Aggressive and chronic periodontitis correlate with distinct cellular sources of key immunoregulatory cytokines.
BACKGROUND
Chronic periodontitis (CP) and aggressive periodontitis (AP) are inflammatory diseases and the main cause of dental loss in adults. We aimed to investigate the expression of adhesion molecules and the source of proinflammatory and anti-inflammatory cytokines in circulating mononuclear cells from patients with CP and AP.


METHODS
Peripheral blood mononuclear cells from healthy controls and CP or AP patients were collected. The expression of the cell adhesion molecules CD11a and CD11b, and the cellular sources of interleukin (IL)-4, IL-10, IL-12, interferon-γ, and tumor necrosis factor-α by distinct subpopulations of circulating leukocytes were determined using flow cytometry.


RESULTS
The expression of CD11a, but not CD11b, was significantly higher within the CD4(+) and CD8(+) T cells in CP and AP than in healthy controls. The frequencies of tumor necrosis factor-α-expressing CD4(+) T cells and CD14(+) cells were higher in AP and CP, compared to healthy controls, respectively. Moreover, the frequency of IL-10 expressing CD14(+) cells was higher in CP, but not AP, compared to healthy controls CD4(+) T cells committed to IL-4 production was higher in CP than in healthy controls.


CONCLUSIONS
These results suggest the participation of CD11a in the pathogenesis of periodontal lesions and show distinct cellular sources of immunoregulatory cytokines in AP versus CP.
Lima
Patrícia Maria A
PM
Department of Morphology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Souza
Paulo Eduardo A
PE
Costa
José Eustáquio
JE
Gomez
Ricardo Santiago
RS
Gollob
Kenneth John
KJ
Dutra
Walderez Ornelas
WO
D000293:Adolescent; D000328:Adult; D010520:Aggressive Periodontitis / Q000097:blood* / Q000276:immunology; D015703:Antigens, CD / Q000097:blood; D018941:Antigens, CD19 / Q000097:blood; D000945:Antigens, Differentiation, T-Lymphocyte / Q000097:blood; D040881:CD11a Antigen / Q000097:blood; D039481:CD11b Antigen / Q000097:blood; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D055113:Chronic Periodontitis / Q000097:blood* / Q000276:immunology; D016207:Cytokines / Q000097:blood*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000276:immunology; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D007371:Interferon-gamma / Q000097:blood; D016753:Interleukin-10 / Q000097:blood; D018664:Interleukin-12 / Q000097:blood; D015847:Interleukin-4 / Q000097:blood; D037181:Lectins, C-Type / Q000097:blood; D007962:Leukocytes / Q000145:classification; D007963:Leukocytes, Mononuclear / Q000276:immunology*; D018950:Lipopolysaccharide Receptors / Q000097:blood; D016169:Lymphocyte Function-Associated Antigen-1 / Q000097:blood; D016177:Macrophage-1 Antigen / Q000097:blood; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D055815:Young Adult; D000099192:CD69 Antigens
D015703:Antigens, CD; D018941:Antigens, CD19; D000945:Antigens, Differentiation, T-Lymphocyte; D040881:CD11a Antigen; D039481:CD11b Antigen; D016207:Cytokines; D018836:Inflammation Mediators; D018799:Intercellular Adhesion Molecule-1; D007371:Interferon-gamma; D016753:Interleukin-10; D018664:Interleukin-12; D015847:Interleukin-4; D037181:Lectins, C-Type; D018950:Lipopolysaccharide Receptors; D016169:Lymphocyte Function-Associated Antigen-1; D016177:Macrophage-1 Antigen; D014409:Tumor Necrosis Factor-alpha; D000099192:CD69 Antigens; C509295:ITGAM protein, human