Defensins are important antimicrobial effector peptides of the innate immune system, which provides protection against bacterial infections in the intestine. Salmonella Choleraesuis and Salmonella Typhimurium are the most commonly isolated serovars in pig, but disease outcome is dependent on the Salmonella serovar. These infections are a serious problem for the swine industry and are also posing a major threat to public health because of Salmonella-related food-borne illnesses in human. To understand the innate immune response of pigs upon Salmonella infections, we studied the effect of these Salmonella serovars on defensin gene expression in the porcine ileal epithelial cell line IPEC-J2. With the use of scanning electron microscopy, we first visualized the surface characteristics of this cell line, and captured the invasion of Salmonella into the epithelial cell. Gene expression levels of porcine beta-defensin 1 and 2 were both induced upon S. Typhimurium infection but S. Choleraesuis had no effect. Invasion, adhesion and defensin susceptibility of both serovars were similar, which could not explain the observed difference in host response to these Salmonellae. In addition, induction of defensins was dependent on viability of S. Typhimurium, since Salmonella cell- or secreted components had no effect on defensin gene expression. These results provide further insight into the porcine innate immune response towards Salmonella infections, and could partially explain the different epidemiology of Salmonella infections in pig.
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http://dx.doi.org/10.1016/j.vetmic.2008.09.072 | DOI Listing |
Mol Biol Cell
January 2025
Department of Biology, The Catholic University of America, Washington, DC, 20064.
MAL2 (myelin and lymphocyte protein 2) and rab17 have been identified as hepatocellular carcinoma tumor suppressors. However, little is known how their functions in hepatic polarized protein sorting/trafficking translates into how they function in the epithelial to mesenchymal transition and/or the mesenchymal to epithelial transition in metastases. To investigate this, we expressed MAL2 and rab17 alone or together in hepatoma-derived Clone 9 cells (that lack endogenous MAL2 and rab17).
View Article and Find Full Text PDFCurr Hypertens Rep
January 2025
Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN, USA.
Purpose Of Review: The role of the lymphatic system in clearing extravasated fluids, lipid transport, and immune surveillance is well established, and lymphatic vasculature can provide a vital role in facilitating crosstalk among various organ systems. Lymphatic vessels rely on intrinsic and local factors to absorb and propel lymph from the interstitium back to the systemic circulation. The biological implications of local influences on lymphatic vessels are underscored by the exquisite sensitivity of these vessels to environmental stimuli.
View Article and Find Full Text PDFJ Cell Biol
February 2025
Department of Cell Biology, Yale University School of Medicine, New Haven, CT, USA.
Mutations that increase LRRK2 kinase activity have been linked to Parkinson's disease and Crohn's disease. LRRK2 is also activated by lysosome damage. However, the endogenous cellular mechanisms that control LRRK2 kinase activity are not well understood.
View Article and Find Full Text PDFJ Exp Med
February 2025
Laboratory of Immunogenetics of Pediatric Autoimmune Diseases, INSERM UMR 1163, Imagine Institute, University Paris Cité, Paris, France.
IKKα, encoded by CHUK, is crucial in the non-canonical NF-κB pathway and part of the IKK complex activating the canonical pathway alongside IKKβ. The absence of IKKα causes fetal encasement syndrome in humans, fatal in utero, while an impaired IKKα-NIK interaction was reported in a single patient and causes combined immunodeficiency. Here, we describe compound heterozygous variants in the kinase domain of IKKα in a female patient with hypogammaglobulinemia, recurrent lung infections, and Hay-Wells syndrome-like features.
View Article and Find Full Text PDFJ Cell Biol
March 2025
Department of Biological Sciences, Laboratory of Cell Biology and Biochemistry, Tokyo Metropolitan University, Tokyo, Japan.
The accumulation of defective polypeptides in cells is a major cause of various diseases. However, probing defective proteins is difficult because no currently available method can retrieve unstable defective translational products in a soluble state. To overcome this issue, there is a need for a molecular device specific to structurally defective polypeptides.
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