Allergic response to common environmental agents has been regarded as a main pathogenetic mechanism of bronchial asthma. However, allergic sensitization (atopy) can not be detected in a siginificant number of adult asthmatic patients. The etiology of nonatopic asthma has not yet been defined. To evaluate the possible involvement of autoimmune response against bronchial mucosa in the pathogenesis of nonatopic asthma, we performed indirect immunofluorescence staining of fresh frozen human bronchial mucosa tissue using serum samples from patients with atopic and nonatopic asthma, healthy controls, and patients with systemic lupus erythematosus. On immunostaining, circulating IgG autoantibodies against bronchial mucosa were detected in 2 (9.1%) of 22 patients with nonatopic asthma and in none of 22 patients with atopic asthma and of 22 healthy controls. IgG autoantibodies from the two patients with nonatopic asthma predominantly stained the cytoplasmic membrane of basal cells in bronchial epithelium. Serum samples from 10 patients with systemic lupus erythematosus immunostained the nucleus of epithelial cells in whole layer of bronchial epithelium. This study showed the presence of circulating IgG autoantibodies against the bronchial epithelial cell in a small portion of patients with nonatopic asthma. Further studies may be necessary to evaluate the possible involvement of autoimmune mechanism in the pathogenesis of nonatopic asthma.
Asthma/immunology* ; Autoantibodies/immunology* ; Autoantibodies/blood ; Bronchi/immunology* ; Epithelial Cells/immunology ; Human ; Immunity, Mucosal/immunology ; Respiratory Mucosa/immunology*

The pathogenetic mechanism of nonatopic asthma has not yet been defined. The idea of a possible involvement of autoimmunity in the pathogenesis of nonatopic asthma has been proposed by earlier studies. To evaluate the possible involvement of autoimmune response against bronchial epithelial cell in the pathogenesis of nonatopic asthma, we measured circulating autoantibodies to cultured human bronchial epithelial cell (BEAS-2B cell line) using enzyme-linked immunosorbent assay. We used stored serum samples form 38 age-matched healthy controls, 26 adult patients with atopic asthma, 16 adult patients with nonatopic asthma, and 12 adult patients with systemic lupus erythematosus. Levels of IgG autoantibodies to bronchial epithelial cell were significantly higher in patients with nonatopic asthma (mean+/-SD of absorbance values; 0.135+/-0.030) and systemic lupus erythematosus (0.293+/-0.181) than in healthy controls (0.112+/-0.016) and patients with atopic asthma (0.116+/-0.031) (p<0.05). This study showed that levels of circulating IgG autoantibodies to bronchial epithelial cell were increased in adult patients with nonatopic asthma. Further studies are needed to evaluate the possible involvement of autoimmune mechanism in the pathogenesis of nonatopic asthma.
Adult ; Asthma/*immunology ; Autoantibodies/*blood ; Bronchi/*immunology ; Cells, Cultured ; Epithelial Cells/immunology ; Human ; Hypersensitivity/immunology ; IgG/blood

OBJECTIVETo observe the immune reaction in the mixed culture of host lymphocytes with allogenic and host endothelial cells.

METHODSThe host epithelial cells and lymphocytes from burn patients and allogenic epithelial cells were mix-cultured in different ratios, so as to simulate the local immune micro-environment of host skin island in intermingled skin grafting. In addition, the cells from normal human subjects were also mix-cultured as control. The lymphocyte cpm values were detected by (3)H-TdR and HLA molecules and T cell subgroup were determined by immunohistological technique.

RESULTS(1) The lymphocyte proliferation reaction could be effectively inhibited by the epithelial cells from burn patients but not from normal control. (2) The inhibition of host lymphocyte proliferation could not be mediated by the HLA-DQ molecules of epithelium from burn patients. (3) The positive expression rate of HLA-DR of epithelia from burn patients was evidently higher that that from normal control (P < 0.05), (4) The CD8 expression of lymphocyte in burn patients was significantly higher than that in normal control (P < 0.01), while the CD4 expression in burn patients was lower than that in normal control (P < 0.01). But there was no obvious difference of the CD3 expression between patients and normal subjects (P > 0.05).

