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PubMed2026

Examining the Relationship Between Physical Neglect, Inflammation and Anterior Cingulate Activation During Facial Emotion Recognition in Patients With Schizophrenia and Healthy Controls: A Functional Magnetic Resonance Imaging Study.

Physical neglect is associated with poorer cognitive functioning in patients with schizophrenia, including deficits in facial emotion recognition. Recent research by our group showed the relationship between physical neglect and facial emotion recognition is mediated by inflammation. While this mediation effect was observed at the level of behaviour, examining the relationship between physical neglect, inflammation and neural activation during facial emotion recognition would help confirm brain regions impacted and support behavioural findings, but these relationships are unclear. Two hundred twelve participants (52 patients with schizophrenia and 160 healthy controls) underwent functional magnetic resonance imaging while performing an established facial emotion recognition task and a subset completed the Childhood Trauma Questionnaire and provided blood samples outside of the scanner. Inflammation was measured using a latent variable that combined basal plasma levels of interleukin-6, tumour necrosis factor-alpha and C-reactive protein. The relationships between physical neglect, inflammation and neural activation were examined using multiple regression. Neither physical neglect nor inflammation predicted altered neural response during facial emotion recognition at p < 0.05, family-wise error corrected for multiple comparisons within an anterior cingulate region of interest, across the whole brain, in the whole sample or separately in patients or controls. Future research should examine relationships between physical neglect, inflammation and brain activation in larger samples, which may have sensitivity to detect smaller effects, and use tasks that require active recognition of emotions, in addition to passive viewing of faces, which might be associated with additional neural responses.

Humans↗

PubMed2025

Cross-omics risk scores of inflammation markers are associated with all-cause mortality: The Canadian Longitudinal Study on Aging.

Inflammation is a critical component of chronic diseases, aging progression, and lifespan. Omics signatures may characterize inflammation status beyond blood biomarkers. We leveraged genetics (polygenic risk score [PRS]), metabolomics (metabolomic risk score [MRS]), and epigenetics (epigenetic risk score [ERS]) to build multi-omics-multi-marker risk scores for inflammation status represented by the level of circulating C-reactive protein (CRP), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-α). We found that multi-omics risk scores generally outperformed single-omics risk scores in predicting all-cause mortality in the Canadian Longitudinal Study on Aging. Compared with circulating inflammation biomarkers, some multi-omics risk scores had a higher hazard ratio (HR) for all-cause mortality when including both score and circulating IL-6 in the same model (1-SD IL-6 MRS-ERS: HR = 2.20 [1.55-3.13] vs. 1-SD circulating IL-6 HR = 0.94 [0.67,1.32]. 1-SD IL-6 PRS-MRS: HR = 1.47 [1.35,1.59] vs. 1-SD circulating IL-6 HR = 1.33 [1.18, 1.51]. 1-SD PRS-MRS-ERS: HR = 1.95 [1.40, 2.70] vs. 1-SD circulating IL-6: HR = 0.99 [0.71, 1.39]). In the Nurses' Health Study (NHS), NHS II, and Health Professional Follow-up Study with available omics, 1 SD of IL-6 PRS and 1-SD IL-6 PRS-MRS had HR = 1.12 [1.00,1.26] and HR = 1.13 [1.01,1.26] among individuals >65 years old without mutual adjustment of the score and circulating IL-6. Our study demonstrates that some multi-omics scores for inflammation markers may characterize important inflammation burden for an individual beyond those represented by blood biomarkers and improve our prediction capability for the aging process and lifespan.

Humans↗

PubMedDate not supplied

Heat, cold and inflammation.

Although therapeutic heat and cold measures are widely used in rheumatic diseases, their application in joint inflammations is still broadly empirical. Animal experiments concerning the effects of systemic hyperthermia and of local heat and cold applications upon experimentally induced inflammations (dextran edema, formol edema, kaolin edema, carrageenan edema, adjuvant arthritis) show that some inflammations are significantly depressed, i.e. they are effected by a useful therapeutic influence, but that cold and heat can also act as enhancing inflammatory stimulus. Under certain conditions, whole-body hyperthermia has immuno-suppressive effects. Although the exact points of intervention of heat and cold investigations, acute exsudative inflammations seem to be better influenced by cold; on the contrary, chronic torpid and proliferous inflammations are better influenced by heat. Prostaglandin mediated inflammations can be aggravated by cold, because it stimulates the prostaglandin synthesis; acute exsudative inflammatory processes are most often aggravated by heat. These results show that both therapeutic agents should be applied within a well-defined range and with care.

