Authorship and contributorship
Antiphospholipid IgM antibody response in acute and chronic Mycobacterium tuberculosis mouse infection model
Article first published online: 1 OCT 2013
© 2013 John Wiley & Sons Ltd
The Clinical Respiratory Journal
How to Cite
Goodridge, A., Zhang, T., Miyata, T., Lu, S. and Riley, L. W. (2013), Antiphospholipid IgM antibody response in acute and chronic Mycobacterium tuberculosis mouse infection model. The Clinical Respiratory Journal. doi: 10.1111/crj.12049
AG, TZ and TM performed experiments and laboratory assays. AG, TZ and SL analyzed the data. AG and LWR designed the study and wrote the manuscript.
This study was approved by the Animal Care and Use Committee-ACUC at UC Berkeley (Animal Use Protocol # R228-1211B).
Conflict of interest
Authors declare that they have no competing interests.
- Article first published online: 1 OCT 2013
- Accepted manuscript online: 1 AUG 2013 02:40AM EST
- Manuscript Accepted: 25 JUL 2013
- Manuscript Revised: 24 JUN 2013
- Manuscript Received: 27 FEB 2013
- a Doctoral Fellowship from SENACYT-Panama 2005–2010
- UBS Optimus Foundation
- antiphospholipid ;
- B-1 B cell ;
- biomarker ;
- IgM ;
- monitoring ;
- treatment ;
Background and Aims
The clinical management of tuberculosis (TB) could be greatly improved by an affordable biomarker test to monitor treatment response. Here, we examined changes in immunoglobulin M (IgM) antibody response to lipids as a potential biomarker for monitoring TB treatment in an experimental mouse model.
We performed enzyme-linked immunosorbent assay to investigate changes in IgM antibody response against cardiolipin (CL), phosphatidylcholine (PTC), phosphatidylethanolamine (PE), phosphatidylinositol (PI) and sphingolipid (SL) in BALB/c mice that were treated after being infected with Mycobacterium tuberculosis for 4 weeks (acute infection) and 20 weeks (chronic infection). Cytokine levels [interleukin (IL)-5, IL-10, interferon-gamma (IFN-γ), monocyte chemoattractant protein-1 (MCP-1)] in lung and spleen homogenates as well as in blood were also compared.
In both acutely and chronically infected mice, lungs were sterilised of M. tuberculosis infection after 8 weeks of treatment. The IgM response to CL, PTC, PE, PI and SL were consistently elevated throughout the course of infection in chronically infected mice compared with acutely infected mice. In acutely infected mice, the IgM antibody response against CL significantly decreased after 8 weeks of treatment, but not against other lipids. In chronically infected mice, the IgM response showed no significant changes against any of the lipids after 8 weeks of treatment. Of the cytokines examined, only MCP-1 levels in lungs decreased significantly after treatment.
These findings demonstrate that antilipid IgM antibody can remain elevated in chronically infected mice, but with treatment, only anti-CL IgM antibody levels decreased together with M. tuberculosis bacterial burden in acutely infected mice. Treatment did not affect antilipid IgM levels in chronically infected mice.