Binding of cholera toxin B subunit to intestinal epithelial cells

Impact of Corona Virus

“…Several years ago we synthesized the peptide LKEKK (Np5) corresponding to the sequence 16-20 of thymosin-α1 and the sequence 131-135 of interferon-α2, and showed that it is able to bind with high affinity and specificity human T and B lymphocytes, rat intestinal epithelial cell membranes, rat IEC-6, and human Caco-2 intestinal epithelial cells, murine Raw 264.7 macrophage-like cells [8][9][10][11][12][13][14]. In all of the above cases, treatment of cells or membranes with proteases did not affect the binding, suggesting the non-protein nature of the peptide binding site.…”

Cholera Toxin B Subunit and Peptide LKEKK Inhibit TNF-α Signaling in Intestinal Epithelial Cells and Reduce Inflammation in a Mouse Model of Colitis

“…Recently we have shown that CT-B and synthetic peptide LKEKK that corresponds to residues 16-20 in TM-α 1 and 131-135 in IFN-α 2 bind with high affinity and specificity to rat IEC-6 and human Caco-2 intestinal epithelial cells. The CT-B and peptide LKEKK binding to the cells leads to an increase in the sGC activity [18]. In this context, it is interesting comparative study of anti-inflammatory action of protein and peptide in vitro and in vivo, as well as clarifying the role of the sGC-dependent signal transduction pathway in the implementation of this action.…”

“…Recently we synthesized peptide LKEKK and found that [ 3 H] LKEKK binds with high affinity to donor blood T lymphocytes, rat intestinal epithelial cell membranes, rat IEC-6 and human Caco-2 intestinal epithelial cells, murine Raw 264.7 macrophage-like cells [13][14][15][16][17][18][19]. Treatment of cells and membranes with proteases did not affect the [3H] LKEKK binding, suggesting the non-protein nature of the peptide receptor.…”

“…We suggested that this receptor could be the CT receptor, which is known to be a GM1-glanglioside [5,6]. It was found that CT-B and the peptide: LKEKK at concentrations of 10 1000 NM increased in a dose-dependent manner the nitric oxide (NO) production and the soluble guanylate cyclase (sGC) activity in IEC-6 and Caco-2 cells [17,18]. Taking into account that NO acts as a primary activator of sGC, it can be assumed that the effect of CT-B and peptide LKEKK on the target cell is realized in the following way: increase in the iNOS expression → increase in the NO production → increase in the sGC activity → increase in intracellular levels of cGMP.…”

The Combined Effect of STAT3 and NF-Κb Inhibitors (The Last Links of the Cholinergic Anti-Inflammatory Pathway) on Mouse Mortality and Blood Concentration of Proinflammatory Cytokines in Sepsis

“…We suggested that this fragment may be involved in the binding of TM-α 1 and IFN-α 2 with a common receptor and synthetic peptide LKEKK may also have the same ability. Recently we synthesized peptide LKEKK and found that [ 3 H] LKEKK binds with high affinity to donor blood T lymphocytes [13,14], rat intestinal epithelial cell membranes [15,16], rat IEC-6 and human Caco-2 intestinal epithelial cells, murine Raw 264.7 macrophage-like cells [17][18][19]. Treatment of cells and membranes with proteases did not affect the [ 3 H] LKEKK binding, suggesting the non-protein nature of the peptide receptor.…”