Abstract:
BACKGROUND:Airway inflammation and asthma have been linked to oxidative stress and the melastatin-related transient receptor potential cation channel, member 2 (TRPM2), which can be activated by reactive oxygen species (ROS), has emerged as a potential therapeutic target for inflammatory diseases. OBJECTIVE:Using TRPM2 deficient (TRPM2-/-) mice, we investigated whether the TRPM2 ion channel, which mediates calcium (Ca2+) influx and lysosomal Ca2+ release, plays a role in the pathophysiology of severe allergic asthma in mouse. METHODS:Severe allergic asthma was initiated in wild type (WT) and TRPM2-/- mice by repeated sensitization with ovalbumin (OVA)/aluminum hydroxide on Days 0, 7 and 14, followed by intranasal challenge on Days 21, 22 and 23. Mice were investigated for the presence of airway responsiveness, airway inflammation, production of allergen-specific antibodies, cytokine response and lung pathology. RESULTS:The absence of TRPM2 channels has no obvious effect on major etiologic markers of severe allergic asthma in this mouse model. Neither airway resistance nor mucus production are affected in TRPM2-/- mice. TRPM2 channel ablation also does not alter airway inflammation or immunocyte infiltration and does not affect antibody response or cytokine levels. CONCLUSIONS:TRPM2 is not required for airway inflammation in OVA-induced severe allergic asthma in mice. Accordingly, TRPM2 might not be a suitable therapeutic target for airway inflammation caused by allergens in humans.
journal_name
J Inflamm (Lond)journal_title
Journal of inflammation (London, England)authors
Sumoza-Toledo A,Fleig A,Penner Rdoi
10.1186/1476-9255-10-19subject
Has Abstractpub_date
2013-05-01 00:00:00pages
19issue
1issn
1476-9255pii
1476-9255-10-19journal_volume
10pub_type
杂志文章abstract::French maritime pine bark extract (Pycnogenol) displays a variety of anti-inflammatory effects in vivo. Aim of this study was to determine whether human plasma after oral intake of Pycnogenol contains sufficient concentrations of active principles to inhibit key mediators of inflammation. Blood samples from seven heal...
journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-3-1
更新日期:2006-01-27 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-7-17
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abstract:BACKGROUND:PTPH1 is a protein tyrosine phosphatase expressed in T cells but its effect on immune response is still controversial. PTPH1 dephosphorylates TCRzeta in vitro, inhibiting the downstream inflammatory signaling pathway, however no immunological phenotype has been detected in primary T cells derived from PTPH1-...
journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-7-16
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-7-18
更新日期:2010-04-20 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/s12950-015-0056-5
更新日期:2015-02-08 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/s12950-020-00265-1
更新日期:2020-11-07 00:00:00
abstract::Eosinophils are often predominant inflammatory leukocytes infiltrating oral squamous carcinoma (OSC) sites. Prostaglandins are secreted by oral carcinomas and may be involved in eosinophil infiltration. The objective of this study was to determine the factors contributing to eosinophil migration and potential anti-neo...
journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-10-4
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-7-51
更新日期:2010-10-25 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-2-9
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-3-4
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/s12950-018-0186-7
更新日期:2018-05-16 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-5-7
更新日期:2008-05-29 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/s12950-014-0026-3
更新日期:2014-08-12 00:00:00
abstract:: Interleukin-6 is a multifunctional cytokine that is critical for T/B-cell differentiation and maturation, immunoglobulin secretion, acute-phase protein production, and macrophage/monocyte functions. Extensive research into the biology of IL-6 has implicated IL-6 in the pathophysiology and pathogenesis of RA. An anti-...
journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-6-10
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-7-21
更新日期:2010-05-12 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-4-4
更新日期:2007-02-16 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type:
doi:10.1186/s12950-017-0157-4
更新日期:2017-05-19 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 社论
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-4-21
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-11-10
更新日期:2014-04-02 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-2-10
更新日期:2005-10-05 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-10-36
更新日期:2013-11-20 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-8-11
更新日期:2011-05-03 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/s12950-019-0228-9
更新日期:2019-12-16 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-8-30
更新日期:2011-11-03 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/1476-9255-10-12
更新日期:2013-03-21 00:00:00
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journal_title:Journal of inflammation (London, England)
pub_type: 杂志文章
doi:10.1186/s12950-020-00264-2
更新日期:2020-10-31 00:00:00