ◽  
Vol 174 (11) ◽  
pp. 7352-7358 ◽  
Author(s):  
Nades Palaniyar ◽  
Howard Clark ◽  
Jeya Nadesalingam ◽  
Michael J. Shih ◽  
Samuel Hawgood ◽  
...  
Keyword(s):  
Surfactant Protein ◽  
Innate Immune ◽  
Surfactant Protein D

Antibody equivalent molecules of the innate immune system: parallels between innate and adaptive immune proteins

2010 ◽  
Vol 16 (3) ◽  
pp. 131-137 ◽  
Author(s):  
Nades Palaniyar
Keyword(s):  
Pattern Recognition ◽  
Immune System ◽  
Innate Immune System ◽  
Adaptive Immune System ◽  
Surfactant Protein ◽  
Innate Immune ◽  
Future Research ◽  
Surfactant Protein D ◽  
Adaptive Immune ◽  
Carbohydrate Arrays

Soluble pattern-recognition innate immune proteins functionally resemble the antibodies of the adaptive immune system. Two major families of such proteins are ficolins and collectins or collagenous lectins (e.g. mannose-binding lectin [MBL], surfactant proteins [SP-A and SP-D] and conglutinin). In general, subunits of ficolins and collectins recognize the carbohydrate arrays of their targets via globular trimeric carbohydrate-recognition domains (CRDs) whereas IgG, IgM and other antibody isotypes recognize proteins via dimeric antigen-binding domains (Fab). Considering the structure and functions of these proteins, ficolins and MBL are analogous to molecules with the complement activating functions of C1q and the target recognition ability of IgG. Although the structure of SP-A is similar to MBL, it does not activate the complement system. Surfactant protein-D and conglutinin could be considered as the collagenous non-complement activating giant IgMs of the innate immune system. Proteins such as peptidoglycan-recognition proteins, pentraxins and agglutinin gp-340/DMBT1 are also pattern-recognition proteins. These proteins may be considered as different isotypes of antibody-like molecules. Proteins such as defensins, cathelicidins and lactoferrins directly or indirectly alter microbes or microbial growth. These proteins may not be considered as antibodies of the innate immune system. Hence, ficolins and collectins could be considered as specialized ‘antibodies of the innate immune system’ instead of ‘ante-antibody’ innate immune molecules. The discovery, structure, functions and future research directions of many of these soluble proteins and receptors such as Toll-like and NOD-like receptors are discussed in this special issue of Innate Immunity.

scholarly journals Surfactant protein D and bronchopulmonary dysplasia: a new way to approach an old problem

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Raquel Arroyo ◽  
Paul S. Kingma
Keyword(s):  
Immune Response ◽  
Preterm Infants ◽  
Bronchopulmonary Dysplasia ◽  
Lung Tissue ◽  
Lung Inflammation ◽  
Tissue Injury ◽  
Surfactant Protein ◽  
Immune Defense ◽  
Innate Immune ◽  
Surfactant Protein D

AbstractSurfactant protein D (SP-D) is a collectin protein synthesized by alveolar type II cells in the lungs. SP-D participates in the innate immune defense of the lungs by helping to clear infectious pathogens and modulating the immune response. SP-D has shown an anti-inflammatory role by down-regulating the release of pro-inflammatory mediators in different signaling pathways such as the TLR4, decreasing the recruitment of inflammatory cells to the lung, and modulating the oxidative metabolism in the lungs. Recombinant human SP-D (rhSP-D) has been successfully produced mimicking the structure and functions of native SP-D. Several in vitro and in vivo experiments using different animal models have shown that treatment with rhSP-D reduces the lung inflammation originated by different insults, and that rhSP-D could be a potential treatment for bronchopulmonary dysplasia (BPD), a rare disease for which there is no effective therapy up to date. BPD is a complex disease in preterm infants whose incidence increases with decreasing gestational age at birth. Lung inflammation, which is caused by different prenatal and postnatal factors like infections, lung hyperoxia and mechanical ventilation, among others, is the key player in BPD. Exacerbated inflammation causes lung tissue injury that results in a deficient gas exchange in the lungs of preterm infants and frequently leads to long-term chronic lung dysfunction during childhood and adulthood. In addition, low SP-D levels and activity in the first days of life in preterm infants have been correlated with a worse pulmonary outcome in BPD. Thus, SP-D mediated functions in the innate immune response could be critical aspects of the pathogenesis in BPD and SP-D could inhibit lung tissue injury in this preterm population. Therefore, administration of rhSP-D has been proposed as promising therapy that could prevent BPD.

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