Host genetic predispositions to dysregulated immune response can influence the development of the aggressive form of periodontitis (AgP) through susceptibility to oral dysbiosis and subsequent host-microbe interaction. This case-control study aimed to perform a multilocus analysis of functional variants in selected interleukin (IL) genes in patients with the generalized form of AgP in a homogenous population. Twelve polymorphisms in IL-1 gene cluster, IL-6 and its receptor, IL-10, IL-17A, and IL-18 were determined in 91 AgP patients and 210 controls. Analysis of seven selected periodontal bacteria in subgingival sulci/pockets was performed with a commercial DNA-microarray kit in a subgroup of 76 individuals. The pilot in vitro study included stimulation of peripheral blood monocytes (PBMC) from 20 individuals with periodontal bacteria and measurement of IL-10 levels using the Luminex method. Only the unctional polymorphism IL‑10-1087 A/G (rs1800896) and specific IL-10 haplotypes were associated with the development of the disease (P < 0.05, Pcorr > 0.05). Four bacterial species occurred more frequently in AgP than in controls (P < 0.01, Pcorr < 0.05). Elevated IL-10 levels were found in AgP patients, carriers of IL‑10-1087GG genotype, and PBMCs stimulated by periodontal bacteria (P < 0.05, Pcorr > 0.05). We therefore conclude that a combination of genetic predisposition to the altered expression of IL-10 and the presence of specific periodontal bacteria may contribute to Th1/Th2 balance disruption and AgP development.
- Klíčová slova
- aggressive periodontitis, genetic predisposition, inflammation, interleukin, oral bacteria, polymorphism,
- MeSH
- agresivní parodontitida genetika imunologie mikrobiologie MeSH
- alely MeSH
- Bacteria genetika MeSH
- dospělí MeSH
- frekvence genu genetika MeSH
- genetická predispozice k nemoci genetika MeSH
- genotyp MeSH
- haplotypy genetika MeSH
- interleukin-1 genetika MeSH
- interleukin-10 genetika MeSH
- interleukin-17 genetika MeSH
- interleukin-18 genetika MeSH
- interleukin-6 genetika MeSH
- interleukiny genetika metabolismus MeSH
- jednonukleotidový polymorfismus genetika MeSH
- lidé MeSH
- parodontitida genetika imunologie MeSH
- studie případů a kontrol MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Geografické názvy
- Česká republika epidemiologie MeSH
- Názvy látek
- interleukin-1 MeSH
- interleukin-10 MeSH
- interleukin-17 MeSH
- interleukin-18 MeSH
- interleukin-6 MeSH
- interleukiny MeSH
Fusarium-derived mycotoxin deoxynivalenol (DON) usually induces diarrhea, vomiting and gastrointestinal inflammation. We studied the cytotoxic effect of DON on porcine small intestinal epithelium using the intestinal porcine epithelial cell line IPEC-J2. We screened out differentially expressed genes (DEGs) using RNA-seq and identified 320 upregulated genes and 160 downregulated genes. The enrichment pathways of these DEGs focused on immune-related pathways. DON induced proinflammatory gene expression, including cytokines, chemokines and other inflammation-related genes. DON increased IL1A, IL6 and TNF-α release and DON activated the phosphorylation of extracellular signal-regulated kinase-1 and-2 (ERK1/2), JUN N-terminal kinase (JNK) and p38 MAPK. A p38 inhibitor attenuated DON-induced IL6, TNF-α, CXCL2, CXCL8, IL12A, IL1A, CCL20, CCL4 and IL15 production, while an ERK1/2 inhibitor had only a small inhibitory effect on IL15 and IL6. An inhibitor of p38 MAPK decreased the release of IL1A, IL6 and TNF-α and an inhibitor of ERK1/2 partly attenuated protein levels of IL6. These data demonstrate that DON induces proinflammatory factor production in IPEC-J2 cells by activating p38 and ERK1/2.
