The production mechanism and immunosuppression effect of pulmonary surfactant protein D via toll like receptor 4 signaling pathway in human corneal epithelial cells during Aspergillus fumigatus infection

Wu, Xian; Zhao, Guiqiu; Lin, Jing; Jiang, Nan; Li, Cui; Hu, Liting; Peng, Xudong; Xu, Qiang; Wang, Qian; Li, Hui; Zhang, Yan

doi:10.1016/j.intimp.2015.10.018

Cited by 16 publications

(14 citation statements)

References 30 publications

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“…As a kind of PRRs, SP-D has been found to contribute remarkably to surfactant homeostasis and innate host defense, and to exhibit specific binding to the extracellular domains of recombinant TLR4 through its CRD [22]. SP-D can inhibit TLR4 expression and inflammatory cytokines in human corneal epithelial cells through TLR4 signaling pathway during fungal infection [23]. SP-D can inhibit cell apoptosis and modulating NF-κB-mediated inflammation in sepsis-stimulated acute pancreatic injury [11].…”

Section: Discussionmentioning

confidence: 99%

Surfactant protein D attenuates nitric oxide-stimulated apoptosis in rat chondrocyte by suppressing p38 MAPK signaling

Zhou

Jiang

et al. 2018

Biochemical and Biophysical Research Communications

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Innate immune molecule surfactant protein D (SP-D), a member of the C-type lectin protein family, plays an indispensable role in host defense and the regulation of inflammation in the lung and other tissues. Osteoarthritis (OA) is a degenerative disease of cartilage, with inflammation that causes pathologic changes and tissue damage. However, it is unknown whether there exist SP-D expression and its potential role in the pathogenesis of OA. In this study, we examined SP-D expression and explored its biological function in a sodium nitroprusside (SNP)-stimulated rat chondrocytes and surgically-induced rat OA model. We found SP-D expression in both human and rat articular chondrocytes, with higher level in normal chondrocytes compared to in OA chondrocytes. Furthermore, In vivo study demonstrated that recombinant human SP-D (rhSP-D) ameliorated cartilage degeneration in surgically-induced rat OA model. In vitro cell culture study showed that rhSP-D markedly inhibited the expression of caspase-3 as an apoptosis biomarker, and decreased phosphorylation of p38 mitogen-activated protein kinase (MAPK), which resulted in maintaining normal nuclear morphology and increasing mitochondrial membrane potential in SNP-stimulated rat chondrocytes. Collectively, these findings indicate that SP-D expresses in articular chondrocytes and suppresses SNP-stimulated chondrocyte apoptosis and ameliorates cartilage degeneration via suppressing p38 MAPK activity.

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Section: Discussionmentioning

confidence: 99%

Surfactant protein D attenuates nitric oxide-stimulated apoptosis in rat chondrocyte by suppressing p38 MAPK signaling

Zhou

Jiang

et al. 2018

Biochemical and Biophysical Research Communications

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“…SP-A and SP-D are ligands for both TLR-2 and TLR-4. Both receptors are present on the cell surface and modulate intracellular signaling either via MyD88 or TRAF adaptors, ultimately increasing protein transcription of cytokines (Akira et al, 2000; Chuang et al, 2011; Wu et al, 2015). The TLR signaling pathway, in association with ligands and expression of cytokines, is depicted in Figure 5.…”

Section: Interaction Of Molecules With Collectins- Ligands and Recmentioning

confidence: 99%

Structure, genetics and function of the pulmonary associated surfactant proteins A and D: The extra-pulmonary role of these C type lectins

Vieira

Kung

Bhatti

2017

Annals of Anatomy - Anatomischer Anzeiger

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The collectins family encompasses several collagenous Ca2+-dependent defense lectins that are described as pathogen recognition molecules. They play an important role in both adaptive and innate immunity. Surfactant protein A and D are two of these proteins which were initially discovered in association with surfactant in the pulmonary system. The structure, immune and inflammatory functions, and genetic variations have been well described in relation to their roles, function and pathophysiology in the pulmonary system. Subsequently, these proteins have been discovered in a wide range of other organs and organ systems. The role of these proteins outside the pulmonary system is currently an active area of research. This review intends to provide a current overview of the genetics, structure and extra-pulmonary functions of the surfactant collectin proteins.

