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Volume 39, Number 1, February 2006

Simultaneous increases in immune-competent cells and nitric oxide in the spleen during Plasmodium berghei infection in mice


Hossein Nahrevanian, Michael J. Dascombe
Department of Parasitology, Pasteur Institute of Iran, Tehran, Iran; and Faculty of Life Sciences, The University of Manchester, Manchester, United Kingdom

Received: April 18, 2005    Revised: August 30, 2005    Accepted: September 12, 2005   

 

Corresponding author:

Dr. Hossein Nahrevanian, Department of Parasitology, Pasteur Institute of Iran, Pasteur Ave., Tehran 13164, Iran. E-mail: mobcghn@yahoo.co.uk This e-mail address is being protected from spam bots, you need JavaScript enabled to view it

 



 

Background and purpose: 

Nitric oxide and other reactive nitrogen intermediates (RNI) are thought to be important mediators of both immunological and pathological responses of the vertebrate host to malaria infection. The role of RNI has been studied most often by assay of stable RNI metabolites (nitrites, nitrates) in blood. This study evaluated the nature of the RNI response of mice to malaria by analyzing the subsets of immune-competent cells within the organ displaying increased RNI in vivo.

 



 

Methods:

We measured RNI production indirectly, as stable metabolites of nitric oxide activity in tissue homogenates (brain, liver, spleen) from mice infected with Plasmodium berghei. Only spleen exhibited an RNI concentration response during rising parasitemia. Subsets of immune-competent cells (B cells, CD19+), macrophages/monocytes (MOMA2+) and T cells (CD4+, CD8+) in the spleen were assayed by fluorescence activated cell scan flow cytometry.

 



 

Results:

The spleen was confirmed as a major source of RNI during mid-phase P. berghei infection. Significant increases in CD19+ and MOMA2+ spleen cells were evident during the mid-phase of P. berghei infection in MF1 mice when RNI are maximally elevated.

 



 

Conclusion:

The time courses of the cellular and RNI responses indicate that CD19+ and MOMA2+ cells may be responsible for the increase in RNI in the spleen. However, experiments in vitro are needed to make a definitive identification of the cell type(s) responsible for the increase in RNI in the mouse spleen during P. berghei infection.

 



 

Key words:

B lymphocytes, macrophages, malaria, nitric oxide, Plasmodium berghei, spleen


 



 

J Microbiol Immunol Infect 2006;39:11-17.