Expression of peroxiredoxin I in plasma cells of oral inflammatory diseases

The participation of reactive oxygen species (ROS) in the immune response, both as pathogen killers and as mediators of signaling pathways, is well established. However, little is known about the enzymes responsible for ROS elimination in immune cells. Peroxiredoxin I (PrdxI) is a multifunctional en...

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Published in:European journal of oral sciences 2007-08, Vol.115 (4), p.334-337
Main Authors: Demasi, Ana P. D., Ceratti, Daniela, Furuse, Cristiane, Cury, Patrícia, Junqueira, José L. C., Araújo, Vera C.
Format: Article
Language:English
Subjects:
B-Lymphocytes - cytology
cancer
Carcinoma, Squamous Cell - enzymology
Carcinoma, Squamous Cell - pathology
Dentistry
Gingival Hyperplasia - enzymology
Gingival Hyperplasia - pathology
Gingivitis - enzymology
Gingivitis - pathology
Humans
inflammation
Mouth Neoplasms - enzymology
Mouth Neoplasms - pathology
oxidative stress
Peroxidases - blood
peroxiredoxin
Peroxiredoxins
plasma cells
Plasma Cells - enzymology
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Summary:The participation of reactive oxygen species (ROS) in the immune response, both as pathogen killers and as mediators of signaling pathways, is well established. However, little is known about the enzymes responsible for ROS elimination in immune cells. Peroxiredoxin I (PrdxI) is a multifunctional enzyme that exhibits thioredoxin‐dependent peroxidase activity. It has been described as a major hydrogen peroxide (H2O2)‐inducible protein in mouse peritoneal macrophages. In order to characterize its participation in the antioxidant defense of inflammatory/immune cells in greater detail, we evaluated its expression at sites of the oral cavity affected by inflammatory disorders induced by different agents (infectious, chemical, mechanical or tumor). In this study we demonstrated, by immunohistochemistry, that PrdxI is expressed in plasma cells, but not in B lymphocytes, regardless of the inflammation‐inducing agent. We suggest that PrdxI induction could be considered a crucial part of the cellular adaptive response to the B‐cell differentiation process to cope with the additional H2O2 associated with massive disulfide bond formation during immunoglobulin folding in the endoplasmic reticulum of plasma cells. PrdxI could diminish the tissue damage that accompanies inflammation.
ISSN:0909-8836
1600-0722
DOI:10.1111/j.1600-0722.2007.00462.x