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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