acid-phosphatase and Dermatitis--Atopic

The aim of this study was to investigate how atopic dermatitis (AD) contributes to root resorption during orthodontic tooth movement.. Atopic dermatitis model mice and wild-type mice were subjected to an excessive orthodontic force (OF) to induce movement of the upper first molars. The expression levels of the tartrate-resistant acid phosphatase (TRAP), IL-17, IL-6, and RANKL proteins were determined in the periodontal ligament (PDL) by an immunohistochemical analysis. Furthermore, the effects of the compression force on co-cultures of CD4(+) cells from AD patients or healthy individuals and human PDL cells were investigated with regard to the levels of secretion and mRNA expression of IL-17, IL-6, RANKL, and osteoprotegerin.. The immunoreactivities for TRAP, IL-17, IL-6, and RANKL in the AD group were found to be significantly increased. The double immunofluorescence analysis for IL-17/CD4 detected immunoreaction. The secretion of IL-17, IL-6, and RANKL, and the mRNA levels of IL-6 and RANKL in the AD patients were increased compared with those in healthy individuals.. Th17 cells may therefore be associated with the deterioration of root resorption of AD mice, and may explain why AD patients are more susceptible to root resorption than healthy individuals when an excessive OF is applied.

Topics: Acid Phosphatase; Adult; Animals; CD4-Positive T-Lymphocytes; Cell Culture Techniques; Coculture Techniques; Dermatitis, Atopic; Disease Models, Animal; Female; Humans; Immunoglobulin E; Interleukin-17; Interleukin-6; Isoenzymes; Male; Mice; Mice, Inbred BALB C; Osteoprotegerin; Periodontal Ligament; RANK Ligand; Root Resorption; Stress, Mechanical; Tartrate-Resistant Acid Phosphatase; Th17 Cells; Tooth Movement Techniques; Young Adult

The neutrophils in 2 patients with atopic disease were studied. Ultrastructurally, a number of abnormal azurophilic granules (AG) with low electron-density (Case 1) and secondary lysosomes with "myelinoid membranes" figures (Case 2) were found. Myeloperoxidase (MPO) and acid phosphatase activity were detected by light cytochemical techniques, and showed significantly low values. The deficiency of MPO and abnormal distribution of AG were also demonstrated by electron microscopic cytochemical technique. The neutrophils from the parents revealed changes similar to the patients. This study suggests that since genetic partial deficiency of neutrophil AG enzymes existed, the phagocytosed substances were only partially degraded, leading to accumulation of substances with antigenicity, and became trigger event of atopic disease.

Topics: Acid Phosphatase; Adolescent; Alkaline Phosphatase; Child, Preschool; Dermatitis, Atopic; Histocytochemistry; Humans; Male; Microscopy, Electron; Neutrophils; Peroxidase

Neutrophils (PMN) from 20 patients with atopic disease (atopy), the parents of 8 of the patients and 10 normal controls were studied by light-microscopic cytochemistry. The results revealed that myeloperoxidase (MPO) and acid phosphatase (ACP) activities in PMN in all cases significantly decreased and alkaline phosphatase activity was normal. Parents or parent of 7 of those patients had PMN enzyme deficiency similar to that of the patients. The results indicated that a primary combined and partial deficiency of MPO and ACP in PMN azurophilic granule existed in atopy. It is postulated that the deficiency led to reduction of PMN bactericidal power and delay of bactericidal action. Foreign bodies which were partially degraded could possess antigenic property. This is believed to be the important cytobiological mechanism of the tendency toward infections and formation of sensitive antigen in atopy.

Topics: Acid Phosphatase; Adolescent; Adult; Alkaline Phosphatase; Asthma; Child; Child, Preschool; Dermatitis, Atopic; Female; Humans; Male; Middle Aged; Neutrophils; Peroxidase; Rhinitis, Allergic, Perennial

Topics: Acid Phosphatase; Adolescent; Adult; Alkaline Phosphatase; Dermatitis, Atopic; Female; Glycerolphosphate Dehydrogenase; Humans; Lymphocytes; Male; Neutrophils; Peroxidase; Succinate Dehydrogenase

Topics: Acid Phosphatase; Adenosine Triphosphatases; Administration, Topical; Adolescent; Adult; Aged; Alkaline Phosphatase; Anti-Inflammatory Agents; Dermatitis, Atopic; Female; Humans; Hydrocortisone; Male; Middle Aged; Skin

Topics: Acid Phosphatase; Adenosine Triphosphatases; Adult; Alkaline Phosphatase; Capillaries; Dermatitis, Atopic; Esterases; Histocytochemistry; Humans; Isocitrate Dehydrogenase; L-Lactate Dehydrogenase; Leucyl Aminopeptidase; NADP; Nucleotidases; Staining and Labeling

Topics: Acid Phosphatase; Dermatitis, Atopic; Esterases; Fructose-Bisphosphate Aldolase; Glucosephosphate Dehydrogenase; Glucuronidase; Glutamate Dehydrogenase; Glyceraldehyde-3-Phosphate Dehydrogenases; Glycerolphosphate Dehydrogenase; Histocytochemistry; Humans; L-Lactate Dehydrogenase; Leucyl Aminopeptidase; Malate Dehydrogenase; Phosphogluconate Dehydrogenase; Psoriasis

Topics: Acid Phosphatase; Alkaline Phosphatase; Amino Acids; Animals; Anura; Dermatitis, Atopic; Eels; Haplorhini; Humans; Lipids; Mucins; Mucus; Neuraminic Acids; Polysaccharides; Proteins; Saliva; Sweat; Sweat Glands

Topics: Acid Phosphatase; Alkaline Phosphatase; Asthma; Dermatitis, Atopic; Eosinophils; Exudates and Transudates; Histocytochemistry; Humans; Injections, Intravenous; Leukocytes; Pyrogens; Skin