- Klíčová slova
- IPEC-J2 cells, MAPKs, RNA-seq, deoxynivalenol, inflammation,
- MeSH
- buněčné linie MeSH
- epitelové buňky účinky léků imunologie metabolismus MeSH
- interleukin-1 genetika MeSH
- interleukin-6 genetika MeSH
- MAP kinasový signální systém účinky léků genetika imunologie MeSH
- mitogenem aktivované proteinkinasy p38 metabolismus MeSH
- prasata MeSH
- střevní sliznice účinky léků imunologie metabolismus MeSH
- TNF-alfa genetika MeSH
- transkriptom účinky léků MeSH
- trichotheceny toxicita MeSH
- viabilita buněk účinky léků MeSH
- zánět MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- deoxynivalenol MeSH Prohlížeč
- interleukin-1 MeSH
- interleukin-6 MeSH
- mitogenem aktivované proteinkinasy p38 MeSH
- TNF-alfa MeSH
- trichotheceny MeSH
Overactivation of the innate immune system together with the impaired downstream pathway of type I interferon-responding genes is a hallmark of rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and systemic sclerosis (SSc). To date, limited data on the cross-disease innate gene signature exists among those diseases. We compared therefore an innate gene signature of Toll-like receptors (TLRs), seven key members of the interleukin (IL)1/IL1R family, and CXCL8/IL8 in peripheral blood mononuclear cells from well-defined patients with active stages of RA (n = 36, DAS28 ≥ 3.2), SLE (n = 28, SLEDAI > 6), and SSc (n = 22, revised EUSTAR index > 2.25). Emerging diversity and abundance of the innate signature in RA patients were detected: RA was characterized by the upregulation of TLR3, TLR5, IL1RAP/IL1R3, IL18R1, and SIGIRR/IL1R8 when compared to SSc (P corr < 0.02) and of TLR2, TLR5, and SIGIRR/IL1R8 when compared to SLE (P corr < 0.02). Applying the association rule analysis, six rules (combinations and expression of genes describing disease) were identified for RA (most frequently included high TLR3 and/or IL1RAP/IL1R3) and three rules for SLE (low IL1RN and IL18R1) and SSc (low TLR5 and IL18R1). This first cross-disease study identified emerging heterogeneity in the innate signature of RA patients with many upregulated innate genes compared to that of SLE and SSc.
- MeSH
- dospělí MeSH
- interleukin-1 genetika metabolismus MeSH
- interleukin-8 genetika metabolismus MeSH
- leukocyty mononukleární metabolismus MeSH
- lidé středního věku MeSH
- lidé MeSH
- přirozená imunita genetika MeSH
- receptory interleukinu-1 - typ I genetika metabolismus MeSH
- revmatoidní artritida krev genetika imunologie MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- systémová sklerodermie krev genetika imunologie MeSH
- systémový lupus erythematodes krev genetika imunologie MeSH
- toll-like receptory genetika metabolismus MeSH
- transkriptom MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- interleukin-1 MeSH
- interleukin-8 MeSH
- receptory interleukinu-1 - typ I MeSH
- toll-like receptory MeSH
BACKGROUND: Recurrent aphthous stomatitis (RAS) is one of the most common oral chronic ulcerative disease in which proinflammatory cytokines such as interleukin-1 (IL-1) and interleukin-6 (IL-6) are thought to play an important role. The aim of this study was to investigate the possible association between polymorphisms in the IL-1 cytokine family, IL-6 or its receptor and RAS in the Czech population. METHODS: A total of 248 subjects, 184 healthy controls, and 64 patients with RAS were genotyped for IL-1A-889C>T, IL-1B-511C>T, IL-1B+3953C>T, IL-1RN86 bp variable number of tandem repeats (VNTRs) in intron 2, IL-6-597G>A, IL-6-572G>C, IL-6-174G>C, and IL-6R+48992A>C by polymerase chain reaction (PCR) methods. RESULTS: No significant differences between investigated polymorphisms in healthy subjects and patients with RAS were detected (P>.05). In addition, complex analysis also revealed similar IL-1 or IL-6 haplotype frequencies between both groups (P>.05). CONCLUSIONS: In conclusion, IL-1 and IL-6 or its receptor gene variants cannot be used as markers for identification of Czech patients with increased risk of recurrent aphthous stomatitis.