Animals↗

PubMed1976

[Inflammation of the tail in swine. Slaughter-house findings during 1972, 1973, and 1974 (author's transl)].

In the Public Salughter-House of Utrecht, a percentage increase in the number of pigs with inflammation of the tail, which had or had not healed, was observed during the period from 1972 to 1974 inclusive. The most common secondary symptoms of inflammation consisted in embolic pneumonia, osteomyelitis of the vertebrae and abscess formation in other parts of the body, particularly the semimebranosus muscles. Osteomyelitis was found to be the most common complication in pigs in which the inflammation of the tail had healed, whereas this usually consisted in embolic pneumonia in those cases in which the inflammation of the tail had not healed. The bacteriological examination carried out in accordance with the Meat Inspection Regulations was positive in 21.7 per cent, 13.5 per cent of the cases respectively in 1972, 1973 and 1974. Micro-organisms were isolated much more frequently from the kidney than they were from the spleen and meat. There was no relationship between the presence of inflammation of the tail and climatological conditions during the fattening period. The losses at slaughter from inflammation of the tail in the Netherlands are estimated at 3-4 million guilders per annum.

Animals↗

PubMed2025

Association of Lung Quantitative CT Scan Textures With Systemic Inflammation and Mortality in COPD.

BACKGROUND: COPD is characterized by persistent inflammation that is responsible for remodeling the bronchovascular bundles (BVBs), which may lead to poor quality of life. Quantitative CT (QCT) scan textures of the lung can capture local disease patterns of inflammation and related respiratory morbidity. RESEARCH QUESTION: Are BVB textures, obtained from the adaptive multiple feature method, associated with systemic inflammation, morbidity, and mortality in COPD? STUDY DESIGN AND METHODS: We analyzed data from the Subpopulations and Intermediate Outcome Measures in COPD Study (SPIROMICS; n = 2,981) and the Genetic Epidemiology of COPD (COPDGene) study (n = 10,305). The predictors included 2 QCT scan biomarkers, the BVB and CT density gradient (CTDG) textures, age, sex, BMI, race, smoking status, pack-years of smoking, CT scan-detected emphysema, and square root of the wall area of a hypothetical airway with a 10-mm lumen perimeter (Pi10). Outcomes included plasma biomarker concentrations from Meso Scale Discovery proteomics assays and CBC counts, both as markers of inflammation, along with FEV1, FEV1 to FVC ratio, St. George's Respiratory Questionnaire score, 6-minute walk distance, and modified Medical Research Council dyspnea scale score. Associations of these QCT scan textures with FEV1 decline and all-cause mortality also were investigated. RESULTS: Increased BVB texture was associated significantly with elevated neutrophil and monocyte counts and the neutrophil to lymphocyte ratio, independent of clinical covariates, CT scan-detected emphysema, and Pi10. Elevated CTDG was associated with increased neutrophil count, NLR, and tumor necrosis factor α. Increased CTDG and BVB textures also were associated with a lower FEV1 and 6-minute walk distance. CTDG at baseline was also associated with decline in FEV1 at the 5-year follow-up in the COPDGene study. We observed a significant association of both BVB texture (SPIROMICS: hazard ratio [HR], 1.084 [95% CI, 1.035-1.135; P < .001]; COPDGene: HR, 1.106 [95% CI, 1.080-1.131; P < .001]) and CTDG texture (SPIROMICS: HR, 1.033 [95% CI, 1.003-1.064; P = .03]; COPDGene: HR, 1.079 [95% CI, 1.061-1.096; P < .001]) with all-cause mortality independent of CT scan-detected emphysema and Pi10. INTERPRETATION: QCT scan textures may provide imaging evidence of the spatial heterogeneity of lung inflammation and overall disease burden in COPD. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov; Nos.: NCT01969344 (SPIROMICS) and NCT00608764 (COPDGene); URL: www. CLINICALTRIALS: gov.

