Multi-omics analysis reveals the molecular regulatory network underlying the prevention of Lactiplantibacillus plantarum against LPS-induced salpingitis in laying hens

Background Salpingitis is one of the common diseases in laying hen production, which greatly decreases the economic outcome of laying hen farming. Lactiplantibacillus plantarum was effective in preventing local or systemic inflammation, however rare studies were reported on its prevention against salpingitis. This study aimed to investigate the preventive molecular regulatory network of microencapsulated Lactiplantibacillus plantarum(MLP) against salpingitis through multi-omics analysis, including microbiome, transcriptome and metabolome analyses.Results The results revealed that supplementation of MLP in diet significantly alleviated the inflammation and atrophy of uterus caused by lipopolysaccharide(LPS) in hens(P < 0.05). The concentrations of plasma IL-2 and IL-10 in hens of MLP-LPS group were higher than those in hens of LPS-stimulation group(CN-LPS group)(P < 0.05). The expression levels of TLR2, MYD88, NF-κB, COX2, and TNF-α were significantly decreased in the hens fed diet supplemented with MLP and suffered with LPS stimulation(MLP-LPS group) compared with those in the hens of CN-LPS group(P < 0.05). Differentially expressed genes(DEGs) induced by MLP were involved in inflammation, reproduction, and calcium ion transport. At the genus level, the MLP supplementation significantly increased the abundance of Phascolarctobacterium, whereas decreased the abundance of Candidatus_Saccharimonas in LPS challenged hens(P < 0.05). The metabolites altered by dietary supplementation with MLP were mainly involved in galactose, uronic acid, histidine, pyruvate and primary bile acid metabolism. Dietary supplementation with MLP inversely regulates LPSinduced differential metabolites such as Lyso PA(24:0/0:0)(P < 0.05).Conclusions In summary, dietary supplementation with microencapsulated Lactiplantibacillus plantarum prevented salpingitis by modulating the abundances of Candidatus_Saccharimonas, Phascolarctobacterium, Ruminococcus_torques_group and Eubacterium_hallii_group while downregulating the levels of plasma metabolites, p-tolyl sulfate, o-cresol and N-acetylhistamine and upregulating S-lactoylglutathione, simultaneously increasing the expressions of CPNE4, CNTN3 and ACAN genes in the uterus, and ultimately inhibiting oviducal inflammation.

Modified Gexiazhuyu decoction(膈下逐瘀汤加减方)alleviates chronic salpingitis via p38 signaling pathway

OBJECTIVE:To investigate pharmacodynamic effects of modified Gexiazhuyu decoction(MGXZYD)and explore the underlying mechanism in the treatment of chronic salpingitis METHODS:Chronic salpingitis model rats were firstly constructed and the blood was collected to detect the whole blood viscosity and plasma viscosity.Rat oviduct were collected to evaluate the macroscopic damage and the pathological injury and fibrosis of oviduct by hematoxylin-eosin(HE)and Masson staining.Elisa assay was to detect the production interleukin-1β(IL-1β)in serum and collagen I(COL-1),matrix metalloprotein 9(MMP-9),tissue inhibitor of metalloproteinases 1(TIMP-1)in oviduct tissue.And immunohistochemical staining with MMP-9 and TIMP-1 in oviduct tissue were examined.Western blot was used to detect the expressions of p38 mitogen-activated protein kinases(p38MAPK),phosphop38MPAK(p-p38MPAK),transforming growth factor-β1(TGF-β1)in oviduct.The expression ofα-smooth muscle actin(α-SMA),p-p38MPAK,in oviduct tissue were detected by immunofluorescence method.The m RNA of p-p38MAPK,α-SMA,COL-1,MMP-9,TIMP-1 was measured by reverse transcription-polymerase chain reaction.RESULTS:Rats administrated with MGXZYD demonstrated decreased the whole blood viscosity and plasma viscosity.MGXZYD obviously improved the tubal wall thickening,swelling and pelvic adhesion.And HE and Masson staining showed MGXZYD improved the pathological injury and fibrosis of oviduct.The results of MTT assay and flow cytometry indicated that MGXZYD could decreased the NIN-3T3 cells viability and improved the apoptosis.Besides,MGXZYD inhibited the protein and/or m RNA of TGF-β1,IL-1β,COL-1,α-SMA,pp38MAPK expressions and increased the production of MMP-9/TIMP-1.CONCLUSION:MGXZYD could prevent the progression of chronic salpingitis by inhibited the fibrocyte and inflammation which via inhibited the p38 MAPK signaling pathway.

