Periodontitis is an inflammatory disease involving the destruction of both soft and hard tissue in the periodontal region. Although dysbiosis of the local microbial community initiates local inflammation, over-activation of the host immune response directly activates osteoclastic activity and alveolar bone loss. Many studies have reported on the cytokine network involved in periodontitis and its crucial and pleiotropic effect on the recruitment of specific immunocytes, control of pathobionts and induction or suppression of osteoclastic activity. Nonetheless, particularities in the stimulation of pathogens in the oral cavity that lead to the specific and complex periodontal cytokine network are far from clarified. Thus, in this review, we begin with an up-to-date aetiological hypothesis of periodontal disease and summarize the roles of cytokines in the host immune response. In addition, we also summarize the latest cytokine-related therapeutic measures for periodontal disease.
Alveolar Bone Loss ; etiology ; Cytokines ; metabolism ; physiology ; Humans ; Inflammation ; Periodontal Diseases ; Periodontitis ; immunology ; microbiology ; Tumor Necrosis Factor-alpha ; physiology

OBJECTIVETo explore the immune mechanism of moxibustion on protecting gastric mucosa injury.

METHODSForty healthy SD rats were randomly divided into four groups: a blank group, a model group, a moxibustion acupoint group and a moxibustion non-acupoint group, 10 rats in each one. Eight days before model establishment, moxibustion at "Zusanli" (ST 36), "Zhongwan" (CV 12), "Guanyuan" (CV 4), "Pishu" (BL 20) and "Weishu" (BL 21) was applied in the moxibustion acupoint group while these acupoints' controlled points were selected in the moxibustion non-acupoint group, and no treatment was given in the model group, once a day in three groups for continuous 16 days. The helicobacter pylori (Hp) model was established by intragastric administration of Hp. HE staining microscopic examination was used to observe inflammation severity in gastric mucosa, and enzyme-linked immunosorbent assay (ELISA) was adapted to measure content of heat shock protein (HSP) 72, TNF-alpha and IL-1beta, and real-time quantitative PCR was used to measure the expression of TLR2 mRNA, TLR4 mRNA, CD14 mRNA and MyD88 mRNA in peripheral blood mononuclear cells, and western blot method was used to measure content of NFkappaB and IkappaBalpha in peripheral blood mononuclear cells.

RESULTSCompared with the blank group, the expression of HP could be seen in the smear of gastric mucosa by Gram's staining in the model group; the inflammation severity score was obviously increased as well as content of serum HSP 72 and TNF-alpha and IL-1beta in gastric tissue; and expression of TLR2, 4 mRNA, CD14 mRNA, MyD88 mRNA, NFkappaB was increased (P < 0.01), but the expression of IkappaBalpha was reduced (P < 0.05). After the moxibustion, the inflammation severity score was reduced in the moxibustion acupoint group, and the content of serum HSP 72 was increased, and the expression of TNF-alpha and IL-1beta in gastric tissue and expression of TLR2 mRNA, TLR4 mRNA, CD14 mRNA, MyD88 mRNA and NFkappaB were reduced (P < 0.01), but the expression of IkappaBalpha was increased (P < 0.05). The differences between the moxibustion non-acupoint group and the model group were not significant (P > 0.05).

CONCLUSIONThe pretreatment of moxibustion at acupoints could induce the over expression of serum HSP 72. By combining TLR 2 and 4 receptors to trigger receptor signal transduction pathways, the releases of downstream signal substances are regulated; as a result, the releases of related immune substances are regulated to relieve the gastric mucosa injury of rats with HP gastritis.

Acupuncture Points ; Animals ; Female ; Gastritis ; immunology ; therapy ; Helicobacter Infections ; genetics ; immunology ; therapy ; Helicobacter pylori ; physiology ; Humans ; Interleukin-1beta ; genetics ; immunology ; Male ; Moxibustion ; NF-kappa B ; genetics ; immunology ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; genetics ; immunology

OBJECTIVETo observe the effect of volatile oil of Schizonepetae Herba (VOSH), and its essential components-menthone and pulegone against anti-influenza virus A/PR/8/34 (H1N1) in vivo and in vitro, as well as the signaling mechanism of its toll-like receptor/interferon (TLR/IFN).