CONCLUSIONThe lymphocyte proliferation reaction could be obviously inhibited by the host epithelium, which might be related to the specific immune state of the host lymphocytes and epithelium of burn patients.

Cell Communication ; immunology ; physiology ; Cell Culture Techniques ; Cell Division ; Epithelial Cells ; immunology ; physiology ; Humans ; Lymphocytes ; immunology ; physiology ; Skin Transplantation ; immunology

Kidney dendritic cells(DC) play important roles in the pathogenesis of kidney diseases. Kidney DC presents anti-inflammatory effects in certain kidney diseases, sometimes presents pro-inflammation in other diseases, and sometimes their effects are changing in different stages of the disease, suggesting that the differentiation and function of kidney DC may be influenced by microenvironment. This article reviews the origin and distribution of kidney DC subsets and their roles in the pathogenesis of kidney diseases such as lupus nephritis and pyelonephritis, and the functional regulation of kidney DC by proximal tubule epithelial cells.
Cell Differentiation ; Dendritic Cells ; cytology ; immunology ; Epithelial Cells ; cytology ; Humans ; Inflammation ; immunology ; Kidney ; cytology ; Kidney Diseases ; immunology ; Lupus Nephritis ; immunology ; Pyelonephritis ; immunology

OBJECTIVETo establish the model of cellular inflammatory responses of gingival epithelial cells in vitro induced by Porphyromonas gingivalis vesicle and to probe into the pathogenesis of Porphyromonas gingivalis in periodontitis.

METHODSThe effect of Porphyromonas gingivalis vesicle on prostaglandin E(2) (PGE(2)) production of gingival epithelial cells was detected by ELISA and the effects of Porphyromonas gingivalis vesicle on cyclooxygenase-2 (COX-2), interleukin (IL)-6 and IL-8 mRNA expression in gingival epithelial cells were determined by Real-time reverse transcription-polymerase chain reaction (RT-PCR).

RESULTSPorphyromonas gingivalis vesicle dose-dependently induced PGE(2) production and up-regulated COX-2, IL-6 and IL-8 mRNA expression in gingival epithelial cells significantly.

CONCLUSIONSCellular inflammatory responses of gingival epithelial cells induced by Porphyromonas gingivalis vesicle may contribute to the initiation and progression of periodontitis.

Bacterial Adhesion ; Cells, Cultured ; Cyclooxygenase 2 ; immunology ; metabolism ; Dinoprostone ; immunology ; metabolism ; Epithelial Cells ; immunology ; metabolism ; microbiology ; Gingiva ; immunology ; metabolism ; microbiology ; Humans ; Interleukin-6 ; immunology ; metabolism ; Interleukin-8 ; immunology ; metabolism ; Porphyromonas gingivalis ; immunology ; pathogenicity

Ambystoma mexicanum/immunology* ; Amputation ; Animals ; Biomarkers/metabolism* ; Blastomeres/immunology* ; Cell Lineage/immunology* ; Connective Tissue Cells/immunology* ; Epithelial Cells/immunology* ; Forelimb ; Gene Expression ; High-Throughput Nucleotide Sequencing ; Humans ; Immunity ; Peroxiredoxins/immunology* ; Regeneration/immunology* ; Regenerative Medicine/methods* ; Single-Cell Analysis/methods*

Epithelial Cells ; immunology ; Humans ; Pulmonary Disease, Chronic Obstructive ; physiopathology ; Respiratory System ; physiopathology

Adaptive Immunity ; Bacterial Infections ; immunology ; prevention & control ; Biological Evolution ; Epithelial Cells ; immunology ; Gastrointestinal Diseases ; immunology ; prevention & control ; Humans ; Immunity, Innate ; Lymphocytes ; immunology ; Mucous Membrane ; cytology ; immunology ; Receptors, Pattern Recognition ; immunology ; Toll-Like Receptors ; immunology