Humans↗

PubMed1979

Prognostic significance of peritumoural inflammation in invasive urothelial bladder carcinoma.

Peritumoural inflammation consisting of lymphocytes, plasma cells and lymph follicles is present in two thirds of invasive urothelial bladder carcinomas. This type of inflammation is significantly rarer in advanced tumour stages (P3, P/) and its presence is a favourable prognostic factor. The mean survival time in patients with this type of inflammation is 26.1 months compared to only 14.8 months in patients without. All other forms of inflammation e. g. eosinophilic or polymorphonuclear leukocytes have no relation with prognosis. The significant prognostic value of lympho-plasmocytic inflammation may be considered as local expression of immunological host resistance.

Aged↗

PubMed1976

Modification of adjuvant inflammation in rats deficient in essential fatty acids.

Rats deficient in essential fatty acids (EFA) did not develop as much foot swelling on receiving injections of complete Freund's adjuvant as did normal controls. Both the acute inflammation and the chronic inflammation were affected. This reduction in the chronic phase of adjuvant inflammation was restored to normal levels by feeding a small supplement of corn oil as a dietary source of EFA. Since the EFA are biologic precursors of prostaglandins (PG), the lack of EFA is thought to influence adjuvant-induced inflammation by reducing available PG mediators of inflammation.

Acute Disease↗

PubMed2014

Persistent inflammation, immunosuppression, and catabolism syndrome after severe blunt trauma.

BACKGROUND: We recently proffered that a new syndrome persistent inflammation, immunosuppression, and catabolism syndrome (PICS) has replaced late multiple-organ failure as a predominant phenotype of chronic critical illness. Our goal was to validate this by determining whether severely injured trauma patients with complicated outcomes have evidence of PICS at the genomic level. METHODS: We performed a secondary analysis of the Inflammation and Host Response to Injury database of adults with severe blunt trauma. Patients were classified into complicated, intermediate, and uncomplicated clinical trajectories. Existing genomic microarray data were compared between cohorts using Ingenuity Pathways Analysis. Epidemiologic data and outcomes were also analyzed between cohorts on admission, Day 7, and Day 14. RESULTS: Complicated patients were older, were sicker, and required increased ventilator days compared with the intermediate/uncomplicated patients. They also had persistent leukocytosis as well as low lymphocyte and albumin levels compared with uncomplicated patients. Total white blood cell leukocyte analysis in complicated patients showed that overall genome-wide expression patterns and those patterns on Days 7 and 14 were more aberrant from control subjects than were patterns from uncomplicated patients. Complicated patients also had significant down-regulation of adaptive immunity and up-regulation of inflammatory genes on Days 7 and 14 (vs. magnitude in fold change compared with control and in magnitude compared with uncomplicated patients). On Day 7, complicated patients had significant changes in functional pathways involved in the suppression of myeloid cell differentiation, increased inflammation, decreased chemotaxis, and defective innate immunity compared with uncomplicated patients and controls. Subset analysis of monocyte, neutrophil, and T-cells supported these findings. CONCLUSION: Genomic analysis of patients with complicated clinical outcomes exhibit persistent genomic expression changes consistent with defects in the adaptive immune response and increased inflammation. Clinical data showed persistent inflammation, immunosuppression, and protein depletion. Overall, the data support the hypothesis that patients with complicated clinical outcomes are exhibiting PICS. LEVEL OF EVIDENCE: Epidemiologic study, level III.

Adolescent↗

PubMed1979

Neutropenia, inflammation, and the kinetics of transfused neutrophils in rabbits.

