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AHR — TNF
Text-mined interactions from Literome
Shore et al., Am J Respir Crit Care Med 2001
(Bronchial Hyperreactivity...) :
The purpose of this study was to determine whether
tumor necrosis factor (TNF) contributes to
airway hyperresponsiveness (AHR) and migration of polymorphonuclear leukocytes ( PMN ) into the airways following exposure to ozone ( O ( 3 ) ) ... Our results indicate that
TNF contributes to the
AHR but not the PMN emigration induced by acute O ( 3 ) exposure
Kanehiro et al., Am J Respir Crit Care Med 2001
(Bronchial Hyperreactivity) :
gammadelta T cells have been shown to be activated by
TNF-alpha and to negatively
regulate AHR
Kibe et al., Am J Respir Crit Care Med 2003
(Eosinophilia...) :
The
effects of
tumor necrosis factor-alpha on IL-13 induced
AHR were also examined ...
Tumor necrosis factor-alpha did not
affect AHR despite marked enhancement of eosinophil infiltration in IL-13 treated mice
Neff-LaFord et al., Cell Immunol 2003
(Orthomyxoviridae Infections) :
Infection caused transient increases in pulmonary
TNFalpha , IL-1, and IFNalpha/beta levels, but neither the kinetics nor magnitude of this response was
affected by
AhR activation
Choi et al., J Allergy Clin Immunol 2005
(Asthma...) :
TNF-alpha blockade
resulted in significant inhibition of the late
AHR without affecting the early AHR, and reduction in airway eosinophilia and inflammation
Nakae et al., J Allergy Clin Immunol 2007
(Asthma...) :
However, studies with TNF-deficient or TNF receptor-deficient mice have not produced a clear picture of the
role of
TNF in the
AHR associated with allergic inflammation in the mouse ... Our findings in mice support the hypothesis that
TNF can
promote the allergic inflammation and
AHR associated with asthma
Kim et al., Eur J Immunol 2007
(Bronchial Hyperreactivity...) :
We have investigated the
role of
TNF-alpha in mast cell mediated late
airway hyperresponsiveness (AHR) using mast cell-deficient WBB6F1-W/W ( v ) ( W/W ( v ) ) mice in a murine model of asthma, which exhibits a biphasic increase in AHR
Guedes et al., Am J Physiol Lung Cell Mol Physiol 2008
(Bronchial Hyperreactivity...) :
In conclusion, CD38 contributes to
TNF-alpha induced
AHR after a brief airway exposure to the cytokine, likely by mediating changes in ASM contractile responses, and is associated with greater AHR remission following chronic airway exposure to TNF-alpha
Jain et al., Immunobiology 2008
(Bronchial Hyperreactivity) :
Here, we investigated the putative involvement of IFNbeta in regulating
TNFalpha induced
airway hyper-responsiveness (AHR) , a defining feature of asthma
Kobayashi et al., Rheumatology (Oxford) 2008
(Arthritis, Rheumatoid...) :
AhR expression in synovial cells was
up-regulated by
TNF-alpha ...
TNF-alpha activates
AhR expression in RA synovial tissue, and that cigarette smoking and exposure to TCDD enhances RA inflammatory processes
Nam et al., Yonsei Med J 2009
(Asthma...) :
This study investigated whether
TNF-alpha blocking therapy
inhibits airway inflammation and
airway hyperresponsiveness (AHR) in a mouse model of asthma
Nishiumi et al., Toxicological sciences : an official journal of the Society of Toxicology 2010
(Insulin Resistance) :
Taken together, TCDD stimulates expression and secretion of TNF-alpha in adipocytes through activation of
AhR , ERK1/2, and JNK, and the secreted
TNF-alpha causes the downregulation of IRbeta, IRS1, and GLUT4 through TNFR1, resulting in insulin resistance
Lee et al., J Asthma 2011
(Bronchial Hyperreactivity) :
Single i.t. instillation of IgG-IC caused the recruitment of neutrophils and macrophages into the airway and
TNF mediated late
AHR , but failed to induce Th2 cell mediated asthmatic phenotypes ... IgG, but not IgE, is the major Ab that induces not only NF-?B activation and NF-?B dependent proinflammatory molecules in the lungs but also subsequent recruitment of inflammatory cells into the airway and
TNF mediated late
AHR
Hsia et al., J Allergy Clin Immunol 2012
(Asthma...) :
Using SP-A ( -/- ) Kit ( W-sh/W-sh ) mice engrafted with TNF-a ( -/- ) or TNF receptor (TNF-R) ( -/- ) MCs, we found that
TNF-a activation of MCs through the TNF-R, but not MC-derived TNF-a,
leads to augmented
AHR during M pneumoniae infection when SP-A is absent