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“…Surfactant protein D (SP‐D), a component of lung surfactants, which reduces surface tension at the pulmonary air–liquid interface and enhances defense against pathogens as the first line of innate pulmonary immunity, has never been investigated with regard to the association between its genetic variants and the risk of RP. Previous study showed that serum levels of SP‐D in RP patients were elevated .…”

Section: Introductionmentioning

confidence: 99%

“…These RP susceptibility genes identified thus far were involved in the DNA repair pathways, [7][8][9] oxidative stress pathways, 10 cellular signaling pathways, 11 and inflammatory response to ionizing radiation. [12][13][14] Surfactant protein D (SP-D), a component of lung surfactants, which reduces surface tension at the pulmonary air-liquid interface [15][16][17] and enhances defense against pathogens as the first line of innate pulmonary immunity, [18][19][20][21] has never been investigated with regard to the association between its genetic variants and the risk of RP. Previous study showed that serum levels of SP-D in RP patients were elevated.…”

Section: Introductionmentioning

confidence: 99%

Genetic variants of SP‐D confer susceptibility to radiation pneumonitis in lung cancer patients undergoing thoracic radiation therapy

Jiang²,

et al. 2019

Cancer Medicine

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Background Surfactant protein D (SP‐D) is an innate immunity molecule in the alveoli. However, the associations between genetic variants of SP‐D and radiation pneumonitis (RP) have never been investigated. Methods The Linkage disequilibrium of SP‐D and tagSNPs were analyzed by using Haploview 4.1. Eight tagSNPs were genotyped among 396 lung cancer patients who received thoracic radiation therapy with follow–up time (median [P25, P75]: 11[6, 18]) using improved multiplex ligation detection reaction (iMLDR). The associations between clinical characteristics, tagSNP alleles, genotypes, haplotypes and onset time of grade ≥2 or ≥3 RP were evaluated by using univariate and multivariate Cox proportional hazard regression model. Results Three tagSNPs of SP‐D (rs1998374, rs911887 and rs2255326) were significantly associated with grade ≥2 RP in multivariate analysis with multiple testing (Q test). The rs199874 had a protective effect for grade ≥2 RP in the dominant model (Hazard ratio (HR), 0.575; 95% confidence interval (CI), 0.378‐0.875). The homozygous mutant genotype for rs911887 had risk effect for grade ≥2 RP (HR, 2.209; 95% CI, 1.251‐3.902). The A mutant allele of rs2255326 also showed an elevated risk for grade ≥2 RP (HR, 1.777; 95% CI, 1.283‐2.461) and this risk effect was still significant in the recessive genetic model (HR, 3.320; 95% CI, 1.659‐6.644) and dominant genetic model (HR, 1.773; 95% CI, 1.166‐2.696). Compared to the lung cancer patients bearing the most common haplotype C‐G‐T, the patients bearing the haplotype T‐A‐C (rs1998374‐rs2255326‐rs911887) showed a significant risk of both grade ≥2 RP (HR, 1.885; 95% CI, 1.284‐2.765) and grade ≥3 RP (HR, 2.256; 95% CI, 1.248‐4.080). Conclusions Genetic variants of SP‐D were associated with risk of RP development in lung cancer patients receiving thoracic radiotherapy.

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The production mechanism and immunosuppression effect of pulmonary surfactant protein D via toll like receptor 4 signaling pathway in human corneal epithelial cells during Aspergillus fumigatus infection

Cited by 16 publications

References 30 publications

Surfactant protein D attenuates nitric oxide-stimulated apoptosis in rat chondrocyte by suppressing p38 MAPK signaling

Surfactant protein D attenuates nitric oxide-stimulated apoptosis in rat chondrocyte by suppressing p38 MAPK signaling

Structure, genetics and function of the pulmonary associated surfactant proteins A and D: The extra-pulmonary role of these C type lectins

Genetic variants of SP‐D confer susceptibility to radiation pneumonitis in lung cancer patients undergoing thoracic radiation therapy

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