Role of Toll-like receptor 2 against Streptococcus uberis infection in primary mouse mammary epithelial cells

Wan, Zhixin; Wang, Xudong; Liu, Ming; Zuo, Jiane; Xu, Yuanyuan; Han, Xiangan; Vanhnaseng, Phoutapane; Miao, Jinfeng

doi:10.1016/j.intimp.2019.106142

Cited by 10 publications

(7 citation statements)

References 31 publications

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“…Cells were pelleted at 1.4× g for 10 min. The same number of cells were lysed with sterile triple distilled water, and CFUs were counted by the spread plate method after incubation for 12 h at 37 • C [22].…”

Section: Viable Bacterial Count Assaymentioning

confidence: 99%

TLR2 Signaling Pathway Combats Streptococcus uberis Infection by Inducing Mitochondrial Reactive Oxygen Species Production

Wan

Wang

et al. 2020

Cells

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Mastitis caused by Streptococcus uberis (S. uberis) is a common and difficult-to-cure clinical disease in dairy cows. In this study, the role of Toll-like receptors (TLRs) and TLR-mediated signaling pathways in mastitis caused by S. uberis was investigated using mouse models and mammary epithelial cells (MECs). We used S. uberis to infect mammary glands of wild type, TLR2−/− and TLR4−/− mice and quantified the adaptor molecules in TLR signaling pathways, proinflammatory cytokines, tissue damage, and bacterial count. When compared with TLR4 deficiency, TLR2 deficiency induced more severe pathological changes through myeloid differentiation primary response 88 (MyD88)-mediated signaling pathways during S. uberis infection. In MECs, TLR2 detected S. uberis infection and induced mitochondrial reactive oxygen species (mROS) to assist host in controlling the secretion of inflammatory factors and the elimination of intracellular S. uberis. Our results demonstrated that TLR2-mediated mROS has a significant effect on S. uberis-induced host defense responses in mammary glands as well as in MECs.

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Section: Viable Bacterial Count Assaymentioning

confidence: 99%

TLR2 Signaling Pathway Combats Streptococcus uberis Infection by Inducing Mitochondrial Reactive Oxygen Species Production

Wan

Wang

et al. 2020

Cells

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“…Bar Shira and Friedman (2018) demonstrated their capacity to take up and process bacteria after establishing primary intestinal epithelial cell cultures. TLR molecules have also been reported in bovine intestinal epithelial cells (Mansilla et al, 2020), mouse mammary epithelium (Wan et al, 2020), as well as airway (Sukkar et al, 2006) and vascular smooth muscle cells (Stoll et al, 2004).…”

Section: Discussionmentioning

confidence: 96%

TLR2 and TLR4 molecules and antigen‐presenting cell compositions in cecal tonsils of broiler chicks (Gallus gallus domesticus) in the first two weeks of the post‐hatch period

Eren

Kum

Nazlıgül

et al. 2021

Anat Histol Embryol

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Chickens do not have lymph nodes. Gut-associated lymphoid tissue is the major immunological organization for the digestive system. Cecal tonsils are an important part of this organization. This study is a descriptive and experimental study that was conducted to determine the histological development of the cecal tonsils and the distribution of Toll-like receptor (TLR) 2, TLR4 and antigen-presenting cells during the first 2 weeks of the chick's life. The tissue sections were stained using Crossmon's triple technique, Gordon and Sweet's silver impregnation, and streptavidin-biotin-peroxidase complex methods. The classical tonsil framework with fossa and tonsillar units were observed in 4 days cecal tissue. The web of reticular fibres forming the stroma of the tissue had the impression that the lymphoid cells filling in time. The development of cecal tonsil was completed histologically on the day 10 and following day 14 samples. Regardless of the antigenic stimulation, TLR2, TLR4 and CD83, major histocompatibility complex (MHC) class II molecules are present in proximal cecal tissue. However, CD83-positive dendritic cells in the germinal centre were first distinguished on day 7. Furthermore, the high antigen presentation capacity of the cecum with an intense MHC class II molecule expression was determined. Histological and immunohistochemical findings in this study revealed that both innate and adaptive cecal defence mechanisms were in the learning period during the first 2 weeks. The learning period of innate immunity may require more detailed research. However, the results obtained in this study will be taken into consideration in the vaccination programmes in chicks.

