Ting Li

Bio: Ting Li is an academic researcher from Huazhong Agricultural University. The author has contributed to research in topics: Mastitis & Gene. The author has an hindex of 2, co-authored 4 publications receiving 12 citations.

A retrospective study of clinical and laboratory features and treatment on cats highly suspected of feline infectious peritonitis in Wuhan, China.

Abstract: Feline infectious peritonitis (FIP) is a systemic, potentially fatal viral disease. The objectives of this study were to review clinical and laboratory features and treatment of cats highly suspected of FIP in Wuhan, China. The clinical records of 127 cats highly suspected of FIP were reviewed for history, clinical signs, physical findings, and diagnostic test results. Sex, neutering status, breed, age, and month of onset of disease were compared with the characteristics of the clinic population. Age and neutering status were significantly correlated with FIP-suspicion. Sex, breed and onset month were not associated with FIP. There were many more FIP-suspected cases in cats in young cats or male intact cats. Effusion was observed in 85.8% of the FIP-suspected cats. Increased serum amyloid A (SAA) and lymphopenia were common laboratory abnormalities in the FIP cases. Furthermore, 91.7% of the cats highly suspected of FIP had an albumin/globulin (A/G) ratio < 0.6, while 85.3% had an A/G ratio < 0.5. The mortality rate for FIP-suspected cats was 67%, and six submitted cases were confirmed by FIP-specific immunohistochemistry. Of the 30 cats treated with GS-441524 and/or GC376, 29 were clinically cured. The study highlights the diverse range of clinical manifestations by clinicians in diagnosing this potentially fatal disease. A/G ratio and SAA were of higher diagnostic value. GS-441524 and GC376 were efficient for the treatment of FIP-suspected cats.

Transcriptome Profiling of m6A mRNA Modification in Bovine Mammary Epithelial Cells Treated with Escherichia coli.

Abstract: Mastitis is a common disease in dairy cows that is mostly caused by E. coli, and it brings massive losses to the dairy industry. N6-Methyladenosine (m6A), a methylation at the N6 position of RNA adenine, is a type of modification strongly associated with many diseases. However, the role of m6A in mastitis has not been investigated. In this study, we used MeRIP-seq to sequence the RNA of bovine mammary epithelial cells treated with inactivated E. coli for 24 h. In this in vitro infection model, there were 16,691 m6A peaks within 7066 mRNA transcripts in the Con group and 10,029 peaks within 4891 transcripts in the E. coli group. Compared with the Con group, 474 mRNAs were hypermethylated and 2101 mRNAs were hypomethylated in the E. coli group. Biological function analyses revealed differential m6A-modified genes mainly enriched in the MAPK, NF-κB, and TGF-β signaling pathways. In order to explore the relationship between m6A and mRNA expression, combined MeRIP-seq and mRNA-seq analyses revealed 212 genes with concomitant changes in the mRNA expression and m6A modification. This study is the first to present a map of RNA m6A modification in mastitis treated with E. coli, providing a basis for future research.

Genome-Wide Analysis of LncRNA in Bovine Mammary Epithelial Cell Injuries Induced by Escherichia Coli and Staphylococcus Aureus

Abstract: Escherichia coli and Staphylococcus aureus are two common pathogenic microorganisms that cause mastitis in dairy cows. They can cause clinical mastitis and subclinical mastitis. In recent studies, lncRNAs have been found to play an important role in the immune responses triggered by microbial inducers. However, the actions of lncRNAs in bovine mastitis remain unclear. The purpose of this study was to investigate the effects of bovine mammary epithelial cell injuries induced by treatment with E. coli and S. aureus, and to explore the lncRNA profile on cell injuries. The lncRNA transcriptome analysis showed a total of 2597 lncRNAs. There were 2234 lncRNAs differentially expressed in the E. coli group and 2334 in the S. aureus group. Moreover, we found that the E. coli and S. aureus groups of maternal genes targeted signaling pathways with similar functions according to KEGG and GO analyses. Two lncRNA-miRNA-mRNA interaction networks were constructed in order to predict the potential molecular mechanisms of regulation in the cell injuries. We believe that this is the first report demonstrating the dysregulation of lncRNAs in cells upon E. coli and S. aureus infections, suggesting that they have the potential to become important diagnostic markers and to provide novel insights into controlling and preventing mastitis.

Gambogic acid ameliorates high glucose- and palmitic acid-induced inflammatory response in ARPE-19 cells via activating Nrf2 signaling pathway: ex vivo.

