Inflammatory Cytokine Expression Pattern Research Articles

The Protective Effect of IDO1 Inhibition in Aβ-Treated Neurons and APP/PS1 Mice.

Alzheimer's disease (AD) is an inflammatory associated disease, in which dysregulated kynurenine pathway (KP) plays a key role. Through KP, L-tryptophan is catabolized into neurotoxic and neuroprotective metabolites. The overactivation of indolamine 2,3-dioxygenase1 (IDO1), the first rate-limiting enzyme of KP, and the abnormal accumulation of KP metabolites have been noted in AD, and blocking IDO1 has been suggested as a therapeutic strategy. However, the expression patterns of KP enzymes in AD, and whether these enzymes are related to AD pathogenesis, have not been fully studied. Herein, we examined the expression patterns of inflammatory cytokines, neurotrophic factors and KP enzymes, and the activity of IDO1 and IDO1 effector pathway AhR (aryl hydrocarbon receptor) in AD mice. We studied the effects of IDO1 inhibitors on Aβ-related neuroinflammation in rat primary neurons, mouse hippocampal neuronal cells, and APP/PS1 mice. The results further demonstrated the importance of IDO1-catalyzed KP in neuroinflammation in Alzheimer's disease.

Immune-related colitis and pancreatitis treated with infliximab.

Patients with various cancers benefit from immune checkpoint inhibitors. However, immune checkpoint inhibitor-induced adverse events have also been reported, such as colitis. Prednisolone is the first-line treatment for immune-related adverse events, but second-line therapy for patients refractory to steroids has not been established. Furthermore, the inflammatory cytokine expression pattern in the intestinal mucosa of patients with steroid-refractory immune-related colitis remains unclear. We present the case of a 48-year-old man diagnosed with immune-related colitis and pancreatitis induced by pembrolizumab for advanced lung cancer. First, we administered 50mg/day of prednisolone, and the patient's abdominal symptoms improved. However, the pancreatic enzyme levels did not return to normal. Furthermore, the patient's diarrhea worsened and hematochezia appeared at a 40mg/day prednisolone dose. A mucosal cytokine analysis identified a low interleukin-10 messenger RNA level, which has been associated with a poor response to prednisolone. Thus, we administered 5mg/kg of infliximab; the patient's diarrhea and hematochezia immediately improved, and the pancreatic enzyme levels returned to normal. Infliximab was administered three times every 2weeks. After, the patient's colitis and pancreatitis did not recur. To our knowledge, this is the first report demonstrating the effectiveness of infliximab for immune-related colitis and pancreatitis.

Different expression patterns of inflammatory cytokines induced by lipopolysaccharides from Escherichia coli or Porphyromonas gingivalis in human dental pulp stem cells

BackgroundLipopolysaccharide (LPS) is one of the leading causes of pulpitis. The differences in establishing an in vitro pulpitis model by using different lipopolysaccharides (LPSs) are unknown. This study aimed to determine the discrepancy in the ability to induce the expression of inflammatory cytokines and the underlying mechanism between Escherichia coli (E. coli) and Porphyromonas gingivalis (P. gingivalis) LPSs in human dental pulp stem cells (hDPSCs).Material and methodsQuantitative real-time polymerase chain reaction (QRT-PCR) was used to evaluate the mRNA levels of inflammatory cytokines including IL-6, IL-8, COX-2, IL-1β, and TNF-α expressed by hDPSCs at each time point. ELISA was used to assess the interleukin-6 (IL-6) protein level. The role of toll-like receptors (TLR)2 and TLR4 in the inflammatory response in hDPSCs initiated by LPSs was assessed by QRT-PCR and flow cytometry.ResultsThe E. coli LPS significantly enhanced the mRNA expression of inflammatory cytokines and the production of the IL-6 protein (p < 0.05) in hDPSCs. The peaks of all observed inflammation mediators’ expression in hDPSCs were reached 3–12 h after stimulation by 1 μg/mL E. coli LPS. E. coli LPS enhanced the TLR4 expression (p < 0.05) but not TLR2 in hDPSCs, whereas P. gingivalis LPS did not affect TLR2 or TLR4 expression in hDPSCs. The TLR4 inhibitor pretreatment significantly inhibited the gene expression of inflammatory cytokines upregulated by E. coli LPS (p < 0.05).ConclusionUnder the condition of this study, E. coli LPS but not P. gingivalis LPS is effective in promoting the expression of inflammatory cytokines by hDPSCs. E. coli LPS increases the TLR4 expression in hDPSCs. P. gingivalis LPS has no effect on TLR2 or TLR4 expression in hDPSCs.