METHODThe lung-adapted PR-8 virus model was prepared in mice. They were administered with preventive and therapeutic drugs, and the hemagglutination titer of model animals was determined to evaluate in vivo effect against H1N1. ELISA test was conducted to observe the effect on IFN-alpha, IFN-beta, IL-2, IL-6 and TNF-alpha in serum, as well as IFN-beta secretion in H1N1 infected MDCK supernatant. Real-time RT-PCR was employed to observe the expression levels of IRAK4 and TLR3 mRNA.

RESULTThe in vivo experiment shows that the hemagglutination titer was significantly decreased when the mice were treated with VOSH (0.266 mg x kg(-1)), menthone(0.5 mg x kg(-1)) and pulegone (0.19 mg x kg(-1)) in therapeutic way; VOSH (0.226 mg x kg(-1)) had a significant effect on increasing serum levels of IFN-alpha, IL-2; Methone (0.5 mg x kg(-1)) had a significant effect on increasing serum levels of IFN-beta; Methone (0.5 mg x kg(-1)) and pulegone (0.19 mg x kg(-1)) had a significant effect on decreasing serum levels of IL-6; VOSH (0.452, 0.226 mg x kg(-1)) and pulegone (0.19 mg x kg(-1)) had a significant effect on decreasing serum levels TNF-alpha. The in vitro experiment showed that the expression levels of IRAK4 mRNA and IFN-beta were significantly increased in VOHS (0.1 g x L(-1)) and pulegone (0.1 g x L(-1)) groups; and the menthone (0.25 g x L(-1)) group showed a significant rise in the expression levels of IRAK4 mRNA, but a notable decline in TLR3 mRNA.

CONCLUSIONThe administration with VOSH, methone and pulegone in therapeutic way can significantly decrease the hemagglutination titer, which demonstrates the anti-virus effect of the administration in therapeutic way, but no notable efficacy of the administration in preventive way. The in vivo anti-virus mechanism is related to regulation of IFN-alpha, IFN-beta and IL-2.

Animals ; Drugs, Chinese Herbal ; pharmacology ; Female ; Humans ; Influenza A Virus, H1N1 Subtype ; drug effects ; physiology ; Influenza, Human ; drug therapy ; genetics ; immunology ; virology ; Interferon-alpha ; genetics ; immunology ; Interleukin-1 Receptor-Associated Kinases ; Interleukin-2 ; genetics ; immunology ; Interleukin-6 ; genetics ; immunology ; Lamiaceae ; chemistry ; Male ; Mice ; Oils, Volatile ; pharmacology ; Tumor Necrosis Factor-alpha ; genetics ; immunology

This study is to investigate the anti-allergic effect of anthocyanidin and to explore its possible mechanism. The experiments of passive cutaneous anaphylaxis reaction (PCA) and colorimetry were used to determine the effect of anthocyanidin on degranulation of mast cells in vivo. For in vitro study, various concentrations of anthocyanidin (100, 50 and 25 micromol x L(-1)) were added to the culture medium of mast cells cultured with 100 microg x L(-1) of dinitrophenyl (DNP) specific IgE overnight. The azelastine (100 micromol x L(-1)) was selected as the positive control. The antigen (DNP-human serum albumin, DNP-HAS)-induced release of degranulation was measured by enzymatic assay, histamine was determined by EIA, and interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were measured by Western blotting, separately. In addition, the effects of anthocyanidin on phosphorylation of NF-kappaB, p38MAPK and Akt were observed by Western blotting. The results showed that treatments with anthocyanidin (100 and 50 mg x kg(-1)) were followed by a decrease in PCA of rats. Anthocyanidin (100 and 50 micromol x L(-1)) obviously suppressed the degranulation from mast cells, whereas results from anthocyanidin (100 and 50 micromol x L(-1)) group indicated significant inhibitory effect on histamine, the calcium uptake, TNF-alpha, IL-6, phosphorylation of NF-kappaB, p38MAPK and Akt of mast cells induced by antigen. Anthocyanidin may suppress the anaphylactic reaction by inhibiting the action of mast cells. NF-kappaB, p38MAPK and Akt at least in part contribute to this event.
Animals ; Anthocyanins ; pharmacology ; Anti-Allergic Agents ; pharmacology ; Calcium ; metabolism ; Cell Degranulation ; drug effects ; Histamine Release ; drug effects ; Immunoglobulin E ; immunology ; Interleukin-6 ; metabolism ; Male ; Mast Cells ; immunology ; metabolism ; physiology ; Passive Cutaneous Anaphylaxis ; drug effects ; Proto-Oncogene Proteins c-akt ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Transcription Factor RelA ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism ; p38 Mitogen-Activated Protein Kinases ; metabolism

