Molecular basis of leukocyte adhesion molecules in early-onset periodontitis patients with decreased CD11/CD18 expression on leukocytes
The purpose of this study was to investigate the adherence characteristics of B lymphocytes with CD11/CD18 reduction and to describe the structure of CD18 at the mRNA level in two types of periodontal patients. The patients selected for the study included one juvenile periodontitis patient with an abnormal neutrophil chemotaxis (LJP-1), and his brother and sister, both of whom had generalized prepubertal periodontitis (GPP1-LAD, GPP2-LAD). Also selected for the study were a patient with localized juvenile periodontitis with normal neutrophil chemotaxis (LJP-2), one patient with localized prepubertal periodontitis (LPP) with normal chemotaxis, and two healthy subjects (H1 and H2). Epstein Barr virus B cell lines were established, and quantitative and qualitative assays were performed to determine the percentage of aggregation. Northern blotting reverse transcription Polymerase chain reaction, and Rnase protection assay were used to determine base mismatches between CD18 mRNA and the RNA probe. Intercellular adherence and CD18 expression on B lymphocytes quantitative and qualitative assays were used to examine the appearance of homotypic adhesion by EBV-transformed B lymphocytes from the patients. GPP1-LAD and GPP2-LAD did not aggregate. LJP-1, H1, H2, and the other periodontal patients demonstrated an aggregation of 65%. The clusters of LJP-1 were smaller in size and greater in number. The homotypic cell aggregate formation was inhibited by anti-CD18 monoclonal antibody. Amounts of CD18 mRNA from GPP1-LAD and GPP2-LAD were too small to be detected during normal exposure. Densities in signals of other patients were the same (except GPP1 and GPP2).The CD18 mRNA from GPP1 and GPP2 was 4.4 Kb, and 3.2 Kb for all the other subjects. There were excessive aberrant fragments in GPP1-LAD and GPP2-LAD, but not in the other subjects. In conclusion, dysfunction of CD18-related intercellular adherence in one LJP patient might be caused by disability of CD11/CD18 conformational changes and not by CD18 mRNA sequence abnormality. [c.c.]
Katsuragi, K., S. Takashiba, H. Kurihara, and Y. Murayama, J Periodont, 65:949,1994