Interleukin-17A Contributed to the Damage of Blood-CNS Barriers During Streptococcus suis Meningitis

Lü, Xi; Peng, Xiao; Liu, Ran; Xia, Kunlong; Wu, Meizhou; Jin, Meilin; Xu, Lei

doi:10.1007/s12035-022-02749-y

Cited by 5 publications

(3 citation statements)

References 58 publications

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“…Cell-cell junctions between epithelial cells, particularly TJs and AJs, are known to play an essential role in maintaining host epithelial permeability ( 30 , 31 ). Changes in the expression of TJs and AJs between epithelial cell monolayers could also be used to evaluate the conditions of epithelial permeability ( 32 , 33 ). In this study, our in vitro tests revealed that P. multocida infection decreased the expression of several key proteins at TJs (ZO-1) and AJs (β-catenin and E-cadherin) in MLE-12 cells ( Fig.…”

Section: Discussionmentioning

confidence: 99%

Vascular Endothelial Growth Factor A Contributes to Increased Mammalian Respiratory Epithelial Permeability Induced by Pasteurella multocida Infection

et al. 2023

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Section: Discussionmentioning

confidence: 99%

Vascular Endothelial Growth Factor A Contributes to Increased Mammalian Respiratory Epithelial Permeability Induced by Pasteurella multocida Infection

et al. 2023

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“…Furthermore, in children with ASD, circulating T H 17 cells are increased, with the T H 17 to regulatory T cell ratio positively correlating with disease severity 207 . IL-17 promotes damage to the blood–brain barrier during Streptococcus suis meningitis 242 . Therefore, infection-induced IL-17 during pregnancy or in infants may contribute to the development of ASD and other developmental disorders.…”

Section: Il-17 In Autoimmunity and Inflammationmentioning

confidence: 99%

IL-17 and IL-17-producing cells in protection versus pathology

2022

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“…12 Cell-cell junctions between epithelial cells, particularly TJs and AJs, are known to play an essential role in maintaining host epithelial permeability (30,31). Changes in expression of TJs and AJs between epithelial cell monolayers could be also used to evaluate the condition of epithelial permeability (32,33). In this study, our in vitro tests revealed that P. multocida and/or S. pneumoniae infection decreased the expression of several key proteins at TJs (ZO-1) and AJs (β-catenin, E-cadherin) in MLE-12 cells (Fig.…”

Section: Discussionmentioning

confidence: 99%

Vascular endothelial growth factor A contributes to the increasing of mammalian respiratory epithelial permeability induced byPasteurella multocidainfection

Lin

Yang

Zhang

et al. 2022

Preprint

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Infections withPasteurella multocidacan cause significant zoonotic respiratory problems in both humans and animals.In vivotests in mouse infection models were used to investigate the mechanisms of respiratory epithelial barrier dysfunction during respiratory bacterial infection with these pathogens. Results revealed thatP. multocidainfection significantly increased epithelial permeability and increased expression of vascular endothelial growth factor A (VEGFA) and endothelial nitric oxide synthase (eNOS) in murine tracheae and lungs. In murine lung epithelial cell (MLE-12) models,P. multocidainfection decreased the expression of tight junctions (ZO-1) and adherens junctions (β-catenin, E-cadherin), but induced the activation of the hypoxia-inducible factor-1α (HIF-1α) and VEGFA signaling. When expression of HIF-1α is suppressed, the induction of VEGFA and ZO-1expression byP. multocidainfection is decreased. We also found that intervention of HIF-1α and VEGFA signaling affected infection outcomes caused by respiratory bacteria in mouse models. Most importantly, we demonstrated thatP. multocidainfection increased permeability of human respiratory epithelial cells and this process was associated with the activation of the HIF-1α and VEGFA signaling and likely contributes to the pathogenesis ofP. multocidain humans.

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Interleukin-17A Contributed to the Damage of Blood-CNS Barriers During Streptococcus suis Meningitis

Cited by 5 publications

References 58 publications

Vascular Endothelial Growth Factor A Contributes to Increased Mammalian Respiratory Epithelial Permeability Induced by Pasteurella multocida Infection

Vascular Endothelial Growth Factor A Contributes to Increased Mammalian Respiratory Epithelial Permeability Induced by Pasteurella multocida Infection

IL-17 and IL-17-producing cells in protection versus pathology

Vascular endothelial growth factor A contributes to the increasing of mammalian respiratory epithelial permeability induced byPasteurella multocidainfection

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