◀ Back to IL13
CPOX — IL13
Text-mined interactions from Literome
Moore et al., J Appl Physiol 2001
:
In human cultured airway smooth muscle cells,
interleukin (IL)-1 beta
increases cyclooxygenase (COX)-2 expression and PGE ( 2 ) release, ultimately resulting in decreased beta-adrenergic responsiveness
Peebles et al., Am J Respir Crit Care Med 2002
(Bronchial Hyperreactivity) :
We conclude that in the BALB/c mouse,
COX inhibition with either a COX-1 or COX-2 inhibitor during allergen sensitization
augments production of
IL-13 and increases airway hyperresponsiveness
Saito et al., Int Arch Allergy Immunol 2003
(Fibrosis) :
IL-4 and
IL-13 stimulate fibroblast proliferation and this effect is at least partly
due to suppressed
COX gene expressions and subsequently decreased PGE ( 2 ) production
Hashimoto et al., J Immunol 2005
(Hypersensitivity...) :
Allergen sensitization and airway challenge alone led to undetectable levels of IL-5 and IL-13 in the lungs of IL-4, IL-4Ralpha, and STAT6 knockout ( KO ) mice, but
COX inhibition during the development of allergic inflammation
resulted in wild-type levels of IL-5 and
IL-13 and heightened airway eosinophilia in each of the three KO mice
Helmersson et al., Free radical research 2005
(Cardiovascular Diseases...) :
This study investigated the longitudinal association between serum selenium ( s-Se ) and a golden standard indicator of oxidative stress in vivo ( 8-iso-prostaglandin F2alpha, a major F2-isoprostane ), an indicator of
cyclooxygenase (COX) mediated inflammation ( prostaglandin F2alpha ), high sensitive C-reactive protein ( hsCRP ),
interleukin-6 (IL-6) and serum amyloid A protein (SAA) in a follow-up study of 27 years
Peebles et al., J Immunol 2005
(Bronchial Hyperreactivity...) :
In contrast, the
COX inhibition mediated increase in AHR is
dependent on
IL-13 , but airway eosinophilia is not
Schwartzbaum et al., Cancer Epidemiol Biomarkers Prev 2007
(Genetic Predisposition to Disease...) :
In addition, recent studies suggest that IL-4 and
IL-13 induce
cyclooxygenase-2 (COX-2) to resolve brain inflammation
Zhou et al., J Immunol 2008
(Inflammation...) :
COX inhibition during sensitization increased the numbers of mature dendritic cells and activated CD4 T cells in the spleen and
augmented OVA-specific IL-5 and
IL-13 responses of the splenic CD4 T cells at day 5 after sensitization
Endo et al., Am J Respir Cell Mol Biol 1998
:
Lipopolysaccharide (LPS) stimulated PGE2 synthesis and
COX activity were suppressed significantly by IL-4, but were not
affected significantly by IL-10,
IL-13 , or IFN-gamma
Dean et al., J Biol Chem 1999
:
We have previously shown that the pyridinyl imidazole SB 203580, which inhibits it, blocks the
interleukin-1 induction of
cyclooxygenase-2 (COX-2) and matrix metalloproteinase 1 and 3 mRNAs in fibroblasts