The purpose of our study was to investigate changes in immunological parameters induced by weaning stress (including milk restriction) in calves. Fifteen Holstein calves were subjected to weaning at 6 weeks of age. Blood samples were collected at -14, -7, -2, 1, 3, and 5 days post-weaning (DPW; 0 DPW = 42 days). Weaning caused significant (p < 0.01) increases in the neutrophil (NE):lymphocyte (LY) ratio at 5 DPW with a significant (p < 0.05) reduction of LYs. The concentration of acute-phase proteins (haptoglobin and serum amyloid A) also increased significantly (p < 0.05) at 3 and 5 DPW compared to -2 DPW. Levels of the iron-binding protein lactoferrin decreased significantly (p < 0.05) after weaning. Serum tumor necrosis factor-alpha and cortisol levels were elevated (p < 0.05) at 3 DPW, while those of serum interferon-gamma decreased (p < 0.05) at 1 and 3 DPW compared to levels observed before weaning. Weaning significantly (p < 0.05) decreased the percentage of CD25+ T cells in the peripheral blood. In conclusion, weaning stress affected the NE:LY ratio along with the levels of acute phase proteins, lactoferrin, cortisol, and inflammatory cytokines in the peripheral blood of calves. Weaning stress may induce an acute phase response possibly through the elevation of cortisol production and modulation of inflammatory cytokines.
Acute-Phase Proteins/*immunology/metabolism ; Acute-Phase Reaction/immunology/*veterinary ; Animals ; Cattle/*immunology ; Female ; Flow Cytometry ; Haptoglobins/analysis/immunology ; Hydrocortisone/blood/immunology ; Interferon-gamma/blood/immunology ; Lactoferrin/analysis/immunology ; Leukocyte Count/veterinary ; Leukocytes/cytology/*immunology ; Male ; Serum Amyloid A Protein/analysis/immunology ; Stress, Physiological/*physiology ; Tumor Necrosis Factor-alpha/blood/immunology ; Weaning

Genetic Predisposition to Disease ; genetics ; Genotype ; HLA Antigens ; genetics ; Hepatitis B virus ; genetics ; physiology ; Hepatitis B, Chronic ; genetics ; immunology ; virology ; Humans ; Interleukin-10 ; genetics ; Mutation ; Polymorphism, Single Nucleotide ; Promoter Regions, Genetic ; genetics ; Tumor Necrosis Factor-alpha ; genetics

OBJECTIVETo explore the effect of Yinqiao detoxifcation oral liquid on activity of natural killer cells (NK) and serum content of TNF-alpha, TGF-beta1 of BALB/C nude mouse infected by influenza virus.

METHODTo establish infected mice model by FM1 followed by intragastric administration of Yinqiao detoxifcation oral liquid for treatment. LDH method was used to observe NK cells. ELISA method was used to determine the levels of TNF-alpha, TGF-beta1, in serum on 1st, 3rd, 5th, 7th days after infection.

RESULTComparing to the normal group, the NK activity of the model group was significantly increased on 1 dpi (day post infection), and significantly decreased on 3, 5, 7 dpi. The NK activity of three dosage groups (5, 10, 20 g x kg(-1)) of Yinqiao detoxifcation oral liquid were respectively higher than that of the model on 3, 5, 7 dpi, especially with high dose (P < 0.01). The serum level of TNF-alpha and TGF-beta1 of model group is higher than that of normal group on 1, 3, 5, 7 d. Compared with model group, the serum level of Yinqiao detoxifcation oral liquid groups (5, 10, 20 g x kg(-1)) were decreased in different degree on every time point, especially the serum level of the higher dose of Yinqiao detoxifcation oral liquid decreased on 3 dpi (P < 0.05), Yinqiao detoxifcation oral liquid inhibit the serum level of TGF-beta1 in a dose-dependent manner.

CONCLUSIONYinqiao detoxifcation oral liquid could enhance the activity of NK cell and decrease the serum level of TNF-alpha and TGF-beta1 of the mice infected by influenza virus.