- Klíčová slova
- aphthous stomatitis, case-control study, gene polymorphism, interleukin-1, interleukin-6,
- MeSH
- aftózní stomatitida genetika MeSH
- dospělí MeSH
- genetické asociační studie MeSH
- interleukin-1 genetika MeSH
- interleukin-6 genetika MeSH
- jednonukleotidový polymorfismus * MeSH
- lidé středního věku MeSH
- lidé MeSH
- recidiva MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- interleukin-1 MeSH
- interleukin-6 MeSH
Interleukin 1 (IL-1) family is a group of cytokines with multiple local and systemic effects, which regulates both innate and adaptive immune responses. Generally, most IL-1 family cytokines express prevailing pro-inflammatory activities (IL-1α, IL-1β, IL-18, IL-33, IL-36 α, β, γ), whereas others are anti-inflammatory (IL-1Ra (IL-1 receptor antagonist), IL-36Ra, IL-38, IL-37). In addition to their immunomodulatory roles, some of them are also involved in the physiological modulation of homeostatic processes and directly affect mRNA transcription. IL-1 family cytokines bind to specific receptors composed of a ligand-binding chain and an accessory chain. The pro-inflammatory effects of IL-1 family cytokines are regulated on the level of transcription, enzymatic processing of precursors, release of soluble antagonists, and expression of decoy receptors. Members of the IL-1 family regulate the recruitment and activation of effector cells involved in innate and adaptive immunity, but they are also involved in the pathogenesis of chronic disorders, including inflammatory bowel disease, rheumatoid arthritis, and various autoimmune and autoinflammatory diseases. There are only limited data regarding the role of IL-1 cytokines in transplantation. In recent years, targeted therapeutics affecting IL-1 have been used in multiple clinical studies. In addition to the recombinant IL-1Ra, anakinra (highly effective in autoinflammatory diseases and tested for other chronic diseases), the monoclonal antibodies canakinumab, gevokizumab, and rilonacept (a long-acting IL-1 receptor fusion protein) provide further options to block IL-1 activity. Furthermore, new inhibitors of IL-18 (GSK 1070806, ABT-325, rIL-18BP (IL-18 binding protein)) and IL-33 (CNTO-7160) are presently under clinical studies and other molecules are being developed to target IL-1 family cytokines.
- Klíčová slova
- IL-1 family, biologic therapy, cytokines, inflammation, transplantation,
- MeSH
- interleukin-1 genetika imunologie MeSH
- lidé MeSH
- multigenová rodina * MeSH
- transplantace orgánů MeSH
- transplantační imunologie * MeSH
- zánět genetika imunologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- interleukin-1 MeSH
OBJECTIVES: Gastroesophageal reflux (GERD) is a one of the major public health problem that can lead to reflux esophagitis (RE), Barrett's esophagus (BE), and esophageal adenocarcinoma (EAC). The aim of our study was to determine the impact of IL-1 gene polymorphisms on the development of GERD, RE and BE. METHODS: Three hundred and thirty-three Czech patients with gastroesophageal reflux and 165 healthy controls were included in this case-control study. Four polymorphisms in the genes of the IL-1 cluster [IL-1A(-889C/T), IL-1B(-511C/T), IL-1B(+3953C/T), and IL-1RN(VNTR)] were analyzed. RESULTS: Significant differences were found in IL-1RN 1/2 genotype between patients with GERD/RE and controls and in IL-1B+3953 T allele between patients with BE and healthy subjects. In addition, complex analysis revealed differences in IL-1 haplotype frequencies between the groups. Specifically, the haplotype TCCL was significantly more frequent (p = 0.016) in GERD patients than in controls and the haplotype CCCL more frequent (p = 0.008) in RE patients than in controls. However, in patients with BE, frequency of haplotype TCTL was lower (p = 0.05) and haplotypes CTCL and TCCL were higher (p = 0.03 and p = 0.02) in comparison with the controls. CONCLUSIONS: Our results suggest that IL-1 haplotypes may be associated with susceptibility to GERD, RE and BE.