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“…TLR2, one of the activators of the inflammatory response and a link between innate and adaptive immune responses, expressed in immune cells and is involved in innate immune recognition of bacteria through recognition of peptidoglycan and lipoteichoic acid in gram‐positive pathogens (Thompson et al., 2014). Research showed that the absence of TLR2 in mMECs has significant damage to cells in the process of S. uberis infection (Wan et al., 2020). Moreover, TLR2‐mediated mROS has a significant effect on S .…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, TLR2‐mediated mROS has a significant effect on S . uberis ‐induced host defense responses in mammary glands as well as in MECs (Wan et al., 2020). TLRs are also associated with the activation of the NF‐κB proinflammatory pathway that ultimately activates the transcription of inflammatory cytokines (Moyes et al., 2014).…”

Section: Discussionmentioning

confidence: 99%

“…Primary mMECs were isolated from the fourth mammary glands of female lactating ICR mice, as described previously with minor modifications (Li et al., 2014; Wan et al., 2020). Following aseptic lymph node removal, mammary tissue was finely minced and placed in DMEM/ F12 (CORNING, USA) containing 1.5 mg/ml collagenase I, 1.5 mg/ml collagenase Ⅱ, 1.5 mg/ml trypsin and 100 U/ml penicillin/streptomycin at 37°C for 3 hr.…”

Section: Methodsmentioning

confidence: 99%

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Infective mastitis due to bovine‐associated Streptococcus dysgalactiae contributes to clinical persistent presentation in a murine mastitis model

Gao

Yue

et al. 2021

Veterinary Medicine & Sci

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Background Mastitis caused by Streptococcus dysgalactiae (GCS) is a major pathology of dairy cows. The mechanisms by which GCS intramammary infection is established and maintained involve not only bacterial adherence and invasion but also modulation of the cytokines and TLR immune response. Objectives The study aimed to evaluate characteristics of persistent infection of GCS collected from bovine mastitis milk in a murine mastitis model whose mammary structure is similar to that of dairy cows; dairy cow mastitis can be well simulated by using mice as models. HLJ2019 was tested for its ability to persistently infected mice by intramammary inoculation. Methods As antibiotics tested, establish an intramammary infection model in murine, histopathology analyses, relative expression of inflammatory cytokines mRNA and adherence and invasion in mMECs. Results It induced a robust inflammatory reaction in the mammary gland, characterized by histopathological changes, increased myeloperoxidase activity and induced expression of inflammatory cytokines (TNF‐α, IL‐6, IFN‐γ, IL‐10, IL‐1α and IL‐1β) and TLR2/4, the exhibited strong LDH release, adhesion and invasive abilities in contact with mMECs. Conclusion These results contribute to increase the available information on host‐pathogen interaction and point out the need for further research to expand the knowledge about these interactions for developing new strategies to intervene in the intramammary persistent infection progress.

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Role of Toll-like receptor 2 against Streptococcus uberis infection in primary mouse mammary epithelial cells

Cited by 10 publications

References 31 publications

TLR2 Signaling Pathway Combats Streptococcus uberis Infection by Inducing Mitochondrial Reactive Oxygen Species Production

TLR2 Signaling Pathway Combats Streptococcus uberis Infection by Inducing Mitochondrial Reactive Oxygen Species Production

TLR2 and TLR4 molecules and antigen‐presenting cell compositions in cecal tonsils of broiler chicks (Gallus gallus domesticus) in the first two weeks of the post‐hatch period

Infective mastitis due to bovine‐associated Streptococcus dysgalactiae contributes to clinical persistent presentation in a murine mastitis model

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