Lipoteichoic acid induces surfactant protein-A biosynthesis in human alveolar type II epithelial cells through activating the MEK1/2-ERK1/2-NF-κB pathway

Liu, Feng Lin; Chuang, Chi Yuan; Tai, Yu‐Ting; Tang, Hsiu Lien; Chen, Tyng-Guey; Chen, Ta-Liang; Chen, Ruei Ming

doi:10.1186/1465-9921-13-88

Cited by 12 publications

(11 citation statements)

References 34 publications

(57 reference statements)

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“…We have demonstrated that rhHsp70, LPS or LTA alone and in combinations did not influence metabolic activity of NCI‐H292 cells. In agreement with our results, it was reported that eHsp70, LPS and LTA do not exert toxic effects on various cell types . For instance, Hsp70 treatment did not alter cell viability of A549 human lung cancer cells, HL‐60 promyelocytic leukaemia cells and neutrophils .…”

Section: Discussionsupporting

confidence: 93%

“…In agreement with our results, it was reported that eHsp70, LPS and LTA do not exert toxic effects on various cell types. [22][23][24][25] For instance, Hsp70 treatment did not alter cell viability of A549 human lung cancer cells, 14 HL-60 promyelocytic leukaemia cells 22 and neutrophils. 25 In addition, treatment of human bronchial epithelial cell line BEAS-2B with LPS did not affect cell viability 24 as well as treatment of human lung carcinoma type II epithelial cells A549 with LTA.…”

Section: Discussionmentioning

confidence: 97%

“…25 In addition, treatment of human bronchial epithelial cell line BEAS-2B with LPS did not affect cell viability 24 as well as treatment of human lung carcinoma type II epithelial cells A549 with LTA. 23 Apoptosis or programmed cell death is a vital process for normal cell turnover or proper development and function of the immune system, and inappropriate apoptosis is associated with different disorders and diseases. 26 Caspases are the central players of the apoptotic machinery.…”

Section: Discussionmentioning

confidence: 99%

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Pro‐inflammatory effects of extracellular Hsp70 on NCI‐H292 human bronchial epithelial cell line

Hulina

Rajković

Jelić³

et al. 2019

Int J Experimental Path

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Summary Extracellular Hsp70 (eHsp70) exerts its biological actions via Toll‐like receptors 2 and 4, and is increased in sera of chronic obstructive pulmonary disease (COPD) patients. The aim of this study was to explore the pro‐inflammatory effects and cytotoxicity of eHsp70 alone and in combination with bacterial components lipoteichoic acid (LTA) and lipopolysaccharide (LPS) on NCI‐H292 airway epithelial cells. NCI‐H292 cells were treated with recombinant human Hsp70 protein (rhHsp70), LPS, LTA and their combinations for 4, 12, 24 and 48 hours. IL‐6, IL‐8 and TNF‐α levels were measured by an ELISA method. Cell viability was determined by the MTS method, and caspase‐3/7, caspase‐8 and caspase‐9 assays. rhHsp70 induced secretion of IL‐6 and IL‐8 in a concentration‐ and time‐dependent manner, with the highest secretion at 24 hours. rhHsp70 combined with LTA had antagonistic and with LPS synergistic effect on IL‐6 secretion, while the interactions between rhHsp70 and LPS or LTA on IL‐8 were synergistic. TNF‐α was not detected in the applied conditions. rhHsp70, LPS or LTA did not affect cell viability, and rhHsp70 even suppressed caspase‐3/7 activities. We suggest that pro‐inflammatory effects of eHsp70, together with other damaging molecules and/or COPD risk factors, might contribute to the aggravation of chronic inflammation in human bronchial epithelium.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Pro‐inflammatory effects of extracellular Hsp70 on NCI‐H292 human bronchial epithelial cell line

Hulina

Rajković

Jelić³

et al. 2019

Int J Experimental Path

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“…Analysis of various signaling pathways in the mutant mice points to a possible mechanism for the surfactant deficiency and consequently, offers other points of potential therapeutic intervention. Synthesis of surfactant proteins has been shown to be driven by a MEK1/2 –ERK1/2 pathway [ 46 , 47 ] and ERK downregulation attenuates expression of both surfactant proteins [ 15 , 48 ] and MMP9 [ 49 ]. The ERK pathway was downregulated in our mutant mice ( Fig 1C ) and correlates with the observed changes in pulmonary surfactant production.…”