- Klíčová slova
- BE, Barrett’s esophagus, CI, DNA, DU, EAC, EC, EE, GAC, GERD, GIQLI, GU, HWE, Hardy–Weinberg equilibrium, IL-1, LD, LES, NERD, OR, PCR, RE, RFLP, SNP, VNTR, adenocarcinoma of the esophagus, confidence intervals, deoxyribonucleic acid, duodenal ulcer, erosive esophagitis, esophageal cancer, gastric adenocarcinoma, gastric ulcer, gastroesophageal reflux disease, gastrointestinal quality of life index, interleukin-1, linkage disequilibrium, lower esophageal sphincter, non-erosive reflux disease, odds ratio, polymerase chain reaction, reflux esophagitis, restriction fragment length polymorphism, single nucleotide polymorphism, variable number tandem repeat,
- MeSH
- Barrettův syndrom genetika imunologie MeSH
- dospělí MeSH
- frekvence genu MeSH
- gastroezofageální reflux genetika imunologie MeSH
- genetické asociační studie MeSH
- genotyp MeSH
- haplotypy MeSH
- interleukin-1 genetika MeSH
- lidé středního věku MeSH
- lidé MeSH
- multigenová rodina imunologie MeSH
- studie případů a kontrol MeSH
- zvířata MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Geografické názvy
- Česká republika MeSH
- Názvy látek
- interleukin-1 MeSH
Expression features of genetic landscape which predispose an individual to the type 1 diabetes are poorly understood. We addressed this question by comparing gene expression profile of freshly isolated peripheral blood mononuclear cells isolated from either patients with type 1 diabetes (T1D), or their first-degree relatives or healthy controls. Our aim was to establish whether a distinct type of 'prodiabetogenic' gene expression pattern in the group of relatives of patients with T1D could be identified. Whole-genome expression profile of nine patients with T1D, their ten first-degree relatives and ten healthy controls was analysed using the human high-density expression microarray chip. Functional aspects of candidate genes were assessed using the MetaCore software. The highest number of differentially expressed genes (547) was found between the autoantibody-negative healthy relatives and the healthy controls. Some of them represent genes critically involved in the regulation of innate immune responses such as TLR signalling and CCR3 signalling in eosinophiles, humoral immune reactions such as BCR pathway, costimulation and cytokine responses mediated by CD137, CD40 and CD28 signalling and IL-1 proinflammatory pathway. Our data demonstrate that expression profile of healthy relatives of patients with T1D is clearly distinct from the pattern found in the healthy controls. That especially concerns differential activation status of genes and signalling pathways involved in proinflammatory processes and those of innate immunity and humoral reactivity. Thus, we posit that the study of the healthy relative's gene expression pattern is instrumental for the identification of novel markers associated with the development of diabetes.
