Systemic Inflammatory Conditions Research Articles

Cytokines and Obstructive Sleep Apnea in Childhood: Study of a Group of Children

Introduction: Obstructive Sleep Apnea (OSA) in children is characterized by repeated episodes of partial or complete obstruction of the upper airways that impair normal ventilation and cause hypoxia and sleep disruption. These episodes activate innate and adaptive immunity resulting in the production of proinflammatory cytokines: IL-1β, IL-6, TNF-α, and reactive oxygen species. The hypothalamic–pituitary–adrenal (HPT) axis is also activated with alteration of the circadian rhythm of cortisol synthesis. OSA in children, and even more in adults, induces a systemic inflammatory condition that contributes to the genesis of clinical complications: poor growth, learning disabilities, cardiovascular changes, insulin resistance, and metabolic syndrome. Methods: A total of 42 non-obese children (age 1–15 years) were enrolled among those sent to our sleep center to perform full polysomnography (PSG). After PSG, 6 children did not show OSA (controls), 20 had mild OSA (m OSA), and 16 had medium-severe OSA (MS OSA). In vitro IL-1β, TNF-α, and serum cortisol levels were measured at 2 and 8 am in the analyzed groups. Results: Cortisol levels did not differ between controls and OSA children. At 2 am, there were no differences between controls and OSA in TNF-α production, whereas at 8 am, TNF-α was reduced in MS-OSA. IL-1β production showed no differences between OSA and controls. Conclusions: In our population, only TNF-α production is suppressed in MS-OSA: this might indicate a role of OSA severity in inducing inflammation. In adults, the phenomenon is more pronounced due to the habitual greater severity/duration of OSA, presence of comorbidities (cardiovascular and metabolic), and different immune system function.

Thyroid hormone may predict treatment failure in Kawasaki disease.

In systemic inflammatory conditions, inflammatory cytokines can cause low thyroid hormone levels. There are no reports discussing the relation between thyroid hormone levels and response to treatment for Kawasaki disease. We investigated 67 patients who underwent treatment in the acute phase of Kawasaki disease. We divided patients into two groups based on their response to initial intravenous immunoglobulin (IVIG) treatment: the responder group (n = 40), and the non-responder group (n = 27). The serum levels of the thyroid hormones free triiodothyronine (FT3), free thyroxine (FT4), and thyroid-stimulating hormone (TSH) were compared before and after treatment in all patients, and between responder and non-responder groups. The FT3, FT4, and TSH levels were low before the initial treatment and increased significantly after treatment (p < 0.05). The FT3, FT4, and TSH levels before treatment were significantly lower in the non-responder group than in the responder group (p < 0.05). Logistic regression analysis suggested that the addition of pre-treatment FT4 values to Gunma score was useful in predicting treatment failure. Thyroid hormone and TSH levels were lower in the non-responder group than in the responder group in the initial IVIG treatment for Kawasaki disease. This study suggests that Kawasaki disease in the acute phase is associated with low thyroid hormone levels and TSH. It is possible that these hormone levels predict response to the initial IVIG.

PAR1 Activation, via LMBR1/BMP Axis, Promotes the Osteogenesis of Periodontal Ligament Stem Cells (PDLSCs) and Alleviates the Inhibitory Effect of Sodium Butyrate on PDLSCs Osteogenesis.

