Isolation and subsequent analysis of murine lamina propria mononuclear cells from colonic tissue

2007 ◽  
Vol 2 (10) ◽  
pp. 2307-2311 ◽  
Author(s):  
Benno Weigmann ◽  
Ingrid Tubbe ◽  
Daniel Seidel ◽  
Alex Nicolaev ◽  
Christoph Becker ◽  
...  
Keyword(s):  
Lamina Propria ◽  
Mononuclear Cells ◽  
Colonic Tissue ◽  
Lamina Propria Mononuclear Cells

Zinc Deficiency Activates the IL-23/Th17 Axis to Aggravate Experimental Colitis in Mice

2019 ◽  
Vol 14 (6) ◽  
pp. 856-866 ◽  
Author(s):  
Yasuki Higashimura ◽  
Tomohisa Takagi ◽  
Yuji Naito ◽  
Kazuhiko Uchiyama ◽  
Katsura Mizushima ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Lamina Propria ◽  
Zinc Deficiency ◽  
Mononuclear Cells ◽  
Interferon Regulatory Factor ◽  
Nuclear Accumulation ◽  
Regulatory Factor ◽  
Colonic Inflammation ◽  
Interferon Regulatory Factor 5 ◽  
Lamina Propria Mononuclear Cells

Abstract Background and Aims Patients with inflammatory bowel disease [IBD], especially Crohn’s disease, often develop zinc deficiency. However, the precise mechanisms by which zinc deficiency affects IBD pathology, particularly intestinal macrophage function, remain unclear. We studied the effects of zinc deficiency on the development and progression of colitis in mice. Methods To induce colitis, mice were treated with 2,4,6-trinitrobenzene sulphonic acid. Rag1−/− mice were then given injections of naïve CD4+CD62L+ T cells. The respective degrees of mucosal injury of mice that had received a zinc chelator (TPEN; N,N,N′,N′-tetrakis [2-pyridylmethyl]ethylenediamine) and of control mice were subsequently compared. Colonic lamina propria mononuclear cells were isolated by enzymatic digestion and were examined using flow cytometry. To generate mouse bone marrow-derived macrophages [BMDMs], bone marrow cells were stimulated with mouse macrophage-colony stimulating factor. Results Zinc deficiency aggravates colonic inflammation through the activation of type 17 helper T [Th17] cells in mice. Flow cytometric analysis revealed that zinc deficiency significantly increases the proportion of pro-inflammatory [M1] macrophages in colonic lamina propria mononuclear cells obtained from inflamed colon. Interferon-γ plus lipopolysaccharide-mediated M1 skewing alters the expression of zinc transporters in BMDMs and thereby decreases the intracellular free zinc. TPEN treatment mimicking the effects of the M1 skewing up-regulates IL-23p19 expression, which is strongly related to Th17 development. Furthermore, the nuclear accumulation of interferon-regulatory factor 5 is closely involved in IL-23p19 induction in zinc-deficient macrophages. Conclusions Zinc deficiency aggravates colonic inflammation through activation of the IL-23/Th17 axis. This activation is controlled by subcellular distribution of interferon-regulatory factor 5.

Tu1922 Genome-Wide Epigenomic Analysis of Lamina Propria Mononuclear Cells of Inflammatory Bowel Disease

2012 ◽  
Vol 142 (5) ◽  
pp. S-878-S-879
Author(s):  
Takeshi Otsubo ◽  
Yuki I. Kawamura ◽  
Kenshiro Oshima ◽  
Takaho A. Endo ◽  
Tetsuro Toyoda ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Lamina Propria ◽  
Bowel Disease ◽  
Mononuclear Cells ◽  
Lamina Propria Mononuclear Cells ◽  
Genome Wide ◽  
Inflammatory Bowel

Lamina propria mononuclear cells (LPMC) apoptosis in relation to different activation pathways

1995 ◽  
Vol 108 (4) ◽  
pp. A785
Author(s):  
M. Boirivant ◽  
R. De Maria ◽  
R. Pica ◽  
R. Testi ◽  
F. Pallone ◽  
...  
Keyword(s):  
Lamina Propria ◽  
Mononuclear Cells ◽  
Lamina Propria Mononuclear Cells ◽  
Activation Pathways
Sign in / Sign up

Export Citation Format

Share Document