A rabbit model was used to study the effects of neutropenia and inflammation on the intravascular distribution, survival, and tissue accumulation of transfused neutrophils. Donor blood labeled with [(3)H]thymidine was infused into normal or neutropenic (vinblastine treated) animals. Inflammation was created by subcutaneous implantation of polyvinyl sponges, some with added endotoxin. Initial circulating neutrophil pool recovery, survival, and inflammatory site accumulation of labeled neutrophils were measured. Neutropenia was associated with a relative increase in the marginal pool size, manifested by a diminished initial circulating pool (CNP) recovery of transfused cells. The CNP recovery was directly proportional to recipient neutrophil count. Neutropenia had no effect on the intravascular survival of transfused cells and was accompanied by only a modest decrease in the inflammatory site recovery of the transfused neutrophils (10.4+/-5.4 vs. 14.4+/-4.0% in normals). Inflammation in the form of subcutaneous polyvinyl sponges was accompanied by an increase in margination with initial CNP recoveries of 24.3+/-4.7 and 27.6+/-8.8% at zero and 4 h after implantation respectively (normal, 38.2+/-9.9%). Transit through the CNP was hastened by inflammation with a t((1/2)) of 2.02+/-0.72 h (normal, 3.2+/-1.0 h). Addition of endotoxin to the sponges further perturbed cell kinetics. CNP recoveries were considerably lower and half-lifes were initially shorter and subsequently uninterpretable in studies done after endotoxin sponge insertion. Inflammatory site accumulation was markedly diminished to 7.4+/-1.9% of injected neutrophil label in the endotoxin sponge animals, suggesting that many of the transfused cells were functionally unavailable rather than marginated. These studies demonstrate that neutropenia and inflammation with or without endotoxin markedly alter the kinetics of transfused neutrophils and that CNP recovery of transfused cells is not necessarily predictive of their inflammatory site accumulation.

Agranulocytosis↗

PubMed1975

Inflammation and its effect on the vitreous.

The role of the vitreous in inflammatory diseases of the eye is now more clearly defined because of improved methods of examination and surgery. Inflammatory diseases of various aetiology produce opacification, liquefaction, and shrinkage. Additional changes include cellular proliferation and transformation leading to fibrosis in cases of prolonged inflammation. In some eyes the fibrosis is primarily cortical while in others it is extensive. Those inflammations with outpouring of a fluid exudate lead to detachment of the vitreous from the posterior eye and extensive shrinkage. In such eyes the vitreous becomes heavily organized and opaque in the central eye behind the lens, obscuring the view of the posterior fundus. In young eyes vitreo-retinal adhesions often form at the sites of inflammation, leading to traction on the retina and ciliary body; retinal tears may result from the traction. Exudate in many inflammatory vitreal inflammations tends to collect at the vitreous base where it organizes into scar tissue. The scar is formed by the retina and ciliary body, but there are also fibrosis-produced monocytes that become transformed into fibroblasts. Shrinkage of the new-formed scar can lead to disinsertion or peripheral tears of the retina. Specific inflammations such as chronic cyclitis and toxoplasmosis produce characteristic changes in the vitreous that can be recognized on clinical examination. Melanomas and reticulum cell sarcomas also produce a characteristic vitreous opacification.

Eye Diseases↗

PubMed1975

[Sephadex induced inflammation in rats (author's transl)].