- MeSH
- anotace sekvence MeSH
- autoimunita MeSH
- autoprotilátky biosyntéza genetika MeSH
- CD antigeny genetika imunologie MeSH
- celogenomová asociační studie MeSH
- diabetes mellitus 1. typu genetika imunologie patologie MeSH
- dítě MeSH
- dospělí MeSH
- humorální imunita MeSH
- interleukin-1 genetika imunologie MeSH
- kojenec MeSH
- leukocyty mononukleární imunologie metabolismus patologie MeSH
- lidé MeSH
- mladiství MeSH
- předškolní dítě MeSH
- primární buněčná kultura MeSH
- přirozená imunita MeSH
- receptory CCR3 genetika imunologie MeSH
- regulace genové exprese imunologie MeSH
- rodina MeSH
- signální transdukce MeSH
- stanovení celkové genové exprese MeSH
- studie případů a kontrol MeSH
- toll-like receptory genetika imunologie MeSH
- Check Tag
- dítě MeSH
- dospělí MeSH
- kojenec MeSH
- lidé MeSH
- mladiství MeSH
- mužské pohlaví MeSH
- předškolní dítě MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- autoprotilátky MeSH
- CCR3 protein, human MeSH Prohlížeč
- CD antigeny MeSH
- interleukin-1 MeSH
- receptory CCR3 MeSH
- toll-like receptory MeSH
Materials on the basis of cycloolefin copolymers (COC) are suitable for subchondral defect repairs. The objective of this study was to evaluate the influence of surface modification of COC and COC/LLDPE blends on the viability and gene expression of chondrocytes. Human chondrocytes were incubated on the surface of the studied materials. Half of the materials were plasmatically modified with a subsequent type II collagen application. The gene expression of matrix metalloproteinases (MMP-1,-3,-13), pro-inflammatory cytokines (IL-1, TNF-alpha) and apoptotic molecules (BAX, Bcl-2) was evaluated using quantitative Taq-Man PCR after 48 h incubation. Chondrocyte viability was evaluated by the MTT test after 2, 4 and 8 days of incubation. The synthesis of MMPs was measured by ELISA assay in cell culture medium after 48 h of incubation. Chondrocytes incubated on plasmatically modified in contrast to unmodified materials demonstrated significantly increased gene expression of IL-1 (p<0.05), MMP-1 and MMP-3 (p<0.05 for both comparisons) as well as MMP-13 (p<0.001). Increased gene expression was confirmed by significantly increased production of active forms of particular MMPs into the cell culture medium. Unlike surface unmodified polymers, the modified materials showed time-dependent reduction of chondrocyte viability. The gene expression of TNF-alpha and apoptotic molecules by chondrocytes was not significantly changed by different materials. Cycloolefin copolymers and their blends may represent suitable materials for tissue engineering, however, their surface modification followed by collagen type II application may, at least under in vitro conditions, reduce the viability of chondrocytes and induce their pro-destructive behavior. The potential benefit or disadvantage of surface modifications of materials for osteochondral defect repairs needs to be further elucidated.
- MeSH
- apoptóza účinky léků MeSH
- biokompatibilní materiály farmakologie MeSH
- buněčné linie MeSH
- chondrocyty cytologie účinky léků fyziologie MeSH
- cykloalkany farmakologie MeSH
- exprese genu účinky léků MeSH
- interleukin-1 genetika MeSH
- kolagen typ II farmakologie MeSH
- lidé MeSH
- matrixová metaloproteinasa 1 genetika metabolismus MeSH
- matrixová metaloproteinasa 13 genetika metabolismus MeSH
- matrixová metaloproteinasa 3 genetika metabolismus MeSH
- osteoartróza farmakoterapie patologie MeSH
- polymery farmakologie MeSH
- protézy a implantáty MeSH
- techniky in vitro MeSH
- testování materiálů MeSH
- TNF-alfa genetika MeSH
- viabilita buněk účinky léků MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- biokompatibilní materiály MeSH
- cykloalkany MeSH
- interleukin-1 MeSH
- kolagen typ II MeSH
- matrixová metaloproteinasa 1 MeSH
- matrixová metaloproteinasa 13 MeSH
- matrixová metaloproteinasa 3 MeSH
- polymery MeSH
- TNF-alfa MeSH
Our 10-year study of early-onset periodontitis (EOP) patients includes repeated clinical observations, microbiological characteristics and analysis of genetic polymorphism of IL-1A and IL-1B genes. Twenty patients (age 15-26 years) were divided according to the clinical status in the 4th year into a group with mean number of teeth with bleeding on probing (BP) 9.8 and mean number of teeth with periodontal pocket (PP) 2.23, and a group with mean number of teeth with BP 5.37 and no PP. Significantly higher values of mean BP and PP were found among the groups during the study but a strong progression of disease was found only in 3 patients. The risk IL-1A allele-2 and IL-1B allele-2 genotype and bacterial presence were analyzed by DNA hybridization methods. No significant differences of bacteria composition (Treponema denticola, Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans) were found between the groups. A higher prevalence of composite IL-1 genotype was detected in the group of EOP patients with progressive disease. Early finding of the disease followed by conservative therapy could positively influence the disease progression. EOP treated in early stages may, but need not, develop into the aggressive form in the presence of risk genotype IL-1.
