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Cholera toxin induces a transient depletion of CD8+ intraepithelial lymphocytes in the rat small intestine as detected by microarray and immunohistochemistry.

Artikel i vetenskaplig tidskrift
Författare Carl-Fredrik Flach
Stefan Lange
Eva Jennische
Ivar Lönnroth
Jan Holmgren
Publicerad i Infection and immunity
Volym 73
Nummer/häfte 9
Sidor 5595-602
ISSN 0019-9567
Publiceringsår 2005
Publicerad vid Institutionen för medicinsk mikrobiologi och immunologi
Institutionen för anatomi och cellbiologi
Institutionen för laboratoriemedicin, Avdelningen för klinisk bakteriologi
Sidor 5595-602
Språk en
Länkar dx.doi.org/10.1128/IAI.73.9.5595-56...
Ämnesord Animals, CD8-Positive T-Lymphocytes, immunology, Cholera Toxin, pharmacology, Immunohistochemistry, Intestinal Mucosa, chemistry, cytology, immunology, Jejunum, chemistry, cytology, immunology, Lymphocyte Depletion, Male, Oligonucleotide Array Sequence Analysis, RANTES, biosynthesis, genetics, RNA, Messenger, biosynthesis, Rats, Rats, Sprague-Dawley, Reverse Transcriptase Polymerase Chain Reaction
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

Cholera toxin (CT), besides causing intestinal hypersecretion after intragastric administration or during cholera infection, affects a multitude of regulatory mechanisms within the gut mucosal network, including T cells. By use of microarray screening, real-time PCR, and immunohistochemistry, we demonstrate here a rapid depletion of jejunal CD8(+) intraepithelial lymphocytes (IEL) in rats after intragastric CT challenge. This depletion may depend on CT-induced migration of IEL, since it was associated with a progressive decrease of CD8(+) cells in the epithelium and a contemporary transient increase of such cells, preferentially at the base of the villi, in the lamina propria. A significant decrease in the total number of villous CD8(+) cells at 6 and 18 h after CT challenge was detected; this possibly reflects an efflux from the jejunal mucosa. The kinetics of the CD8(+) IEL demonstrate the return to normal intraepithelial position at original numbers already 72 h after the single CT dose. The induced migration seems to be dependent on the enzymatic A-subunit of CT, since challenge with neither sorbitol nor CT B-subunit did mimic the effects of CT on CD8(+) IEL. Furthermore, a decrease in the level of both RANTES transcript and protein was detected, most likely as a consequence of the CT-induced migration of CD8(+) IEL. These results point to a complex interaction between CT, epithelial cells, and IEL, resulting in a disturbance of the gut homeostasis, which might have relevance for the strong immunomodulatory effects of intragastrically administered CT.

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