Electroacupuncture attenuates chronic salpingitis via transforming growth factor-β1/p38 mitogen-activated protein kinase signaling pathway

OBJECTIVE:To explore the effect of electroacupuncture(EA)on rats with chronic fallopian tube inflammation and its potential mechanisms.METHODS:Thirty-six female Sprague-Dawley rats were divided into Control,Model and EA groups.The pathological morphology of the fallopian tubes was observed by hematoxylin-eosin(HE)and Masson staining.The results of transforming growth factor-β1(TGF-β1),P38 mitogen-activated protein kinase(MAPK),phosphorylation(p)-p38MAPK in rat oviduct tissues were detected by immunohistochemistry.Results of P38MAPK,p-P38MAPK and TGF-β1 in rat oviduct tissues were detected by immunofluorescence.The expression level of p38MAPK,p-P38MAPK,TGF-β1 protein in rats was detected by Western blot.Quantitative real-time polymerase chain reaction(RT-q PCR)was used to detect m RNA expression levels of TGF-β1.RESULTS:It found that collagen fibers counts decreased significantly in EA group compared to Model group.The phosphorylation of P38MAPK in EA group was significantly reduced compared to Model group.The serum TGF-β1 expressions in EA group increased decreased significantly.CONCLUSION:Electroacupuncture was able to attenuate chronic salpingitis through down-regulating TGF-β1/MAPK signaling pathway.

Expressions of β_3 Integrin and Fibronectin in Salpingitis

Objective To investigate the association between β3 integrin-fibronectin signaling and salpingitis. Methods Thirteen chronically inflamed tubal samples were included in the case group, while 29 normal fallopian tube samples were set as the controls. Immunohistochemistry was used to determine the distribution patterns and expressions of β3 integrin and fibronectin in the fallopian tube samples. Results β3 integrin was presented in the ciliated cells within the whole length of the normal fallopian tube, but no staining was detected in the tubal epithelium of salpingitis. A similar distribution pattern offibronectin was revealed between the cases and the controls, with exclusive staining in the tubal mucosal matrix and the basement membranes of the tubal epithelium and mucosal vessels, whereas no staining was detected in the tubal epithelial cells. Fibronectin in the samples of salpingitis showed a remarkably stronger-staining than that of the normal controls （P〈0.01）. Conclusion Salpingitis could reduce β3 integrin expression and raise fibronectin expression in the fallopian tube epithelium, concomitantly changed concentrations of β3 integrin and fibronectin seem to have impacts on the onset of salpingitis.

Fallopian tube:Its role in infertility and gynecological oncology

Disorders of the fallopian tube play a very important role in both infertility and gynaecological oncology. Tubal factor infertility is considered among the leading causes of female factor infertility. Many tubal disorders are related to infertility including congenital anomalies, acute and chronic inflammatory diseases, endometriosis and other pathologies that result in partial or total fallopian tube obstruction. In the field of gynaecological oncology, ovarian surface epithelial tumors remain one of the most fatal malignancies in women worldwide carrying the worst prognosis among female genital malignancies. For decades, the cell of origin of epithelial tumors has remained controversial and was largely believed to be surface ovarian epithelium. Recently several studies suggested that there is a major role of the fallopian tube in the development of ovarian surface epithelial tumors, mainly high grade serous carcinoma and other tumour types. In this article we review the role of the fallopian tube in both infertility and gynaecological oncology.