Profiles of Cytokines Secreted by ARPE-19 Cells Exposed to Light and Incubated with Anti-VEGF Antibody.

The retinal pigment epithelium (RPE) is the major source of cytokines in the retina regulating the intraocular immune environment, and a primary target of photodamage. Here, we examined 27 types of cytokines secreted by ARPE-19 cells exposed to visible light and incubated with aflibercept or ranibizumab, which are two anti-vascular endothelial growth factor (VEGF) antibodies. The cells were cultured for 24 h in the dark or under 2000 lux irradiation from a daylight-colored fluorescent lamp, and cytokine levels in the culture supernatant were measured. In the light-irradiated culture, the levels of IL-9, IL-17A and bFGF were higher, and the levels of IL-6, IL-7, IL-8 and MCP-1 were lower than those in the dark culture, while there was no significant difference with the VEGF-A level. In subgroup analyses of the light-irradiated culture, the bFGF level under 250 to 2000 lux irradiation was elevated in a light intensity-dependent manner. In culture exposed to blue, green or red light, the bFGF level was elevated by blue light and was high compared to that by green or red light. In culture with aflibercept or ranibizumab in the dark, the levels of IL-6, IL-8, bFGF and MCP-1 were increased, and the IL-12 level decreased synchronously with a reduction in the VEGF-A level. Our findings indicate that continuous irradiation of visible light and VEGF suppression may be an influential factor in expression patterns of inflammatory cytokines secreted by human RPE cells.

Cytokine expression patterns in hospitalized children with Bordetella pertussis, Rhinovirus or co-infection

Mechanisms of interaction between Bordetella pertussis and other viral agents are yet to be fully explored. We studied the inflammatory cytokine expression patterns among children with both viral-bacterial infections. Nasopharyngeal aspirate (NPA) samples were taken from children, aged < 1 year, positive for Rhinovirus, Bordetella pertussis and for Rhinovirus and Bordetella pertussis. Forty cytokines were evaluated in NPA by using human cytokine protein arrays and a quantitative analysis was performed on significantly altered cytokines. Forty cytokines were evaluated in NPA by using human cytokine protein arrays and a quantitative analysis was performed on significantly altered cytokines. Our results show that co-infections display a different inflammatory pattern compared to single infections, suggesting that a chronic inflammation caused by one of the two pathogens could be the trigger for exacerbation in co-infections.

Shared microbiological and immunological patterns in periodontitis and IBD: A scoping review

ObjectivesTo extract the microbiological and immunological evidence underpinning the association between periodontitis and inflammatory bowel disease (IBD).MethodsRelevant articles were sorted through a systematic search on PubMed, Embase, Scopus and Web of Science up to October 2020. Available evidence was grouped in three different clusters: (a) studies that examined oral microbial alterations in IBD patients; (b) studies that investigated intestinal dysbiosis in patients with periodontitis; and (c) evidence for a shared immunological pattern between the two conditions.ResultsA total of 15 studies involving 1,171 patients were included. Oral microbiome, either subgingival or salivary, was consistently altered in patients with IBD compared to healthy subjects (a) Additionally, gut dysbiotic microbiota of IBD patients was colonized by pathobionts from oral origin, either via haematogenous or enteric route. Suffering from periodontitis is associated with lower alpha diversity in the gut microbiome (b) Lastly, both IBD and periodontitis are characterized by similar expression patterns of inflammatory cytokines at the gingival and gut levels that are exacerbated when both diseases are present (c).ConclusionsPeriodontitis and IBD share common dysbiotic and immunological traits. Well‐designed preclinical models and longitudinal cohort studies are required to better explore the causal pathways between the two conditions (PROSPERO CRD42020194379).