QUESTION: A single s.c. injection of Dextran is very suitable in producing an inflammatory response in the rat. The Dextran edema has become a standard method. It seems not uhlikely that Sephadex, the Dextran gel widely used in the gelchromatography may have a similar effect. Sephadex, because of its physiochemical properties, would offer some advantages in the studies of inflammatory reactions. But first of all the following questions have to be answered: 1. Does one single s.c. injection of Sephadex produce an inflammation at all and what are the characteristics on the microscopical level? 2 Does it make any difference if Sephadex of different types are injected? MATERIAL AND METHODS: Male and female Wistar rats (100-250 g) in groups of 5 animals each. Diet: Rat pellets "Tagger" and tap water ad libitum. Sephadex (Pharmacia Fine Chemicals) of the types G-25 m, G-50 m, G-100, and G-200 were soaked in 0.9% saline for the prescribed time and afterwards preserved until the Sephadex gel had settled on the bottom of the vessels. 1 ml of this Sephadex gel slurry each were subcutaneously injected to the shaved dorsal skin of the rats (right below). At different intervals (3, 6, 24 and 72 hours: 6, 14, 20 and 28 days) the Sephadex depot and the surrounding tissue were exstirpated and examined histologically. During all the procedures the animals were subjected to ether anesthesia. From the tissue samples frozen sections (Kryocut, -30 degrees C) were prepared and stained with hematoxylin and eosin or after van Gieson. Moreover, several preparations were stained after Pappenheim and Weigert (fibrin) or with PAS and toluidine blue. For recording of probable differences in the effect of the particular Sephadex types always 2 values were determined histometrically. The number of exudate cells emigrated between the Sephadex beads within the area of an ocular-net (edge length 1.66 mm) were counted at 500-fold magnification. Furthermore, the number of eosinophils was determined by the technique. However, because of poor occurrence the eosinophils were counted in 10 fields of view. Tests with Sephadex G-10 were omitted as preliminary tests had shown that it is not suitable for s.c. injections because of its gritty consistency (due to poor soaking properties). RESULTS: One single s.c. injection of Sephadex in the rat induces an acute inflammation. The exudative phase marked by a massive leucocytic infiltration (especially PMN leucocytes) is followed by the appearance of mononuclear leucocytes and fibroblasts after the 2nd day. The inflammation declines within approximately 3 weeks. Thereafter the Sephadex depot is encapsulated by a fibrous tissue. A chronic inflammation was never observed. In the microscopical aspect of the inflammation produced by the different types of Sephadex were detectable. The Sephadex lying in the tissue does not change its original shape, it is insoluble and is not disintegrated. The size of the particles prevents the transport into the blood or lymph vessels...

Animals↗

PubMed1978

Experimental pneumococcal meningitis. IV. The effect of methyl prednisolone on meningeal inflammation.

This study was undertaken to determine whether adrenal corticosteroids suppress meningeal inflammation in experimental pneumococcal meningitis in rabbits and, if so, whether the mechanism of suppression involves inhibition of chemotactic activity in CSF or modification of granulocyte responses to inflammation mediators. It was found that methyl prednisolone, administered intramuscularly in doses of 15 or 30 mg/kg 24 hr and 48 hr after induction of meningitis, significantly reduced (p less than 0.01) the mass of granulocytes present in the meninges 72 hr after infection, the time of maximum meningeal inflammation. The larger dose of steroid produced approximately twice the suppressive effect of the smaller dose (p less than 0.05). The regime of methyl prednisolone that produced maximal suppression of meningeal inflammation (30 mg/kg/day) did not alter CSF chemotactic activity or chemotactic responsiveness and phagocytic activities of granulocytes from rabbits with meningitis. However, steroid therapy inhibited an increase in granulocyte adherence that was observed in untreated animals with meningitis (p less than 0.05). Thus methyl prednisolone in doses of 15 and 30 mg/kg given daily to rabbits with pneumococcal meningitis produced a suppressive effect on meningeal inflammation that was dose-dependent and was possibly mediated by inhibition of granulocyte adherence.

Animals↗

PubMed1976

[Posttraumatic pyogenic and granulomatous encephalitis. An animal experimental contribution on inflammation (author's transl)].

The present studies were performed to elucidate the factors responsible for the relative resistance of the brain to bacterial infections. As a model, group A streptococci were used to produce an experimental brain infection in mice. Attention was focussed on the activity of brain macrophages, the function of which to date is poorly understood. The primary purpose of the experiments was to compare the types of inflammation elicited in the brain by the injection of either killed or living group A streptococci. As a result, two fundamentally different types of encephalitis were observed histologically. A granulomatous inflammation was induced by killed streptococci; when deposited in the brain by intracerebral injection, these were phagocytosed by invading mononuclear macrophages and polymorphonuclear granulocytes during the first day p.i. There was no necrosis of brain tissue excepting the stab wound at the site of injection. The number of granulocytes in the inflammatory infiltrates decreased during the first week p.i. whereas, during the same period, the number of macrophages forming granuloma-like cell accummulations increased. At the beginning of the third week a fading of the granulomatous encephalitis was observed. In contrast, living streptococci produced a pyogenic inflammation of the meninges as well as of the grey and white matter in the region of the stab wound combined with extended tissue necrosis surrounding deposits of bacteria. This pyogenic infection progressed until the end of the first week, forming a brain abscess. A phlegmonous spreading of the pyogenic inflammation predominantly in the white matter and pyocephalus internus was also observed. In contrast to the increase of mononuclear macrophages in the border zone of the abscesses, the granulocytic inflammation decreased. During the second and third weeks p.i. granulation tissue consisting of proliferating connective tissue cells, macrophages and lymphocytes replaced pyogenic necrosis. A secondary purpose was to determine the fate of living and killed streptococci within the pyogenic and granulomatous encephalitis. In these studies immunohistologic, electron microscopic, bacteriologic and serologic methods were employed in addition to the techniques already mentioned. In the majority of the experimental animals streptococci were killed by granulocytes within the first week after injection of the living bacteria. At this time, most of the streptococci were contained within granulocytes and macrophages located to the periphery of the brain abscesses. Corresponding to the granulomatous encephalitis produced by injection of killed streptococci it was possible to detect persistent cell wall material in macrophages by immunohistology. By electronmicroscopy streptococci and their cell walls were found within the phagocytic vacuoles of macrophages. During the course of degradation the group-specific cell wall carbohydrate was enzymatically converted into the group A-variant specific structure...

