Sulfasalazine augments a pro-inflammatory response in interleukin-1β-stimulated amniocytes and myocytes

Autor:	Phillip R. Bennett, Kacie Thomson, Yun S. Lee, David A. MacIntyre, Lynne Sykes, Emily J. Boyce, Zahirrah B. M. Rasheed, T. G. Teoh
Rok vydání:	2015
Předmět:	medicine.medical_specialty Necrosis medicine.medical_treatment Interleukin-1beta Myocytes Smooth Muscle Immunology nuclear factor-κB Inflammation Pregnancy Fetal membrane Sulfasalazine Internal medicine 1114 Paediatrics And Reproductive Medicine Humans Immunology and Allergy Medicine Amnion Cells Cultured Nuclear Factor κ B (NF-κB) Myocytes Fetus Amniocytes business.industry Interleukins Sulfasalazine (SASP) NF-kappa B Interleukin Epithelial Cells Original Articles NFKB1 Transcription Factor AP-1 Activator of protein -1 (AP-1) Endocrinology Cytokine 1107 Immunology Cyclooxygenase 2 Cytokines Female Inflammation Mediators medicine.symptom business activator of protein-1 medicine.drug
Zdroj:	Immunology. 146:630-644
ISSN:	0019-2805
DOI:	10.1111/imm.12534
Popis:	Preterm birth occurs in 10% of pregnancies and is a major cause of neonatal morbidity and mortality. The majority of cases of early preterm labour are associated with infection/inflammation, which places the fetal central nervous system at risk. Targeting immune activation is therefore an appealing therapeutic strategy for the prevention of preterm labour and neonatal brain injury. The expression of many labour‐associated and inflammatory‐response genes is controlled by the transcription factors nuclear factor‐κB (NF‐κB) and activator protein‐1 (AP‐1), which makes them therapeutic targets of interest. Sulfasalazine (SASP) has been shown to inhibit NF‐κB and reduce lipopolysaccharide‐induced cytokine concentrations in fetal membrane explants and reduce the rate of Escherichia coli‐induced preterm labour in mice. Its effects upon AP‐1 in the context of pregnancy are unknown. In this study the effect of SASP on interleukin‐1β (IL‐1β) ‐induced NF‐κB and AP‐1 activity, cytokine production and cyclo‐oxygenase‐2 (COX‐2) expression was examined in amniocytes and myocytes. A supra‐therapeutic concentration (5 mm) was required to inhibit IL‐1β‐induced NF‐κB (P
Databáze:	OpenAIRE
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