Anti-Inflammatory Effect of Adipose-Derived Stromal Vascular Fraction on Osteoarthritic Temporomandibular Joint Synoviocytes.

Osteoarthritis (OA) in the temporomandibular joint (TMJ) in the TMJ (TMJ-OA) is difficult to treat, and new alternative treatments are needed. Recently, adipose-derived stem cells (ASCs) have been introduced as a promising cell source because of their anti-inflammatory effects. However, the cost and availability of these cells limited broader applications of stem cell therapy. Thus, Thus, stromal vascular fraction (SVF) containing sufficient amount of ASCs at low cost can be an alternative. In this study, we aimed to demonstrate the use of uncultured, optimally isolated SVF for the treatment of TMJ-OA. First, we optimized the method of isolation to harvest high-quality SVFs with a large yield of ASCs. Then, we analyzed the quantity of ASCs in the SVF and performed characterization of stem cell homology. Subsequently, to evaluate the anti-inflammatory effect of high-quality SVF, an in vitro study was performed to assess the expression patterns of inflammatory cytokines including prostaglandin E2 (PGE2), IL-6, and CXCL8/IL-8, COX2, TNF, IFN, CCL2/MCP-1 and CCL5/RANTES in co-culture with synoviocytes derived from the synovial fluid in the TMJ-OA patients. The SVF containing approximately 32% ASCs was isolated via the our optimized isolation method. The SVF significantly down-regulated certain inflammatory cytokines such as PGE2, CXCL8/IL-8 in TMJ-OA tissue-derived synoviocytes. Although further study is needed, our study suggests that transplantation of adipose tissue-derived SVF cells might be a feasible and a novel therapeutic option for TMJ-OA in the future.

Comprehensive expression patterns of inflammatory cytokines in aqueous humor of patients with neovascular age-related macular degeneration

Neovascular age-related macular degeneration (nAMD) is a complex and multi-factorial disease, and low-grade inflammation is associated with pathogenesis of nAMD. Aqueous humor could reflect intraocular immune environments in various eye diseases. The research so far used aqueous humor samples and revealed that inflammation is involved in pathophysiology of nAMD, although immunological roles of cytokines were evaluated inadequately with aspect to individual effects. Here we used 27 kinds of cytokines covering general immunologic reactions, examined specific expression patterns of cytokines, and assessed relationships between inflammation and pathophysiology of nAMD by multivariate analyses. In nAMD eyes, principal component analysis showed that IL-7, MCP-1, MIP-1β and VEGF had high principal component loadings of over 0.6 in the first principal component constituting 32.6% of all variability of the data. In exploratory factor analysis, IL-6, MCP-1 and MIP-1β had high factor loadings (FL) of over 0.5 in Factor 1 constituting 32.6% of all variability, while VEGF had FL of over 1.0 in Factor 3 constituting 10.7% of all variability. In hierarchical cluster analysis, MCP-1 and VEGF were located in the cluster of first proximate mutual distance to central retinal thickness. These data could suggest that low-grade inflammation is a principal contributor in nAMD.

Alteration of specific cytokine expression patterns in patients with breast cancer

Systemic inflammation has been associated with aggressive tumor growth, invasion, and metastasis. Here we performed a comprehensive analysis of 26 kinds of inflammatory cytokine expression patterns among 185 patients with breast cancer and 54 healthy volunteers followed by chemometric analysis. We identified the specific cytokine expression patterns of breast cancer patients compared to healthy volunteers with (1) VEGF, IL-9, GM-CSF, IL-13, IL-4, and IFNγ, (2) IL-8, IL-10, IL-12, IL-5, IL-7, IL-1α, GCSF, IL-1β, and TNFα and (3) IL-2, Eotaxin, MIP1β, MIP1α, IL-17, and bFGF. Among the patients with breast cancer, we identified the specific cytokine signature of metastatic patients compared to non-metastatic patients. We also established a mathematical model for distinguishing patients with breast cancer from healthy volunteers and metastatic patients from non-metastatic patients. This cytokine network analysis could provide new insights into early intervention and effective therapeutic strategy for patients with breast cancer.