Animals↗

PubMed2026

Glial Connexin-43 Is a Pathogenic Mechanism Promoting Gut Inflammation in Postoperative Ileus Induced by Gut Surgical Manipulation With Potential Relevance to Humans.

BACKGROUND & AIMS: Abdominal surgery often precipitates postoperative ileus (POI), a frequent and severe gastrointestinal (GI) motility disorder, through mechanisms that involve intestinal inflammation. Emerging data show that enteric glia acquire a reactive phenotype that aggravates POI, but how glia exert this effect remains unclear. Enteric glia express connexin-43 hemichannels (gCx43), which are implicated in neurological and inflammatory disorders. Thus, we aimed to decipher contributions of glial connexin-43 (Cx43) in the pathophysiology of POI. METHODS: We induced POI in mice using in vivo intestinal manipulation and used glial Cx43cKO (Sox10CreERT2;Cx43fl/fl) or RiboTag (Sox10CreERT2/Rpl22HA/+) mice to evaluate Cx43-dependent signaling. Human enteric glial cultures (hEGC) and muscularis externa obtained during intestinal surgery translated findings to patients. Transcriptome analysis, immunofluorescence co-labeling, Western blots, and Cx43 hemichannel activation were used for quantitative analysis. RESULTS: Cx43 is the highest expressed connexin in enteric glia in mice and humans. Up-regulation of Cx43 occurs in various disease models linked to POI, GI surgical trauma, inflammation, immune cell activation, and enteric gliosis. In the mouse POI model, glial Cx43-deletion reduces glial reactivity, pro-inflammatory signals, upregulates host protection genes, regulates immune cell activation, and prevents enteric neuropathy. In hEGCs, interleukin (IL)-1β induction opens Cx43 and stimulates release of IL-6 and C-C motif ligand 2 (CCL2). The Cx43 peptide inhibitor, 43Gap26, inhibits glial Cx43 activation, reduces IL-6 release, and blocks upregulation of macrophage activation factors and immune cell regulation factors. Surgical intestinal trauma in patients upregulates Cx43 during inflammation and enteric gliosis in mouse POI. CONCLUSIONS: Glial Cx43 signaling promotes enteric gliosis, immune cell activation, inflammation, and enteric neuropathy in mice with potential translatability to humans after intestinal surgical trauma and mechanical stress in POI. Interventions that block glial Cx43 activation may be protective against POI development.

Animals↗

PubMed2024

Blood-based epigenome-wide analyses of chronic low-grade inflammation across diverse population cohorts.