Administration, Oral ; Animals ; Disease Models, Animal ; Drugs, Chinese Herbal ; administration & dosage ; Humans ; Influenza A virus ; immunology ; physiology ; Influenza, Human ; drug therapy ; immunology ; virology ; Killer Cells, Natural ; drug effects ; immunology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Random Allocation ; Transforming Growth Factor beta1 ; immunology ; Tumor Necrosis Factor-alpha ; immunology

OBJECTIVETo study the roles of serum and urinary interleukins (IL)-13Ralpha2, IL-4, IL-6, IL-8 and tumor necrosis factor-alpha(TNF-alpha) in pediatric Henoch-Schonlein purpura (HSP).

METHODSSerum and urinary levels of IL-13Ralpha2, IL-4, IL-6, IL-8 and TNF-alpha were examined using ELISA in 52 children with HSP and 45 healthy children. The results were compared between the two groups.

RESULTSSerum levels of IL-13Ralpha2, IL-4, IL-6, IL-8 and TNF-alpha in HSP patients with or without renal lesions were higher than those in the control group (p<0.01 or 0.05). Urinary levels of IL-6 and TNF-alpha in HSP patients without renal lesions were higher than those in the control group (p<0.05). Except for urinary levels of IL-6 and TNF-alpha, urinary IL-13Ralpha2 levels in HSP patients with renal lesions (HSPN) were higher than those in the control group (p<0.05).

CONCLUSIONSCytokines IL-13Ralpha2, IL-4, IL-6, IL-8 and TNF-alpha may play roles in the pathogenesis of pediatric HSP/HSPN.

Adolescent ; Child ; Child, Preschool ; Cytokines ; physiology ; Female ; Humans ; Interleukin-13 Receptor alpha2 Subunit ; blood ; physiology ; Interleukin-6 ; physiology ; Male ; Purpura, Schoenlein-Henoch ; etiology ; immunology ; Tumor Necrosis Factor-alpha ; physiology

Dominant inflammatory cytokines might be different depending on the underlying causes of acute lung injury (ALI). The role of kertinocyte-derived chemokine (KC), a potent chemoattractant for neutrophils, has not been clearly established in hemorrhage-induced ALI. In this study, lung injury and cytokine expressison were evaluated in LPS- or hemorrhage-induced ALI models of BALB/c mice. The myeloperoxidase activities at 4 hr after hemorrhage and LPS-injection were 47.4+/-13.0 and 56.5+/-16.4 U/g, respectively. NF-kappa B activity peaked at 4 hr after hemorrhage, which was suppressed to the control level by anti-high mobility group B1 (HMGB1) antibody. Lung expressions of TNF-alpha, MIP-2, and IL-1beta were increased by LPS injection. However, there was only a minimal increase in IL-1beta and no expressions of TNF-alpha or MIP-2 in hemorrhage-induced ALI. In contrast, lung KC increased significantly at 4 hr after hemorrhage compared to control levels (83.1+/-12.3 vs. 14.2+/-1.6 pg/mL/mg by ELISA) (P<0.05). By immunohistochemical staining, lung neutrophils stained positive for KC. Increased KC was also observed in bronchoalveolar lavage fluid and plasma. KC plays an important role in hemorrhage-induced ALI.
Acute Lung Injury/etiology/*metabolism ; Animals ; Antibodies/immunology/metabolism ; Chemokine CXCL2/analysis ; Chemokines/analysis/blood/*physiology ; Chickens ; HMGB1 Protein/metabolism ; Humans ; Interleukin-1beta/analysis ; Lipopolysaccharides/toxicity ; Mice ; Mice, Inbred BALB C ; NF-kappa B/metabolism ; Neutrophils/immunology/metabolism ; Peroxidase/analysis ; Shock, Hemorrhagic/*complications ; Time Factors ; Tumor Necrosis Factor-alpha/analysis

Cytokines ; physiology ; Humans ; Interferon-gamma ; physiology ; Interleukin-1 ; physiology ; Interleukin-10 ; physiology ; Interleukin-12 ; physiology ; Interleukin-6 ; physiology ; Interleukin-8 ; physiology ; Rotavirus Infections ; immunology ; Tumor Necrosis Factor-alpha ; physiology