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Updated: Jul 28, 2026
Isolation and Characterization of Dendritic Cells and Macrophages from the Mouse Intestine
Published on: May 21, 2012
Intestinal macrophages lack CD14 and CD89 and consequently are down-regulated for LPS- and IgA-mediated activities
P D Smith1, L E Smythies, M Mosteller-Barnum
1Department of Medicine, University of Alabama, and Veterans Affairs Medical Center, Birmingham, AL 35294, USA. pdsmith@uab.edu
Abstract:
The intestinal mucosa normally displays minimal inflammation despite the close proximity between mucosal macrophages and lumenal bacteria. Macrophages interact with bacteria and their products through CD14, a surface receptor involved in the response to LPS, and CD89, the receptor for IgA (FcalphaR). Here we show that resident macrophages isolated from normal human intestine lack CD14 and CD89. The absence of CD14 and CD89 was not due to the isolation procedure or mucosal cell products, but was evident at the transcriptional level, as the macrophages expressed neither CD14- nor CD89-specific mRNAs, but did express Toll-like receptor 2 and 4 transcripts. Consistent with their CD14(-) phenotype, lamina propria macrophages displayed markedly reduced LPS-induced cytokine production and LPS-enhanced phagocytosis. In addition, IgA-enhanced phagocytosis was sharply reduced in lamina propria macrophages. Thus, the absence of CD14 and CD89 on resident intestinal macrophages, due to down-regulated gene transcription, causes down-modulated LPS- and IgA-mediated functions and probably contributes to the low level of inflammation in normal human intestinal mucosa.
Insights
Resident intestinal macrophages lack CD14 and CD89 receptors, reducing their response to bacterial products like LPS and IgA. This absence, due to down-regulated gene transcription, helps maintain low inflammation in the gut mucosa.
Area of Science:
- Immunology
- Gastroenterology
- Cell Biology
Background:
- The intestinal mucosa maintains low inflammation despite constant bacterial presence.
- Macrophages are key immune cells interacting with bacteria via receptors like CD14 and CD89 (FcalphaR).
Purpose of the Study:
- To investigate the expression of CD14 and CD89 on resident intestinal macrophages.
- To determine the functional consequences of CD14 and CD89 absence on macrophage activity.
Main Methods:
- Isolation of resident macrophages from normal human intestine.
- Analysis of CD14 and CD89 gene and protein expression using transcript analysis.
- Assessment of lipopolysaccharide (LPS)- and IgA-mediated cytokine production and phagocytosis.
Main Results:
- Normal human intestinal macrophages lack CD14 and CD89 expression at both transcriptional and protein levels.
- These macrophages exhibit reduced lipopolysaccharide (LPS)-induced cytokine production and phagocytosis.
- IgA-enhanced phagocytosis is also significantly diminished in these intestinal macrophages.
Conclusions:
- The absence of CD14 and CD89 on intestinal macrophages, driven by transcriptional down-regulation, modulates their response to LPS and IgA.
- This functional down-modulation likely contributes to the normally low inflammatory state of the human intestinal mucosa.
