scholarly journals Antimicrobial Effect of Zophobas morio Hemolymph against Bovine Mastitis Pathogens

2020 ◽  
Vol 8 (10) ◽  
pp. 1488
Author(s):  
Mengze Du ◽  
Xiaodan Liu ◽  
Jiajia Xu ◽  
Shuxian Li ◽  
Shenghua Wang ◽  
...  

Coliforms and Staphylococcus spp. infections are the leading causes of bovine mastitis. Despite extensive research and development in antibiotics, they have remained inadequately effective in treating bovine mastitis induced by multiple pathogen infection. In the present study, we showed the protective effect of Zophobas morio (Z. morio) hemolymph on bovine mammary epithelial cells against bacterial infection. Z. morio hemolymph directly kills both Gram-positive and Gram-negative bacteria through membrane permeation and prevents the adhesion of E. coli or the clinically isolated S. simulans strain to bovine mammary epithelial (MAC-T) cells. In addition, Z. morio hemolymph downregulates the expression of nucleotide-binding oligomerization domain (NOD)-like receptor family member pyrin domain-containing protein 3 (NLRP3), caspase-1, and NLRP6, as well as inhibits the secretion of interleukin-1β (IL-1β) and IL-18, which attenuates E. coli or S. simulans-induced pyroptosis. Overall, our results suggest the potential role of Z. morio hemolymph as a novel therapeutic candidate for bovine mastitis.

2021 ◽  
Vol 8 ◽  
Author(s):  
Jin-Peng Wang ◽  
Qi-Chao Hu ◽  
Jian Yang ◽  
Zhuo-Ma Luoreng ◽  
Xing-Ping Wang ◽  
...  

Bovine mastitis is an inflammatory response of mammary glands caused by pathogenic microorganisms such as Escherichia coli (E. coli). As a key virulence factor of E. coli, lipopolysaccharide (LPS) triggers innate immune responses via activation of the toll-like-receptor 4 (TLR4) signaling pathway. However, the molecular regulatory network of LPS-induced bovine mastitis has yet to be fully mapped. In this study, bovine mammary epithelial cell lines MAC-T were exposed to LPS for 0, 6 and 12 h to assess the expression profiles of long non-coding RNAs (lncRNAs) using RNA-seq. Differentially expressed lncRNAs (DElncRNAs) were filtered out of the raw data for subsequent analyses. A total of 2,257 lncRNAs, including 210 annotated and 2047 novel lncRNAs were detected in all samples. A large proportion of lncRNAs were present in a high abundance, and 112 DElncRNAs were screened out at different time points. Compared with 0 h, there were 22 up- and 25 down-regulated lncRNAs in the 6 h of post-infection (hpi) group, and 27 up- and 22 down-regulated lncRNAs in the 12 hpi group. Compared with the 6 hpi group, 32 lncRNAs were up-regulated and 25 lncRNAs were down-regulated in the 12 hpi group. These DElncRNAs are involved in the regulation of a variety of immune-related processes including inflammatory responses bMECs exposed to LPS. Furthermore, lncRNA TCONS_00039271 and TCONS_00139850 were respectively significance down- and up-regulated, and their target genes involve in regulating inflammation-related signaling pathways (i.e.,Notch, NF-κB, MAPK, PI3K-Akt and mTOR signaling pathway), thereby regulating the occurrence and development of E. coli mastitis. This study provides a resource for lncRNA research on the molecular regulation of bovine mastitis


2021 ◽  
Vol 88 (3) ◽  
pp. 293-301
Author(s):  
Run Wang ◽  
Wen Zhang ◽  
Lumei Wang ◽  
Na Geng ◽  
Xiaozhou Wang ◽  
...  

AbstractStaphylococcus aureus is a common pathogen of bovine mastitis which can induce autophagy and inhibit autophagy flux, resulting in intracellular survival and persistent infection. The aim of the current study was to investigate the role of p38α in the autophagy induced by intracellular S. aureus in bovine mammary epithelial cells. An intracellular infection model of MAC-T cells was constructed, and activation of p38α was examined after S. aureus invasion. Through activating/inhibiting p38α by anisomycin/SB203580, the autophagosomes, LC3 and p62 level were analyzed by immunofluorescence and western blot. To further study the detailed mechanism of p38α, phosphorylation of ULK1ser757 was also detected. The results showed that intracellular S. aureus activated p38α, and the activation developed in a time-dependent manner. Inhibition of p38α promoted intracellular S. aureus-induced autophagy flow, up-regulated the ratio of LC3 II/I, reduced the level of p62 and inhibited the phosphorylation of ULK1ser757, whereas the above results were reversed after activation of p38α. The current study indicated that intracellular S. aureus can inhibit autophagy flow by activating p38α in bovine mammary epithelial cells.


2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Zhuo-Ma Luoreng ◽  
Da-Wei Wei ◽  
Xing-Ping Wang

AbstractMastitis is a complex inflammatory disease caused by pathogenic infection of mammary tissue in dairy cows. The molecular mechanism behind its occurrence, development, and regulation consists of a multi-gene network including microRNA (miRNA). Until now, there is no report on the role of miR-125b in regulating mastitis in dairy cows. This study found that miR-125b expression is significantly decreased in lipopolysaccharide (LPS)-induced MAC-T bovine mammary epithelial cells. Also, its expression is negatively correlated with the expression of NF-κB inhibitor interacting Ras-like 2 (NKIRAS2) gene. MiR-125b target genes were identified using a double luciferase reporter gene assay, which showed that miR-125b can bind to the 3′ untranslated region (3′ UTR) of the NKIRAS2, but not the 3′UTR of the TNF-α induced protein 3 (TNFAIP3). In addition, miR-125b overexpression and silencing were used to investigate the role of miR-125b on inflammation in LPS-induced MAC-T. The results demonstrate that a reduction in miR-125b expression in LPS-induced MAC-T cells increases NKIRAS2 expression, which then reduces NF-κB activity, leading to low expression of the inflammatory factors IL-6 and TNF-α. Ultimately, this reduces the inflammatory response in MAC-T cells. These results indicate that miR-125b is a pro-inflammatory regulator and that its silencing can alleviate bovine mastitis. These findings lay a foundation for elucidating the molecular regulation mechanism of cow mastitis.