Comprehensive Expression Patterns of Inflammatory Cytokines in Aqueous Humor of Patients with Neovascular Age-Related Macular Degeneration

Comprehensive Expression Patterns of Inflammatory Cytokines in Aqueous Humor of Patients with Neovascular Age-Related Macular Degeneration

Fucoidan Inhibits Radiation-Induced Pneumonitis and Lung Fibrosis by Reducing Inflammatory Cytokine Expression in Lung Tissues.

Purpose: Radiotherapy is a crucial treatment approach for many types of cancer. Radiation pneumonitis (RP) is one of the major complications in chest irradiation. Fucoidan is a sulfated polysaccharide found mainly in various species of brown seaweed. Recent studies have demonstrated the anti-inflammatory effects of fucoidan. However, no study has reported a well-established prophylactic agent for RP. Therefore, we investigated the effects of fucoidan on RP and radiotherapy (RT)-induced lung fibrosis. Materials and Methods: We compared RP and RT-induced fibrosis in lung tissue specimens obtained from irradiated (10 Gy/shot) C57BL/6 mice with or without fucoidan administration (200 mg/kg/day, oral gavage for 14 days). The expression patterns of cytokines in the pleural fluid were determined using a cytokine array and confirmed through enzyme immunoassays. Results: Fucoidan administration attenuated RP and RT-induced fibrosis in lung tissues. Decreased neutrophil and macrophage accumulation was observed in irradiated lung tissues, and radiation-induced lung fibrosis, as demonstrated by Masson trichrome staining, was attenuated. We investigated the expression patterns of inflammatory cytokines in the irradiated lung pleural fluid through the protein array; results revealed that fucoidan administration changed the expression patterns of inflammatory cytokines in irradiated lung tissues. Furthermore, the expression levels of TIMP-1, CXCL1, MCP-1, MIP-2, and interleukin-1Ra were substantially enhanced in the pleural fluid, but fucoidan administration significantly reduced their expression. Conclusions: Fucoidan changes the expression patterns of inflammatory cytokines, which may consequently attenuate RP and RT-induced lung fibrosis.

Do all roads lead to the Rome? The glycation perspective!

Oxidative, carbonyl, and glycative stress have gained substantial attention recently for their alleged influence on cancer progression. Oxidative stress can trigger variable transcription factors, such as nuclear factor erythroid-2-related factor (Nrf2), nuclear factor kappa B (NF-κB), protein-53 (p-53), activating protein-1 (AP-1), hypoxia-inducible factor-1α (HIF-1α), β-catenin/Wnt and peroxisome proliferator-activated receptor-γ (PPAR-γ). Activated transcription factors can lead to approximately 500 different alterations in gene expression, and can alter expression patterns of inflammatory cytokines, growth factors, regulatory cell cycle molecules, and anti-inflammatory molecules. These alterations of gene expression can induce a normal cell to become a tumor cell. Glycative stress resulting from advanced glycation end products (AGEs) and reactive dicarbonyls can significantly affect cancer progression. AGEs are fashioned from the multifaceted chemical reaction of reducing sugars with a compound containing an amino group. AGEs bind to and trigger the receptor for AGEs (RAGE) through AGE-RAGE interaction, which is a major modulator of inflammation allied tumors. Dicarbonyls like, GO (glyoxal), MG (methylglyoxal) and 3-DG (3-deoxyglucosone) fashioned throughout lipid peroxidation, glycolysis, and protein degradation are viewed as key precursors of AGEs. These dicarbonyls lead to the carbonyl stress in living organisms, possibly resulting in carbonyl impairment of proteins, carbohydrates, DNA, and lipoproteins. The damage caused by carbonyls results in numerous lesions, some of which are involved in cancer pathogenesis. In this review, the effects of oxidative, carbonyl and glycative stress on cancer initiation and progression are thoroughly discussed, including probable signaling pathways and the effects on tumorigenesis.