Abstract: Diabetic retinopathy (DR) is a serious microvascular complication of diabetes. Gambogic acid has been reported to have anti-inflammatory effect. However, the effect of GA on inflammatory response of ARPE-19 cells remains unclear. In our study, ARPE-19 cells were stimulated by palmitic acid (PA) induction in the presence of 30 mM glucose and then treated with 0.5, 1, 2, 5, 10, or 20 μM GA. CCK-8 assay showed that cell viability was increased by GA treatment at doses of 0.5, 1, and 2 μM instead of higher doses. ELISA analysis found that GA dose-dependently reduced the production of pro-inflammatory mediators TNF-α and IL-1β. Western blot indicated that GA downregulated the expression of NLRP3 inflammasome components including TXNIP, NLRP3, ASC, cleaved-caspase-1, and cleaved-IL-1β in a dose-dependent manner. In addition, Western blot and immunofluorescence analysis suggested that GA effectively increased the protein level of nuclear factor E2-related factor-2 (Nrf2). RT-qPCR showed that GA significantly increased the mRNA levels of Heme oxygenase-1 (HO-1) and NADPH:quinone oxidoreductase1 (NQO1). Furthermore, Nrf2 siRNA transfection confirmed the above effects of GA. In total, subtoxic doses of GA significantly flattened the inflammatory response induced by HG and PA in ARPE-19 cells via modulating the Nrf2 signaling pathway.

Curing Cats with Feline Infectious Peritonitis with an Oral Multi-Component Drug Containing GS-441524.

Abstract: Feline infectious peritonitis (FIP) caused by feline coronavirus (FCoV) is a common dis-ease in cats, fatal if untreated, and no effective treatment is currently legally available. The aim of this study was to evaluate efficacy and toxicity of the multi-component drug Xraphconn® in vitro and as oral treatment in cats with spontaneous FIP by examining survival rate, development of clinical and laboratory parameters, viral loads, anti-FCoV antibodies, and adverse effects. Mass spectrometry and nuclear magnetic resonance identified GS-441524 as an active component of Xraphconn®. Eighteen cats with FIP were prospectively followed up while being treated orally for 84 days. Values of key parameters on each examination day were compared to values before treatment initiation using linear mixed-effect models. Xraphconn® displayed high virucidal activity in cell culture. All cats recovered with dramatic improvement of clinical and laboratory parameters and massive reduction in viral loads within the first few days of treatment without serious adverse effects. Oral treatment with Xraphconn® containing GS-441524 was highly effective for FIP without causing serious adverse effects. This drug is an excellent option for the oral treatment of FIP and should be trialed as potential effective treatment option for other severe coronavirus-associated diseases across species.

Outbreak of feline infectious peritonitis (FIP) in shelter-housed cats: molecular analysis of the feline coronavirus S1/S2 cleavage site consistent with a ‘circulating virulent–avirulent theory’ of FIP pathogenesis

Abstract: Case series summary This case series describes three shelter-housed cats concurrently diagnosed with feline infectious peritonitis (FIP). The cats were from a cohort of seven surrendered from the site of a house fire. The three cats presented with mild upper respiratory signs. Within 10 days they clinically declined: progressive signs included pyrexia, icterus, lethargy, anorexia and cavitary effusions. Necropsy followed by histopathology and immunohistochemistry confirmed a diagnosis of FIP in all three. Molecular analysis of the causative feline coronavirus (FCoV) revealed varied amino acid alterations in the spike gene both between cats and between sample types in individual cats. A fourth cat from the cohort remained healthy in the shelter but succumbed to FIP 6 weeks post-adoption. Relevance and novel information This case series places FCoV genetic sequences in the context of clinical signs in a small shelter outbreak. Each of the three cats concurrently developed a slightly different clinical presentation. PCR amplification and genetic sequencing revealed that two cats shared an S1/S2 cleavage site mutation (R790S) previously described to be associated with the development of FIP; one of the cats had an additional S1/S2 cleavage site mutation (R793S). The third cat had a single, identical S1/S2 point mutation (R790G) unique from the other two cats; the R790G mutation has not been previously reported. This case series provides interesting data on point mutations associated with the development of FIP and provides support for a ‘circulating virulent–avirulent theory’ of FIP pathogenesis in a small shelter outbreak.

Vitamin D3 mitigates lipopolysaccharide-induced oxidative stress, tight junction damage and intestinal inflammatory response in yellow catfish, Pelteobagrus fulvidraco.

Abstract: The present study explored the possible mitigative effects of vitamin D3 (VD3) on lipopolysaccharide (LPS)-induced intestinal oxidative stress, inflammatory response and tight junction damage in yellow catfish, Pelteobagrus fulvidraco. Herein, four experimental groups were established by injecting yellow catfish with NaCl, LPS, VD3 or LPS plus VD3. The results showed that LPS induced oxidative stress and that exogenous VD3 mitigated the adverse effects of LPS. Additionally, LPS suppressed the activity of antioxidant enzymes (Cat, Sod and Gr) and upregulated the mRNA expression of proinflammatory cytokines (Tnf-α, Il-1β, Il-8). Furthermore, the mRNA expression of "fencing" tight junctions (Claudin-1, Claudin-5, Occludin, Zo-1) was downregulated, while that of "pore-forming" tight junctions (Claudin-2, Claudin-12) was upregulated, however no effect on apoptosis genes was observed (p53, Bax, Caspase-3 and Caspase-9). These LPS-induced effects were significantly reversed by pretreatment with VD3. Taken together, this study suggests that exogenous VD3 substantially alleviates LPS-induced intestinal inflammation by upregulating antioxidant activity, suppressing inflammation and promoting fencing tight junctions in the intestine.