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In vivo expression of the heat stable (estA) and heat labile (eltB) toxin genes of enterotoxigenic Escherichia coli (ETEC).

Artikel i vetenskaplig tidskrift
Författare Åsa Sjöling
Firdausi Qadri
Matilda Nicklasson
Yasmin Ara Begum
Gudrun Wiklund
Ann-Mari Svennerholm
Publicerad i Microbes and infection / Institut Pasteur
Volym 8
Nummer/häfte 12-13
Sidor 2797-802
ISSN 1286-4579
Publiceringsår 2006
Publicerad vid Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Sidor 2797-802
Språk en
Länkar dx.doi.org/10.1016/j.micinf.2006.08...
Ämnesord Adaptation, Physiological, Bacterial Toxins, biosynthesis, genetics, Diarrhea, microbiology, Enterotoxins, biosynthesis, genetics, Escherichia coli, genetics, isolation & purification, metabolism, Escherichia coli Infections, microbiology, Escherichia coli Proteins, biosynthesis, genetics, Feces, microbiology, Gene Expression Regulation, Bacterial, Humans, RNA, Bacterial, analysis, genetics, RNA, Messenger, analysis, genetics, Reverse Transcriptase Polymerase Chain Reaction, Virulence, Virulence Factors, biosynthesis
Ämneskategorier Mikrobiologi inom det medicinska området

Sammanfattning

Enterotoxigenic Escherichia coli (ETEC) colonize the intestine and adhere to the epithelium by means of different host specific colonization factors (CFs). Colonizing ETEC produce one or both of two enterotoxins; the heat stable (ST) and heat labile (LT) toxins which are both able to cause diarrhoea. The regulation of virulence genes in ETEC during infection of the human intestine is mainly unknown. In this study we analysed the level of mRNA expression of estA, coding for ST, and eltB, coding for the B subunit of LT, during human infection. The expressions of the toxins in ETEC strains expressing both ST and LT were investigated in bacteria isolated directly from patient stool without sub-culturing, (in vivo) and compared to the expression pattern of the corresponding ST/LT strains grown in liquid broth (in vitro) by quantitative competitive RT-PCR using fluorescent primers. We found that estA and eltB are expressed in the in vivo samples but no significant up-or down regulation of the expression levels of either estA or eltB could be determined in vivo as compared to in vitro.

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