Chronic inflammation is a hallmark of age-related disease states. The effectiveness of inflammatory proteins including C-reactive protein (CRP) in assessing long-term inflammation is hindered by their phasic nature. DNA methylation (DNAm) signatures of CRP may act as more reliable markers of chronic inflammation. We show that inter-individual differences in DNAm capture 50% of the variance in circulating CRP (N = 17,936, Generation Scotland). We develop a series of DNAm predictors of CRP using state-of-the-art algorithms. An elastic-net-regression-based predictor outperformed competing methods and explained 18% of phenotypic variance in the Lothian Birth Cohort of 1936 (LBC1936) cohort, doubling that of existing DNAm predictors. DNAm predictors performed comparably in four additional test cohorts (Avon Longitudinal Study of Parents and Children, Health for Life in Singapore, Southall and Brent Revisited, and LBC1921), including for individuals of diverse genetic ancestry and different age groups. The best-performing predictor surpassed assay-measured CRP and a genetic score in its associations with 26 health outcomes. Our findings forge new avenues for assessing chronic low-grade inflammation in diverse populations.

Humans↗

PubMed1978

On the relationship between inflammation and altered cAMP metabolism in lungs of B pertussis-vaccinated mice.

Bordetella pertussis-vaccinated mice were examined for evidence of inflammation. Using polymorphonuclear leukocyte and fluid accumulation as markers, inflammation was evidenced in the lungs and to a lesser extent in the livers of such mice. Both heart and kidney showed no evidence of inflammation. Development of the inflammatory lesion followed a time course similar to that previously reported for increased sensitivity to histamine-mediated cAMP accumulation. This close parrallelism between inflammation and altered cAMP metabolism supports the hypothesis that the increased cAMP accumulation might be related to a feedback mechanism regulating inflammatory mediator release.

Animals↗

PubMed1976

Differences in the mode of exucative reaction between early phase and late phase of carrageenin-induced inflammation in rats.

Differences in the mode of vascular permeability change induced by some stimulants such as chemical mediators between the early phase and the late phase of the carrageenin-induced granulomatous inflammation were investigated with the aid of 131I-human serum albumin as an indicator for the measurement of vascular permeability. In the early pregranulomatous phase of the inflammation, histamine injection into the inflammation locus markedly elevated local vascular permeability, while prostaglandins E1 and E2 showed no effect. On the other hand, in the late phase of the inflammation, where permanent granuloma tissue had been formed, prostaglandins E1 and E2 significantly enhanced the local vascular permeability, while histamine was inert.

Animals↗

PubMed2026

Targeted Epigenetic Silencing of Jumonji Domain-Containing Protein 3 Alleviates Nuclear Factor-Kappa B-Mediated Inflammation in Familial Mediterranean Fever.

BACKGROUND: Familial Mediterranean fever (FMF) is an inherited autoinflammatory condition caused by variants in the MEFV gene encoding pyrin, the essential component of the NLRP3/NF-κB complex of inflammasomes. Deregulation of nuclear factor-kappa B (NF-κB), a key proinflammatory mediator, leads to chronic inflammation in autoinflammatory/autoimmune diseases. Epigenetic modulation offers a new approach to regulate inflammasome activity, with Jumonji domain-containing protein 3 (JMJD3) being a promising target for managing inflammatory illnesses. GSK-J4 is a selective inhibitor of JMJD3, restricting pro-inflammatory cytokines and inflammation. AIM: Our research aimed to elucidate the role of JMJD3 and the NF-κB-JMJD3 signaling pathways in regulating inflammation in an in vitro model, and to investigate GSK-J4's effect in inhibiting inflammasome activation in primed peripheral blood mononuclear cells (PBMCs) isolated from FMF cases. METHODS: PBMCs were cultured and primed with LPS, and then treated with GSK-J4. JMJD3 knockdown was achieved using siRNA interference. Cellular inflammatory dynamics were assessed by Western blotting (WB) and ELISA. The qRT-PCR was used for gene expression quantification. Untreated cells served as a negative control. RESULTS: Our results showed significantly downregulated gene expression of NF-κB, NLRP3, and inflammatory cytokines in GSK-J4-treated cells compared to untreated cells, as confirmed by ELISA. WB reported a reduction of NF-κB in induced cells following GSK-J4 treatment. Knocking down JMJD3 also showed decreased levels of JMJD3, NF-κB, and inflammatory cytokines, indicating its proinflammatory role. CONCLUSION: The study showed that selective inhibition or silencing of JMJD3 significantly suppressed the inflammasome in FMF cases, suggesting its role as a therapeutic target for alleviating inflammation in various autoinflammatory diseases.

Humans↗