2020 ◽  
Vol 103 (4) ◽  
pp. 3493-3504
Author(s):  
Jia Cheng ◽  
Jv Zhang ◽  
Bo Han ◽  
Herman W. Barkema ◽  
Eduardo R. Cobo ◽  
...  

2015 ◽  
Vol 6 (6) ◽  
pp. 879-886 ◽  
Author(s):  
B. Seridan Assis ◽  
P. Germon ◽  
A.M. Silva ◽  
S. Even ◽  
J.R. Nicoli ◽  
...  

Bovine mastitis, an inflammatory disease of the mammary gland often associated to bacterial infection, is the first cause of antibiotic use in dairy cattle. Because of the risk of antibioresistance emergence, alternative non-antibiotic strategies are needed to prevent or to cure bovine mastitis and reduce the antibiotic use in veterinary medicine. In this work, we investigated Lactococcus lactis V7, a strain isolated from the mammary gland, as a probiotic option against bovine mastitis. Using bovine mammary epithelial cell (bMEC) culture, and two representative strains for Escherichia coli and for Staphylococcus aureus, two major mastitis pathogens, we investigated L. lactis V7 ability to inhibit cell invasion (i.e. adhesion and internalization) of these pathogens into bMEC. L. lactis V7 ability to modulate the production of CXCL8, a key chemokine IL-8 responsible for neutrophil influx, in bMEC upon challenge with E. coli was investigated by an ELISA dosage of CXCL8 in bMEC culture supernatants. We showed that L. lactis V7 inhibited the internalisation of both E. coli and S. aureus strains into bMEC, whereas it inhibited the adhesion of only one out of the two S. aureus strains and of none of the E. coli strains tested. Investigation of the bMEC immune response showed that L. lactis V7 alone induced a slight increase in CXCL8 production in bMEC and that it increased the inflammatory response in bMEC challenged with the E. coli strains. Altogether these features of L. lactis V7 make it a potential promising candidate for a probiotic prevention strategy against bovine mastitis.


2020 ◽  
Author(s):  
Danru Yang ◽  
Yinghuan Wu ◽  
Yanying Zhao

Abstract Background Bovine mastitis is the inflammatory response of the mammary gland with an utmost threat to the dairy industry worldwide. Cytokine networks fuel inflammation. The sensitive and subtle changes of the inflammatory cytokine network in healthy and mastitic bovine mammary gland may encourage the use of cytokines in the diagnosis and prognosis of bovine mastitis. Allograft inflammatory factor-1 (AIF-1) is a proinflammatory cytokine mainly secreted by immune cells and it plays a central role in the complex signaling network of inflammation activation. Therefore, we explored the possible role of bovine AIF-1 related to bovine mastitis in the present study. Results The average concentration of AIF-1 in milks suffering from mastitis was 2.5 fold of that in the healthy cows, while its value decreased in cows recovered from mastitis. Furthermore, recombinant bovine AIF-1 up-regulated TNF-α, IL-6, and monocyte chemoattractant protein 1 secretion from bovine mammary epithelial cells with NF-κB activating, then NF-κB signaling inhibitor BAY 11-7085 abolished the increase of these inflammatory cytokines secretion induced by AIF-1. Thereafter, AIF-1 impaired bovine mammary epithelial cell viability, induced cell membrane permeability and cell apoptosis with exacerbated nitric oxide and oxidative stress, activated caspase 3, decreased mitochondrial membrane potential and intracellular ATP concentration. Conclusion These results indicated that AIF-1 prompted inflammation mediator production of bovine mammary epithelial cells via NF-κB signaling. Moreover, it damaged epithelial cells by depressing cell viability, inducing cell membrane permeability and cell apoptosis, which might be related to bovine mastitis.


2016 ◽  
Vol 84 (6) ◽  
pp. 1682-1692 ◽  
Author(s):  
Martine Deplanche ◽  
Ludmila Alekseeva ◽  
Ksenia Semenovskaya ◽  
Chih-Lung Fu ◽  
Frederic Dessauge ◽  
...  

The role of the recently described interleukin-32 (IL-32) inStaphylococcus aureus-induced mastitis, an inflammation of the mammary gland, is unclear. We determined expression of IL-32, IL-6, and IL-8 inS. aureus- andEscherichia coli-infected bovine mammary gland epithelial cells. Using live bacteria, we found that inS. aureus-infected cells, induction of IL-6 and IL-8 expression was less pronounced than inE. coli-infected cells. Notably, IL-32 expression was decreased inS. aureus-infected cells, while it was increased inE. coli-infected cells. We identified the staphylococcal phenol-soluble modulin (PSM) peptides as key contributors to these effects, as IL-32, IL-6, and IL-8 expression by epithelial cells exposed topsmmutant strains was significantly increased compared to that in cells exposed to the isogenicS. aureuswild-type strain, indicating that PSMs inhibit the production of these interleukins. The use of genetically complemented strains confirmed this observation. Inasmuch as the decreased expression of IL-32, which is involved in dendritic cell maturation, impairs immune responses, our results support a PSM-dependent mechanism that allows for the development of chronicS. aureus-related mastitis.


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