Search PubMed⌕ Search

PubMed · 11397127

Integrin expression, enterocyte maturation, and bacterial internalization.

Abstract

BACKGROUND: Little is known about the molecular mechanisms involved in the translocation of enteric bacteria. Adhesion molecules mediate interactions between some enteric pathogens and mammalian cells, but no such interactions have been identified for enterocytes and normal enteric bacteria. Using enteric pathogens, adhesion molecule expression has been linked to bacterial internalization and to enterocyte differentiation. Therefore, experiments were designed to study enterocyte integrin expression and differentiation, as well as enterocyte internalization of Salmonella typhimurium, Proteus mirabilis, and Escherichia coli. MATERIALS AND METHODS: Relative expression of the alpha2, alpha3, and beta1 integrin subunits on Caco-2 and HT-29 enterocytes (mature and immature) was measured by ELISA. Bacteria-enterocyte surface interactions were observed by light and scanning electron microscopy. Bacterial internalization by enterocytes was quantified using the gentamicin protection assay. RESULTS: Expression of the alpha2, alpha3, and beta1 integrin subunits was consistently increased in immature compared to mature Caco-2 enterocytes; however, compared to mature enterocytes, immature HT-29 enterocytes had similar expression of alpha3 and beta1 but decreased alpha2. Compared to untreated mature enterocytes, bacterial internalization was increased in immature enterocytes as well as mature enterocytes with lateral membranes artifactually exposed. However, there was no difference in bacterial internalization between immature enterocytes and mature enterocytes treated to expose the lateral membrane. CONCLUSIONS: Bacterial internalization by enterocytes appeared to be due to factors other than integrin expression or enterocyte differentiation. Exposure of the lateral enterocyte membrane may play an important role in facilitating bacterial internalization by enterocytes.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

D J Hess, M J Henry-Stanley, E A Moore, C L Wells. 2001-06-15. Integrin expression, enterocyte maturation, and bacterial internalization.. https://doi.org/10.1006/jsre.2001.6191

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Autophagic-like cell death in neutrophils induced by autoantibodies.

Human neutrophils undergo autophagic-like cell death following Sialic acid binding immunoglobulin-like lectin-9 (Siglec-9) ligation and concurrent stimulation with certain, but not all, neutrophil survival cytokines. Caspase inhibition by these cytokines is required, but is not sufficient, to trigger this particular form of cell death. Additional mechanisms may involve reactive oxygen species (ROS), and blocking of ROS or prevention of ROS production prevents autophagic-like neutrophil death. Interestingly, human intravenous immunoglobulin (IVIg) preparations contain natural anti-Siglec-9 autoantibodies, which are able to ligate Siglec-9 on neutrophils and induce autophagic-like cell death in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF) and some other survival cytokines. Here, we discuss the pathophysiological and therapeutic implications of these recent findings.

Antigens, CD↗

Bias in association studies of systemic lupus erythematosus susceptibility due to geographical variation in the frequency of a programmed cell death 1 polymorphism across Europe.

We obtained eight collections of DNA samples from ethnically matched systemic lupus erythematosus (SLE) patients and controls from five European countries totaling 783 patients and 1210 controls. A highly significant cline in the frequency of the PD1.3 A allele was found among controls but not among SLE patients. The frequency of the PD1.3 A allele increased from the Northeast to the Southwest of Europe. The cline was clearly apparent (P=1.2 x 10(-6)) when data from controls of other five SLE susceptibility studies were included in the analysis. This variation has severely biased SLE association studies owing to the lack of parallel changes in SLE patients. As a consequence, the PD1.3 A allele was more common in SLE patients than in controls in the Northeast and Center of Europe, similar to controls in Southeast Europe, and less frequent than in the controls in the Southwest of the Continent. This dissociation in allele frequencies between SLE patients and controls in different subpopulations indicated that programmed cell death 1 variation and disease susceptibility are not independent but the type of relationship is currently unclear. As allele frequency clines are common in other polymorphisms their impact in genetic epidemiology studies should be carefully considered.

Antigens, CD↗