Lipopolysaccharide-induced cytokine expression pattern in peripheral blood mononuclear cells in childhood obesity.

Obesity is characterized by the abnormal or excessive fat accumulation that may impair health and extensive increase in body mass index (BMI). Childhood obesity may occur due to disturbances in metabolic regulation, which lead to metabolic syndrome and other diseases. Peripheral blood suspended immune cells are responsible for immune surveillance. The aim of the present study was to map the inflammatory cytokine expression pattern of isolated peripheral blood mononuclear cells (PBMCs) following lipopolysaccharide (LPS) stress invitro and clinical chemistry parameters in the plasma of subjects. PBMCs were isolated through density gradient ultracentrifugation of the blood from obese infants that would reflect the cytokine response. Isolated PBMCs were cultured invitro in RPMI‑1640 medium and stressed with 1µg LPS in order to investigate the expression pattern of cytokines, such as interleukin (IL)‑2, interferon (IFN)‑γ, IFN‑α, tumor necrosis factor‑α and IL‑6 using enzyme‑linked immunosorbent assays and reverse transcription‑quantitative polymerase chain reaction. Levels of NO, lipid levels, total protein, albumin, marker enzymes aspartate transaminase and alanine transaminase, malondialdehyde (MDA), and reduced glutathione in the plasma were detected. Reduction in the expression of the inflammatory cytokines in PBMCs, reduced protein and globulins, and altered MDA and GSH levels in the plasma were observed. Altered or compromised pro‑inflammatory signals from PBMCs invitro and the clinical chemistry parameters of the plasma suggested that there were compromised immunological responses in obese children compared with matched controls.

Apoptosis induction and release of inflammatory cytokines in the oviduct of egg-laying hens experimentally infected with H9N2 avian influenza virus

The H9N2 subtype avian influenza virus (AIV) can cause serious damage to the reproductive tract of egg-laying hens, leading to severe egg-drop and poor egg shell quality. However, previous studies in relation to the oviductal-dysfunction resulted from this agent have not clearly been elucidated. In this study, apoptosis and pathologic changes in the oviducts of egg-laying hens caused by H9N2 AIV were evaluated. To understand the immune response in the pathogenic processes, 30-week old specific pathogen free (SPF) egg-laying hens inoculated with H9N2 subtype of AIV through combined intra-ocular and intra-nasal routes. H9N2 AIV infection resulted in oviductal lesions, triggered apoptosis and expression of immune related genes accompanied with infiltration of CD3+CD4+ and CD3+CD8α+ cells. Significant tissue damage and apoptosis were observed in the five oviductal parts (infundibulum, magnum, isthmus, uterus and vagina) at 5 days post-inoculation (dpi). Furthermore, immune-related genes, including chicken TLR3 (7, 21), MDA5, IL-2, IFN-β, CXCLi1, CXCLi2, XCL1, XCR1 and CCR5 showed variation in the egg-laying hens infected with H9N2 AIV. Notably, mRNA expression of IFN-α was suppressed during the infection. These results show distinct expression patterns of inflammatory cytokines and chemokines amongst segments of the oviduct. Differential gene expression of inflammatory cytokines and lymphocytes aggregation occurring in oviducts may initiate the infected tissue in response to virus replication which may eventually lead to excessive cellular apoptosis and tissue damage.