- MeSH
- Aggregatibacter actinomycetemcomitans izolace a purifikace MeSH
- Bacteria izolace a purifikace MeSH
- dospělí MeSH
- genetická predispozice k nemoci MeSH
- genotyp MeSH
- interleukin-1 genetika MeSH
- lidé MeSH
- městské obyvatelstvo MeSH
- mladiství MeSH
- orální hygiena MeSH
- parodontální index MeSH
- parodontitida diagnóza genetika mikrobiologie prevence a kontrola MeSH
- polymorfismus genetický MeSH
- Porphyromonas gingivalis izolace a purifikace MeSH
- Prevotella intermedia izolace a purifikace MeSH
- Treponema denticola izolace a purifikace MeSH
- zuby - přehledy zdravotního stavu MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- mladiství MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Geografické názvy
- Česká republika epidemiologie MeSH
- Názvy látek
- interleukin-1 MeSH
OBJECTIVE: Several interleukins (ILs) including IL-1 beta and IL-6 are produced in the anterior pituitary (AP) where they probably participate in the local regulation of hormone production. Immune challenge brings about the dysregulation of immune-endocrine interaction and enhanced the expression of pituitary IL-1 beta and IL-6. Little is known about regulation of their production, and therefore the purpose of the present work was to describe the relationship between circulating corticosterone and the mRNA expression of proopiomelanocortin (POMC), IL-1 beta and IL-6 in the AP during a 24-hour cycle in normal rats and rats with acute adjuvant arthritis (AA). METHODS: Groups of intact male Long-Evans rats and rats 23 days after induction of AA kept on a 12-hour light/dark cycle (light on at 6:00 a.m.) were killed at 4-hour intervals starting at 2:00 p.m. Trunk blood was used for corticosterone determination by radioimmunoassay. Adenopituitaries were extracted for total RNA and the message of interest was quantitated by real-time PCR using specific primers and TaqMan probes. Parameters of rhythms were evaluated by cosinor analysis. RESULTS: In normal rats, serum corticosterone showed a circadian rhythm with the peak at 6:00 p.m. and the nadir in the morning hours (p < 0.001). POMC mRNA in AP also showed a circadian rhythm (p < 0.05) which was inversely related to corticosterone levels. IL-1beta and IL-6 expression in normal rats showed clear-cut daily rhythms (p < 0.001) with the nadirs in the dark period, in contrast to the corticosterone peak in plasma. In arthritic rats, rhythmic corticosterone secretion was suppressed with a plateau pattern of the rhythm. The mean POMC expression was higher than in controls, and the rhythm failed to be significant. IL-1 beta expression was suppressed by AA (p < 0.001) but the rhythm was still present (p < 0.05). The rhythmic pattern of IL-6 expression was similar to that of controls, but with higher mesor values (p < 0.05). CONCLUSION: These results suggest a regulatory relationship between circulating corticosterone and the expression of POMC, IL-1 beta and IL-6 in AP of normal rats. Arthritis induced a higher expression of POMC and IL-6 in the AP and a suppression of IL-1 beta mRNA during the 24-hour cycle which suggests the involvement of different regulatory mechanisms compared to normal conditions.
- MeSH
- adenohypofýza fyziologie MeSH
- artritida experimentální imunologie metabolismus patofyziologie MeSH
- cirkadiánní rytmus imunologie MeSH
- exprese genu imunologie MeSH
- Freundovo adjuvans farmakologie MeSH
- interleukin-1 genetika MeSH
- interleukin-6 genetika MeSH
- kortikosteron krev MeSH
- krysa rodu Rattus MeSH
- messenger RNA analýza MeSH
- neuroimunomodulace fyziologie MeSH
- potkani Long-Evans MeSH
- pro-opiomelanokortin genetika MeSH
- tělesná hmotnost MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- Freundovo adjuvans MeSH
- interleukin-1 MeSH
- interleukin-6 MeSH
- kortikosteron MeSH
- messenger RNA MeSH
- pro-opiomelanokortin MeSH