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Production of tumor necrosis factor-a is increased in urinary tract infections
Oleh:
Susilaningsih, Neni
;
Karjono, Bambang Joni
;
Purnawati, Ratna Damma
Jenis:
Article from Journal - ilmiah nasional - terakreditasi DIKTI - non-atma jaya
Dalam koleksi:
Universa Medicina vol. 31 no. 03 (Sep. 2012)
,
page 167-174.
Topik:
Urinary tract infection
;
E. coli
;
serum TNF-a
;
TNF-a gene polymorphism
Fulltext:
tumor necrosis.pdf
(56.45KB)
Ketersediaan
Perpustakaan FK
Nomor Panggil:
U01.K
Non-tandon:
1 (dapat dipinjam: 0)
Tandon:
tidak ada
Lihat Detail Induk
Isi artikel
BACKGROUND Urinary tract infection (UTI) is a common source of bacteriemia. The most common cause of UTI is Escherichia coli (E. coli). Tumor Necrosis Factor (TNF)-a gene polymorphism has been reported to be responsible for an excessive production of TNF-a and eventual disruption of pro-inflammatory cytokine regulation. The aim of this study was to compare TNF-a serum levels and TNF-a allele polymorphisms in patients with UTI due to E.coli and in non-UTI controls. METHODS A cross-sectional study was conducted at Dr. Kariadi Central Hospital and the Center for Biomedical Research, Faculty of Medicine, Diponegoro University, Semarang. In 68 patients with UTI the TNF-a serum levels were determined by means of ELISA and compared to those of non-UTI controls (n=55). TNF-a-308G>A gene polymorphism was analyzed by polymerase chain reaction restriction fragment length using the NcoI enzyme. Fragments were visualized on polyacrylamide gel with silver staining. RESULTS TNF-a serum level in patients with UTI had a median of 8.9 pg/mL, which was significantly higher than the median of 3.7 pg/mL in the control group (p<0.001). TNF-a-308G>A gene polymorphisms found in the patient group were G/G=61 (90%), G/A=7(10%) and A/A=0, while in the control group were G/G=48 (87%), G/A=7 (13%) and A/A =0. There was no significant differences (p=0.578) in gene polymorphisms between the two groups. CONCLUSIONS TNF-a serum levels in patients with UTI due to E. coli were significantly higher than in non-UTI controls, but for the TNF-a-380 gene polymorphisms no significant difference was found between the two groups. There are presumably more important factors than host genotype that influence UTI pathogenesis.
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