IL-6 deficiency exacerbates skin inflammation in a murine model of irritant dermatitis

Contact dermatitis is the second most reported occupational injury associated with workers compensation. Inflammatory cytokines are closely involved with the development of dermatitis, and their modulation could exacerbate skin damage, thus contributing to increased irritancy. IL-6 is a pro-inflammatory cytokine paradoxically associated with both skin healing and inflammation. To determine what role this pleiotropic cytokine plays in chemically-induced irritant dermatitis, IL-6 deficient (KO), IL-6 over-expressing transgenic (TgIL6), and corresponding wild-type (WT) mice were exposed to acetone or the irritants JP-8 jet fuel or benzalkonium chloride (BKC) daily for 7 days. Histological analysis of exposed skin was performed, as was tissue mRNA and protein expression patterns of inflammatory cytokines via QPCR and multiplex ELISA. The results indicated that, following JP-8 exposure, IL-6KO mice had greatly increased skin IL-1β, TNFα, CCL2, CCL3, and CXCL1 mRNA and corresponding product protein expression when compared to that of samples from WT counterparts and acetone-exposed control mice. BKC treatment induced the expression of all cytokines examined as compared to acetone, with CCL2 significantly higher in skin from IL-6KO mice. Histological analysis showed that IL-6KO mice displayed significantly more inflammatory cell infiltration as compared to WT and TgIL6 mice in response to jet fuel. Analysis of mRNA for the M2 macrophage marker CD206 indicated a 4-fold decrease in skin of IL-6KO mice treated with either irritant as compared to WT. Taken together, these observations suggest that IL-6 acts in an anti-inflammatory manner during irritant dermatitis, and these effects are dependent on the chemical nature of the irritant.

Bin1 Attenuation Suppresses Experimental Colitis by Enforcing Intestinal Barrier Function

Inflammatory bowel disease (IBD) is associated with defects in intestinal barriers that rely upon cellular tight junctions. Thus, identifying genes that could be targeted to enforce tight junctions and improve barrier function may lead to new treatment strategies for IBD. This preclinical study aimed to evaluate an hypothesized role for the tumor suppressor gene Bin1 as a modifier of the severity of experimental colitis. We ablated the Bin1 gene in a mosaic mouse model to evaluate its effects on experimental colitis and intestinal barrier function. Gross pathology, histology and inflammatory cytokine expression patterns were characterized and ex vivo physiology determinations were conducted to evaluate barrier function in intact colon tissue. Bin1 attenuation limited experimental colitis in a sexually dimorphic manner with stronger protection in female subjects. Colitis suppression was associated with an increase in basal transepithelial electrical resistance (TER) and a decrease in paracellular transepithelial flux, compared to control wild-type animals. In contrast, Bin1 attenuation did not affect short circuit current, nor did it alter the epithelial barrier response to non-inflammatory permeability enhancers in the absence of inflammatory stimuli. Bin1 is a genetic modifier of experimental colitis that controls the paracellular pathway of transcellular ion transport regulated by cellular tight junctions. Our findings offer a preclinical validation of Bin1 as a novel therapeutic target for IBD treatment.

The involvement of inflammatory cytokines in the pathogenesis of recurrent miscarriage

ObjectiveTo investigate the inflammatory cytokine expression pattern in trophoblastic tissue from women with unexplained recurrent miscarriage (RM). Study designTrophoblasts were obtained during uterine evacuation from 11 women with RM and from 20 healthy pregnant women undergoing elective termination of pregnancy, who served as controls. The array was performed using GEArray Q Series Human Inflammatory Cytokines & Receptors Gene Array HS-015 membranes. Data were confirmed by quantitative real-time PCR. The Mann–Whitney U test was performed for statistical analysis. ResultsMicroarray analysis identified three genes that were differentially expressed between RM patients and controls. We observed significant downregulation of Transforming Growth Factor beta 3 (TGF-β3) and Interleukin 25 (IL-25) (5-fold reduction and 2.5-fold reduction, respectively) and significant upregulation of CD-25, also known as Interleukin 2 receptor alpha (IL-2RA) (7-fold increase) in women with RM compared with controls.The median ΔCt of TGF-β3 was 8.2 (interquartile range, 7.67–8.9) in RM patients vs. 5.85 (interquartile range, 5.3–6.09) in controls; the median ΔCt of IL-25 was 5.18 (interquartile range, 4.46–5.76) in RM patients vs. 3.85 (interquartile range, 3.6–4.51) in controls, and the median ΔCt of CD-25 was 9.62 (interquartile range, 7.81–12.42) in RM patients vs. 12.44 (interquartile range, 11.02–13.86) in controls. DiscussionOur results suggest that the immunological and inflammatory regulation mechanisms of the placental environment play a key role in recurrent miscarriage. The observed trophoblast cytokine expression pattern at the maternal–fetal interface confirms the immunotrophic theory, as demonstrated by a switch from a T-helper-1 (Th1) profile to a T-helper-2 (Th2) profile in women who experience recurrent miscarriages.