Helicobacter pylori (H. pylori) has been a major concern as a gastric pathogen with unique features since discovered in the end of the 20th century. Recent data on comparative genome study have revealed that H. pylori has successfully survived with its host though over 58,000 years of evolution and migration from continent to continent. To maintain the symbiotic relationship with human, H. pylori has come up with ways to induce host tolerance as well as exert harmful injuries. Studies about H. pylori have accumulated the knowledge about how the cellular and molecular interactions are controlled and regulated to decide whether the symbiotic relationship is directed to diseases or peaceful mutualism. We reviewed recent literatures and research outcomes about the H. pylori and host interaction in molecular and cellular basis.
Adaptive Immunity ; Epithelial Cells/metabolism/microbiology/pathology ; Helicobacter Infections/immunology/metabolism/*pathology ; Helicobacter pylori/*immunology ; *Host-Pathogen Interactions ; Humans ; Symbiosis ; T-Lymphocytes/immunology/metabolism

OBJECTIVETo explore the feature of nasal mucosa remodeling in experimental allergic rhinitis.

METHODSTwenty-four male Hartley guinea pigs (4 weeks, 250 -300 g) were randomly divided into four groups (control group and allergen exposure groups 1 - 3), each group had 6 guinea pigs. Allergen exposure animals were sensitized by intraperitoneal (ip) injection of ovalbumin (OVA). Sensitized guinea pigs were subjected to either brief or prolonged exposure to allergen. Both brief exposure group (allergen exposure groups) and prolonged exposure group (allergen exposure group 2 and 3) received a daily intranasal challenge with 5% OVA in 0.9% saline from Day 22 to Day 28, the prolonged exposure group (allergen exposure group 2 and 3) followed by twice weekly exposure to 5% OVA intranasal for an additional 8 and 12 weeks respectively. Control animals were given saline only. At 24 h after the last intranasal challenge, the guinea pigs were killed and the heads of the animals were removed and fixed in 10% neutral buffered formalin for 24 hours, then decalcified in 5% trichloroacetic acid for 10 days. The tissue blocks were embedded in paraffin. The paraffin sections 3 microm thick were stained with hematoxylin and eosin (HE), alcian blue (pH, 2. 6)-periodic acid-Schiff (AB-PAS), and Masson's Trichrome (MT). The infiltrating eosinophils in nasal mucosa were examined, AB-PAS-positive cells in the surface epithelium in nasal septal mucosa were counted. The percentage area of MT stained extracellular matrix in septal mucosa and conchae and damage of epithelium were determined by an image analyzer.

RESULTSThe control group only presented a few eosinophils. Significant eosinophil infiltration was observed in the sensitized groups. Compared with control group (intact epithelium 87.7% +/- 11.1%), there was no significant epithelial damage in 1 week exposure group. Significant epithelial damage were observed in 8 and 12 weeks groups (intact epithelium 36.7% +/- 16.9%, 37.9% +/- 12.9%, respectively). An increase in AB-PAS-positive cells was observed in the mucosa of nasal septum in the prolonged allergen exposure groups, but not in the brief allergic inflammation group in comparison with the control. The brief OVA exposure group did not show increased collagen fibrils within the mucosa of nasal septum and conchae. In contrast, after prolonged OVA exposure an increase in matrix was observed. Furthermore, in both the nasal septum and conchae, significant increasing of ECM deposition was found in a further prolonged exposure for 12 weeks compared to 8 weeks.

CONCLUSIONSEpithelial damage, goblet cells hyperplasia and extracellular matrix deposition were observed as the features of remodeling in this guinea pig model of allergic rhinitis.

Animals ; Disease Models, Animal ; Eosinophils ; immunology ; Epithelial Cells ; pathology ; Extracellular Matrix ; pathology ; Goblet Cells ; pathology ; Guinea Pigs ; Male ; Mice ; Nasal Mucosa ; cytology ; pathology ; Rhinitis, Allergic, Perennial ; immunology ; pathology