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Journal: Cellular and Molecular Gastroenterology and Hepatology
Article Title: Role of Innate Oral Immunity and the Salivary Fluid in Inflammatory Bowel Disease
doi: 10.1016/j.jcmgh.2025.101713
Figure Lengend Snippet: Scavenging saliva fluid MIF and TFF2 ameliorates effects of saliva fluid on development of DSS-induced colitis. ( A and B ) Standard curves ( left ) and the level of MIF ( A ) and TFF2 ( B ) in saliva from control ( black ) and DSS-treated mice ( red ) and saliva treated with the respective antibodies ( green ). ( C and E ) WT ( C ) and Aqp5 -/- mice ( E ) were fed with water ( black ) or 3% DSS ( blue, green and red ) for 6 days and allowed to recover for 6 days. The mice were gavaged with the salivary fluid treated with anti-MIF ( green ) and anti-TFF2 antibodies ( red ) on days 1, 3, and 6, as indicated. Mice were 18 to 22 weeks old, and the numbers in parenthesis indicate the number of mice in each group. The P values are relative to mice fed with DSS. The results with DSS shown in dotted lines were taken from and are shown to better illustrate the effect of MIF and TFF2 depletion. ( D and F ) Time course of development of disease activity of the mice in ( C and E ), respectively. ( G ) Intestinal length measured on day 8. ( H and I ) Analysis of cell proliferation ( left ) and goblet cell density ( right ). ( J and K ) Intestinal ( J ) and serum ( K ) MPO levels. ( L ) Intestinal permeability expressed as fold change measured on day 8. ( M and N ) Analysis of ZO1 ( M ) and Occludin ( N ) measured on day 8.
Article Snippet: The depletion of MIF or TFF2 protein from the saliva fluid was by incubation of the fluid for overnight at 4°C with anti-MIF (Cell Signaling, Cat no.88186S) or
Techniques: Control, Activity Assay, Permeability
Journal: Gastro Hep Advances
Article Title: Helicobacter pylori Exploit Short-Chain Fatty Acids-Induced CAPZA1 Overexpression to Emerge CD44v9-Positive Stemness
doi: 10.1016/j.gastha.2025.100860
Figure Lengend Snippet: Stem cell characteristics of CD44v9-positive cells induced by H pylori G27 strains (CagA-positive H pylori ) infection in the presence of butyrate (But). Immunofluorescence analysis of colocalization between CD44v9 and stem cell markers (LGR5, KLF5, and SALL4) in mucosoids derived from the gastric corpus and antrum of mice infected with H pylori G27 strains (CagA-positive H pylori ) or H pylori G27 cag PAI-deletion mutant strains (Δ cag PAI) in the presence of But. Colocalization of CD44v9 and the SPEM marker TFF2 was also assessed. Scale bar = 50 μm.
Article Snippet: The following antibodies were used for fluorescence immunocytochemistry: anti-CAPZA1 (OTI2G4) (Thermo Fisher Scientific, cat# MA5-25093; 1:500 or Abcam, Cambridge, UK, cat# ab166892; 1:500), anti-CD44v9 (Cosmo Bio, Tokyo, Japan, cat# CAC-LKG-M001; 1:500), anti-CagA (Austral Biologicals, cat# HPM-5001–5; 1:500), anti-LGR5 (Atlas antibodies, Stockholm, Sweden, cat# HPA012530; 1:200), anti-KLF5 (GeneTex, Irvine, CA, cat#GTX103289; 1:200), anti-SALL4 (Abcam, cat# ab29112; 1:200), and
Techniques: Infection, Immunofluorescence, Derivative Assay, Mutagenesis, Marker