Insulin therapy induces changes in the inflammatory response in a murine 2-hit model

Post-traumatic complications commonly seen on intensive care units include sepsis and associated disorders, which are accompanied by alterations in inflammatory cytokine expression patterns and in activation of neutrophils. Hyperglycaemia, often occurring after trauma and sepsis, is a further risk factor for morbidity and mortality among critically ill people. Clinical investigations have suggested that strict glycaemic control by insulin titration reduces overall mortality. This study aimed to further elucidate the pathophysiological and immunomodulative actions of insulin. Femoral fracture was induced in a murine model, followed by 1 h of haemorrhage. Two days after the first hit, sepsis was induced by caecal ligation and puncture (CLP). In control animals, laparotomy only was performed. Insulin in two different concentrations (10 IU or 20 IU) or vehicle was administered daily. Insulin therapy was associated with improvement of clinical parameters, slightly improved survival rates and, in lungs and liver, fewer infiltrating neutrophils and reduced IL-6 and IL-10 mRNA expression. These results suggested that, in this animal model, insulin had a direct anti-inflammatory effect that was independent of modulation of blood glucose levels.

Inflammatory Cytokine Expression Patterns in Rat Skin Exposed to JP-8 Jet Fuel

One of the main complaints of personnel exposed to JP-8 jet fuel is irritant dermatitis. The purpose of this investigation is to describe the JP-8 induced inflammatory cytokine response in skin over various periods of exposure. JP-8 jet fuel or acetone control (300 μL) was applied to the denuded skin of rats once a day for up to seven days. Skin samples from the exposed area were collected after one, three, five and seven days of exposure. RT-PCR was performed utilizing total skin RNA to examine the expression of various inflammatory cytokines. The mRNA’s for the chemokines CXCL1, 2, 3 and 10, as well as CCL3, 5, 11 and 20 were variably modulated during the course of exposure, favoring the expression of those that attract PMN. IL-1β and IL-6 mRNA’s were significantly induced by five days, while IL-10 was not significantly different from control at any time point. Paradoxically, skin IL-6 protein content was found to decrease continually throughout the time course as determined by ELISA. Data from the present study indicates that repeated JP-8 exposure induces numerous proinflammatory cytokines in skin that tend to favor neutrophil accumulation. The increased expression of these cytokines and chemokines may lead to increased inflammatory infiltrate and injury of the skin, resulting in JP-8 induced irritant dermatitis.

Inflammatory Cytokine Expressions of the Subacromial Bursitis and Glenohumeral Joint Synovitis in the Patients with Full Thickness Rotator Cuff Tear

PURPOSE: The purpose of this study was to compare expression patterns of inflammatory cytokines between subacromial bursitis and glenohumeral (GH) joint synovitis in full thickness rotator cuff (RC) tear patients with severe pain.MATERIALS AND METHODS: We were able to obtain enough tissue from nine subacromial bursitis and GH synovitis patients at the same time during surgery and evaluate them. We compared mRNA expression of inflammatory cytokines between the two groups using Reverse Transcription-Polymerase Chain Reaction (RT-PCR).RESULTS: Relative mean mRNA expression of IL-1beta, IL-6, TNF-alpha, COX-1, COX-2 and SDF-1 in the tissues of subacromial bursitis and GH synovitis patients did not show significant differences.CONCLUSION: GH synovitis may be another source of shoulder pain with subacromial bursitis in full thickness RC tear patients with severe pain.