Section: Discussionmentioning

confidence: 99%

Sequestration of Vascular Endothelial Growth Factor (VEGF) Induces Late Restrictive Lung Disease

Wieck¹,

Spurrier²,

Levin³

et al. 2016

PLoS ONE

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RationaleNeonatal respiratory distress syndrome is a restrictive lung disease characterized by surfactant deficiency. Decreased vascular endothelial growth factor (VEGF), which demonstrates important roles in angiogenesis and vasculogenesis, has been implicated in the pathogenesis of restrictive lung diseases. Current animal models investigating VEGF in the etiology and outcomes of RDS require premature delivery, hypoxia, anatomically or temporally limited inhibition, or other supplemental interventions. Consequently, little is known about the isolated effects of chronic VEGF inhibition, started at birth, on subsequent developing lung structure and function.ObjectivesTo determine whether inducible, mesenchyme-specific VEGF inhibition in the neonatal mouse lung results in long-term modulation of AECII and whole lung function.MethodsTriple transgenic mice expressing the soluble VEGF receptor sFlt-1 specifically in the mesenchyme (Dermo-1/rtTA/sFlt-1) were generated and compared to littermate controls at 3 months to determine the impact of neonatal downregulation of mesenchymal VEGF expression on lung structure, cell composition and function. Reduced tissue VEGF bioavailability has previously been demonstrated with this model.Measurements and Main ResultsTriple transgenic mice demonstrated restrictive lung pathology. No differences in gross vascular development or protein levels of vascular endothelial markers was noted, but there was a significant decrease in perivascular smooth muscle and type I collagen. Mutants had decreased expression levels of surfactant protein C and hypoxia inducible factor 1-alpha without a difference in number of type II pneumocytes.ConclusionsThese data show that mesenchyme-specific inhibition of VEGF in neonatal mice results in late restrictive disease, making this transgenic mouse a novel model for future investigations on the consequences of neonatal RDS and potential interventions.

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“…aureus infection. A previous study reported that exposure to LTA increased Surfactant protein A (SP-A) expression in human alveolar type II epithelial cells through sequentially activating the MEK1-ERK1/2-NF-κB-dependent pathway [ 59 ]. S .…”

Section: Discussionmentioning

confidence: 99%

Protective Role of Surfactant Protein D in Ocular Staphylococcus aureus Infection

et al. 2015

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Staphylococcus aureus is one of the most common pathogens causing keratitis. Surfactant protein D (SP-D) plays a critical role in host defense and innate immunity. In order to investigate the role of SP-D in ocular S. aureus infection, the eyes of wild-type (WT) and SP-D knockout (SP-D KO) C57BL/6 mice were infected with S. aureus (107 CFU/eye) in the presence and absence of cysteine protease inhibitor(E64).Bacterial counts in the ocular surface were examined 3, 6, 12, 24 hrs after infection. Bacterial phagocytosis by neutrophils and bacterial invasion in ocular epithelial cells were evaluated quantitatively. S. aureus-induced ocular injury was determined with corneal fluorescein staining. The results demonstrated that SP-D is expressed in ocular surface epithelium and the lacrimal gland; WT mice had increased clearance of S. aureus from the ocular surface (p<0.05) and reduced ocular injury compared with SP-D KO mice. The protective effects of SP-D include increased bacterial phagocytosis by neutrophils (p<0.05) and decreased bacterial invasion into epithelial cells (p<0.05) in WT mice compared to in SP-D KO mice. In the presence of inhibitor (E64), WT mice showed enhanced bacterial clearance (p<0.05) and reduced ocular injury compared to absent E64 while SP-D KO mice did not. Collectively, we concluded that SP-D protects the ocular surface from S. aureus infection but cysteine protease impairs SP-D function in this murine model, and that cysteine protease inhibitor may be a potential therapeutic agent in S. aureus keratitis.

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Lipoteichoic acid induces surfactant protein-A biosynthesis in human alveolar type II epithelial cells through activating the MEK1/2-ERK1/2-NF-κB pathway

Cited by 12 publications

References 34 publications

Pro‐inflammatory effects of extracellular Hsp70 on NCI‐H292 human bronchial epithelial cell line

Pro‐inflammatory effects of extracellular Hsp70 on NCI‐H292 human bronchial epithelial cell line

Sequestration of Vascular Endothelial Growth Factor (VEGF) Induces Late Restrictive Lung Disease

Protective Role of Surfactant Protein D in Ocular Staphylococcus aureus Infection

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