Lactate dehydrogenase and the severity of adenoviral pneumonia in children: A meta-analysis

Zou, Min; Zhai, Yang; Mei, Xiaoping; Wei, Xing

doi:10.3389/fped.2022.1059728

Cited by 4 publications

(3 citation statements)

References 49 publications

(45 reference statements)

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“…LDH is a cytoplasmic enzyme that is present in most cells. LDH activity changes when the cell membrane is damaged; therefore, the amount of LDH released can reflect the degree of cell damage [ 37 , 38 ]. Cytotoxicity assay results indicated that lnc001776 overexpression significantly increased LDH levels ( Figure 3 E).…”

Section: Resultsmentioning

confidence: 99%

lnc001776 Affects CPB2 Toxin-Induced Excessive Injury of Porcine Intestinal Epithelial Cells via Activating JNK/NF-kB Pathway through ssc-let-7i-5p/IL-6 Axis

Xie

Yan

Yang

et al. 2023

Cells

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Piglet diarrhea caused by Clostridium perfringens (C. perfringens) type C (CpC) seriously endangers the development of the pig production industry. C. perfringens beta2 (CPB2) toxin is a virulent toxin produced by CpC. Long non-coding RNAs (lncRNAs) are key regulators in the immune inflammatory response to bacterial infection. Nevertheless, the functional mechanism of lncRNAs in bacterial piglet diarrhea is unclear. Herein, a novel lncRNA lnc001776 expression was confirmed to be substantially elevated in the ileum tissue of CpC-infected diarrhea piglets and in CPB2 toxin-treated porcine small intestinal epithelial cells (IPEC-J2). lnc001776 knockdown restrained CPB2 toxin-induced apoptosis, inflammatory injury, barrier dysfunction and activation of JNK/NF-kB pathway in IPEC-J2 cells. Additionally, ssc-let-7i-5p was identified as sponge for lnc001776. Overexpression of ssc-let-7i-5p repressed CPB2-induced injury in IPEC-J2 cells. Interleukin 6 (IL-6), a target gene of ssc-let-7i-5p, was enhanced in CPB2 toxin-treated IPEC-J2 cells. Rescue experiments demonstrated that a ssc-let-7i-5p mimic reversed the effect of lnc001776 overexpression on CPB2 toxin-induced IPEC-J2 cell injury and JNK/NF-kB pathway, whereas IL-6 overexpression partially restored the impact of lnc001776. Overall, lnc001776 overexpression exacerbated CPB2 toxin-induced IPEC-J2 cell damage by sponging ssc-let-7i-5p to regulate IL-6 to activate JNK/NF-kB pathway, indicating that lnc001776 could be a key target for piglet resistance to CpC-induced diarrhea.

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Section: Resultsmentioning

confidence: 99%

lnc001776 Affects CPB2 Toxin-Induced Excessive Injury of Porcine Intestinal Epithelial Cells via Activating JNK/NF-kB Pathway through ssc-let-7i-5p/IL-6 Axis

Xie

Yan

Yang

et al. 2023

Cells

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“…Some studies have found that the LDH level is an independent risk factor for the development of BO after MP pneumonia ( 17 – 19 ), but there are no reports in ADV-PIBO. Although the study of Zou et al also suggests that pretreatment LDH was significantly higher in children with severe ADV pneumonia who developed PIBO than in those who did not, it was not an independent risk factor ( 20 ). The increase in LDH levels suggested severe lung injury, which may induce excessive abnormal repair, may play a role in the pathogenesis of BO.…”

Section: Discussionmentioning

confidence: 99%

Risk factors for the development of bronchiolitis obliterans in children after suffering from adenovirus pneumonia

Yuan,

Wei,

Chen

et al. 2024

Front. Pediatr.

