New insights in gut-liver axis in wild-type murine imiquimod-induced lupus

Background Intestinal and hepatic manifestations of lupus seem to be underestimated in comparison to other major organ lesions. Although recent data point to gut-liver axis involvement in lupus, gut permeability dysfunction and liver inflammation need to be more investigated. Objective This study aims to assess fecal calprotectin, intestinal tight junction proteins and liver inflammation pathway in wild-type murine imiquimod- induced lupus. Methods C57BL/6 mice were topically treated on their right ears with 1.25 mg of 5% imiquimod cream, three times per week for six weeks. Fecal calprotectin was collected at day 0, 22 and 45. Renal, liver and intestinal pathology, as well as inflammatory markers, intestinal tight junction proteins, and E. coli protein in liver were assessed at sacrifice. Results At six weeks, lupus nephritis was confirmed on histopathology and NGAL and KIM-1 expression. Calprotectin rise started at day 22 and persists at day 45. Protein expression of Claudine, ZO-1 and occludin was significantly decreased. E. coli protein was significantly increased in liver with necro-inflammation and increased TLR4, TLR7, and pNFκB/NFκB liver expression. Conclusion This study is the first to demonstrate early fecal calprotectin increase and liver activation of TLR4- NFκB pathway in wild-type murine imiquimod-induced lupus.

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Vitamin D strengthens the bladder epithelial barrier by inducing tight junction proteins during E. coli urinary tract infection

Cell and Tissue Research ◽

10.1007/s00441-019-03162-z ◽

2020 ◽

Vol 380 (3) ◽

pp. 669-673 ◽

Cited By ~ 1

Author(s):

Soumitra Mohanty ◽

Witchuda Kamolvit ◽

Olof Hertting ◽

Annelie Brauner

Keyword(s):

Vitamin D ◽

Urinary Tract Infection ◽

Urinary Tract ◽

Tract Infection ◽

Tight Junction ◽

Epithelial Barrier ◽

Tight Junction Proteins ◽

E Coli ◽

Junction Proteins

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Lactobacillus casei Zhang Counteracts Blood-Milk Barrier Disruption and Moderates the Inflammatory Response in Escherichia coli-Induced Mastitis

Frontiers in Microbiology ◽

10.3389/fmicb.2021.675492 ◽

2021 ◽

Vol 12 ◽

Author(s):

Yuhui Zheng ◽

Gang Liu ◽

Wei Wang ◽

Yajing Wang ◽

Zhijun Cao ◽

...

Keyword(s):

Escherichia Coli ◽

Inflammatory Response ◽

Tight Junction ◽

Lactobacillus Casei ◽

Mammary Tissue ◽

Tight Junction Proteins ◽

E Coli ◽

Tnf Α ◽

Injury Models ◽

Junction Proteins

Escherichia coli is a common mastitis-causing pathogen that can disrupt the blood-milk barrier of mammals. Although Lactobacillus casei Zhang (LCZ) can alleviate mice mastitis, whether it has a prophylactic effect on E. coli-induced mastitis through intramammary infusion, as well as its underlying mechanism, remains unclear. In this study, E. coli-induced injury models of bovine mammary epithelial cells (BMECs) and mice in lactation were used to fill this research gap. In vitro tests of BMECs revealed that LCZ significantly inhibited the E. coli adhesion (p < 0.01); reduced the cell desmosome damage; increased the expression of the tight junction proteins claudin-1, claudin-4, occludin, and zonula occludens-1 (ZO-1; p < 0.01); and decreased the expression of the inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 (p < 0.01), thereby increasing trans-epithelial electric resistance (p < 0.01) and attenuating the lactate dehydrogenase release induced by E. coli (p < 0.01). In vivo tests indicated that LCZ significantly reduced the injury and histological score of mice mammary tissues in E. coli-induced mastitis (p < 0.01) by significantly promoting the expression of the tight junction proteins claudin-3, occludin, and ZO-1 (p < 0.01), which ameliorated blood-milk barrier disruption, and decreasing the expression of the inflammatory cytokines (TNF-α, IL-1β, and IL-6) in mice mammary tissue (p < 0.01). Our study suggested that LCZ counteracted the disrupted blood-milk barrier and moderated the inflammatory response in E. coli-induced injury models, indicating that LCZ can ameliorate the injury of mammary tissue in mastitis.

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Indigenous lactobacilli strains of food and human sources reverse enteropathogenic E. coli O26:H11-induced damage in intestinal epithelial cell lines: effect on redistribution of tight junction proteins

Microbiology ◽

10.1099/mic.0.000507 ◽

2017 ◽

Vol 163 (9) ◽

pp. 1263-1272 ◽

Cited By ~ 4

Author(s):

Ruchi Jariwala ◽

Hemanti Mandal ◽

Tamishraha Bagchi

Keyword(s):

Epithelial Cell ◽

Tight Junction ◽

Cell Lines ◽

Intestinal Epithelial Cell ◽

Intestinal Epithelial ◽

Tight Junction Proteins ◽

E Coli ◽

Epithelial Cell Lines ◽

Junction Proteins

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PSVIII-18 Protective effect of Lactobacillus Casei Zhang on E. coli induced mastitis in mice

Journal of Animal Science ◽

10.1093/jas/skaa278.469 ◽

2020 ◽

Vol 98 (Supplement_4) ◽

pp. 259-260

Author(s):

Yuhui Zheng ◽

Shengli Li

Keyword(s):

Mammary Gland ◽

Tight Junction ◽

Protective Effect ◽

Lactobacillus Casei ◽

Tight Junction Proteins ◽

E Coli ◽

First Choice ◽

Model Control ◽

Lactobacillus Casei Zhang ◽

Junction Proteins

Abstract Mastitis is an acute, obvious and harmful clinical disease in mammals. It is also one of the productive diseases with high incidence, rapid epidemic and great economic loss in dairy farming. Antibiotics are the first choice for the treatment of infectious mastitis, but the long-term use of antibiotics in large quantities will lead to the emergence of antibiotic residues and bacterial resistance, which is harmful to the health of both human and animals. As a potential substitute of antibiotics, Lactobacillus has great potential in the control of pathogenic microorganisms. The purpose of this study was to explore the effect of Lactobacillus casei Zhang (L. Casei Zhang) on the prevention of E. coli-induced mastitis in mice and its protective effect on the damage of the blood and milk barrier. Intramammary administration of E. coli was used to establish a mouse mastitis model. Control group (PBS), E. coli administration group, and L. casei Zhang pretreatment plus E. coli administration group were set up respectively and the mammary gland samples were collected for analysis. The results showed that: L. casei Zhang could significantly reduce the degree of breast tissue damage and the content of inflammatory factors TNF-α，IL-6 and IL-1β (P < 0.05). In addition, the expression of tight junction proteins ZO-1, Claudin-3 and Occludin in the mammary gland tissues of mice was significantly promoted (P < 0.05). In conclusion, intramammary administration of L. casei Zhang could effectively reduce the inflammation of the mouse mammary gland induced by E. coli, and this protection is achieved by promoting the expression of the blood-milk barrier tight junction proteins.

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