N-acetylglucosaminyltransferase V-deficiency increases susceptibility to murine malaria.

Abstract

It is considered that several glycoproteins on erythrocytes in mammalian species are involved in malaria parasite infection. To elucidate the role of N-glycans on malaria parasite infection, we induced experimental murine malaria infection (using Plasmodium berghei ANKA) in mice deficient in N-acetylglucosaminyltransferase V (Mgat5), which is one of the enzymes involved in β1,6-GlcNAc N-glycan biosynthesis. After infection, Mgat5(-/-) mice showed severe body weight loss and parasitemia compared with wild-type mice. The Mgat5(-/-) mice, but not wild-type mice, also showed severe pathology accompanied by marked infiltration of plasma cells into the lungs and liver. These results suggest that β1,6-GlcNAc N-glycans on/in host erythrocytes may interfere with invasion of the parasites and progression to severe malaria.

• Authors: Akiko Shibui, Junko Doi, Mohammed E M Tolba, Chiharu Shiraishi, Yoshitaka Sato, Shumpei Ishikawa, Junichi Watanabe, Sadao Nogami, Susumu Nakae, Sumio Sugano, Nobumichi Hozumi
• Journal: Experimental parasitology (Exp Parasitol) Vol. 129 Issue 3 Pg. 318-21 (Nov 2011) ISSN: 1090-2449 [Electronic] United States
• PMID: 21767537 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2011 Elsevier Inc. All rights reserved.

Chemical References

• Interferon-gamma
• N-Acetylglucosaminyltransferases
• alpha-1,6-mannosylglycoprotein beta 1,6-N-acetylglucosaminyltransferase

Topics

• Animals
• Disease Susceptibility (enzymology)
• Erythrocytes (parasitology)
• Female
• Interferon-gamma (genetics, metabolism)
• Malaria (immunology)
• Mice
• Mice, Inbred BALB C
• Mice, Inbred ICR
• N-Acetylglucosaminyltransferases (deficiency)
• Parasitemia (immunology)
• Plasmodium berghei
• Specific Pathogen-Free Organisms
• Spleen (immunology)