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IntroductionBronchiolitis obliterans (BO) is an irreversible chronic obstructive lung disease in small airways. The aim of this study was to identify the relevant risk factors for the development of BO in children after suffering from adenovirus (ADV) pneumonia.MethodsAn observational cohort study that included 112 children suffering from ADV pneumonia in our institution from March 2019 to March 2020 was performed. We divided the children into a BO group and a non-BO group based on whether they did develop BO or not. Univariate analysis and multivariate logistic regression analysis were applied to identify risk factors for the development of BO. The prediction probability model was evaluated by receiver operating characteristic (ROC) curve analysis.ResultsTwenty-eight children (25%) did develop BO after suffering from ADV pneumonia, while 84 children did not. Respiratory support (OR 6.772, 95% CI 2.060–22.260, P = 0.002), extended length of wheezing days (OR 1.112, 95% CI 1.040–1.189, P = 0.002) and higher lactic dehydrogenase (LDH) levels (OR 1.002, 95% CI 1.000–1.003, P = 0.012) were independently associated with the development of BO. The predictive value of this prediction probability model was validated by the ROC curve, with an area under the curve of 0.870 (95% CI 0.801–0.939, P < 0.001), a standard error of 0.035, a maximum Youden's index of 0.608, a sensitivity of 0.929, and a specificity of 0.679.ConclusionsAfter suffering an ADV pneumonia, children who have needed respiratory support, had a longer length of wheezing days or had higher LDH levels are more likely to develop BO.

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“…LDH is present in the cytoplasm of all tissues and cells. In damaged tissues or cells, LDH levels increase, which is a crucial indicator of the inflammatory response [36,37]. Hong et al [38] revealed that lncRNA NONHSAT217600.1 knockdown attenuated neodymium oxide (Nd 2 O 3 )-induced LDH release and reduced inflammatory damage in 16HBE human bronchial epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

Identification of a Novel lncRNA LNC_001186 and Its Effects on CPB2 Toxin-Induced Apoptosis of IPEC-J2 Cells

Xie

Yang

Yan

et al. 2023

Genes

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The Clostridium perfringens (C. perfringen) beta2 (CPB2) toxin produced by C. perfringens type C (CpC) can cause necrotizing enteritis in piglets. Immune system activation in response to inflammation and pathogen infection is aided by long non-coding RNAs (lncRNAs). In our previous work, we revealed the differential expression of the novel lncRNA LNC_001186 in CpC-infected ileum versus healthy piglets. This implied that LNC_001186 may be a regulatory factor essential for CpC infection in piglets. Herein, we analyzed the coding ability, chromosomal location and subcellular localization of LNC_001186 and explored its regulatory role in CPB2 toxin-induced apoptosis of porcine small intestinal epithelial (IPEC-J2) cells. RT-qPCR results indicated that LNC_001186 expression was highly enriched in the intestines of healthy piglets and significantly increased in CpC-infected piglets’ ileum tissue and CPB2 toxin-treated IPEC-J2 cells. The total sequence length of LNC_001186 was 1323 bp through RACE assay. CPC and CPAT, two online databases, both confirmed that LNC_001186 had a low coding ability. It was present on pig chromosome 3. Cytoplasmic and nuclear RNA isolation and RNA-FISH assays showed that LNC_001186 was present in the nucleus and cytoplasm of IPEC-J2 cells. Furthermore, six target genes of LNC_001186 were predicted using cis and trans approaches. Meanwhile, we constructed ceRNA regulatory networks with LNC_001186 as the center. Finally, LNC_001186 overexpression inhibited IPEC-J2 cells’ apoptosis caused by CPB2 toxin and promoted cell viability. In summary, we determined the role of LNC_001186 in IPEC-J2 cells’ apoptosis caused by CPB2 toxin, which assisted us in exploring the molecular mechanism of LNC_001186 in CpC-induced diarrhea in piglets.

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Lactate dehydrogenase and the severity of adenoviral pneumonia in children: A meta-analysis

Cited by 4 publications

References 49 publications

lnc001776 Affects CPB2 Toxin-Induced Excessive Injury of Porcine Intestinal Epithelial Cells via Activating JNK/NF-kB Pathway through ssc-let-7i-5p/IL-6 Axis

lnc001776 Affects CPB2 Toxin-Induced Excessive Injury of Porcine Intestinal Epithelial Cells via Activating JNK/NF-kB Pathway through ssc-let-7i-5p/IL-6 Axis

Risk factors for the development of bronchiolitis obliterans in children after suffering from adenovirus pneumonia

Identification of a Novel lncRNA LNC_001186 and Its Effects on CPB2 Toxin-Induced Apoptosis of IPEC-J2 Cells

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