Periodontitis is the leading cause of tooth loss and can exacerbate various systemic inflammatory conditions. Periodontal ligament stem cells (PDLSCs) stand out as prominent and favorable candidates for promoting periodontal tissue regeneration. This study aimed to investigate whether the protease-activated receptor type 1 (PAR1) can mitigate the sodium butyrate (NaB)-induced PDLSCs osteogenesis inhibition and unravel the underlying mechanism. Public datasets from the Gene Expression Omnibus (GEO) were utilized to analyze differentially expressed genes (DEGs) in periodontitis and subsequent Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment. PDLSCs were cultured normally in control medium (CM) as the negative control or in osteogenic medium (OM) to induce osteogenesis. PAR1 was either activated or suppressed using a selective agonist or antagonist (OM+agonist and OM+antagonist). The evaluation of PDLSCs osteogenesis was based on the levels of osteogenesis-related markers, including runt-related transcription factor 2 (RUNX2), osterix (OSX), osteocalcin (OCN), and osteopontin (OPN), alkaline phosphatase (ALP) activity, and calcium concentration. Additionally, cell proliferation and osteogenic differentiation were measured through the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and Alizarin Red Staining. To determine the PAR1 targeting the limb development membrane protein 1 (LMBR1)/bone morphogenetic protein (BMP) pathway, LMBR1 was upregulated through cell transfection and BMP2 was inhibited using the selective inhibitor Noggin protein. Finally, NaB was introduced into PDLSCs to investigate the effect on NaB-induced inhibition of PDLSCs osteogenesis. PAR1, RUNX2, OSX, OCN, OPN, proliferation, ALP activity, calcium concentration, osteogenic differentiation, BMP2, and BMP4 exhibited significant increases in PDLSCs cultured in OM (p < 0.01). These parameters were further elevated by PAR1 agonist and conversely reduced by PAR1 antagonist (p < 0.01). Conversely, LMBR1 was decreased in PDLSCs cultured in OM (p < 0.001), with further reduction induced by PAR1 agonist and a reverse increase observed with PAR1 antagonist (p < 0.001). OE-LMBR1 transfection successfully elevated LMBR1 levels, subsequently inhibiting BMP2 and BMP4 (p < 0.001). Meanwhile, the Noggin protein effectively suppressed BMP2 and BMP4 (p < 0.001). All observed osteogenesis-related changes were reversed by the increased LMBR1 or inhibition of the BMP pathway (p < 0.001). Furthermore, NaB suppressed osteogenesis-related changes in OM-cultured PDLSCs (p < 0.001), and these effects were entirely reversed by PAR1 agonist (p < 0.001). Conversely, the increased LMBR1 or inhibited BMP pathway disrupted the osteogenesis reversion induced by PAR1 agonist (p < 0.001). The activation of PAR1, through suppressing LMBR1 signaling and activating BMP pathway, demonstrates the ability to enhance the osteogenesis of PDLSCs and mitigate the inhibitory effects on PDLSCs osteogenesis caused by NaB.

Acute phase proteins patterns as biomarkers in bacterial infection: Recent insights.

Escherichia coli is a bacterium with command and pathogenic variants. It has been implicated in the induction of several inflammatory conditions. Finding a biomarker for infection began many years ago. The challenge of using acute phase proteins (APPs) as biomarkers for infection is a promising target for many researchers in this field. Many APPs have been studied for their roles as biomarkers of E. coli infection. The following review aims to highlight recent trials that have approved the use of adiponectin, amyloid A, ceruloplasmin, C-reactive protein, Haptoglobin, and Pentraxin 3 as biomarkers for E. coli infection and assess the obtained results. In conclusion, despite the existing approaches for the use of APPs as biomarkers in E. coli infection, we recommend more precise studies to enable these markers to be more specific and applicable in clinical fields. APPs could be markers for systemic inflammatory conditions, regardless of the causative agent.

A case report of posterior reversible encephalopathy syndrome in a patient diagnosed with emphysematous necrotizing biliary pancreatitis

Posterior reversible encephalopathy syndrome (PRES), a clinical radiological syndrome, is characterized by the abrupt development of neurological symptoms such as headaches, convulsions, altered sensorium, and visual problems. PRES has been linked to a number of risk factors or etiologies, including the use of immunosuppressants or cytotoxins, hypertensive encephalopathy, eclampsia, preeclampsia, and underlying autoimmune diseases. A 41-year-old female was admitted with acute necrotizing emphysematous pancreatitis complicated by posterior reversible encephalopathy syndrome. She remained normotensive on presentation and during the hospital stay. All her investigations were within normal except double-stranded DNA, which came positive. This could explain the immune-mediated mechanism leading to endothelial dysfunction. This case has been presented for its rarity. When acute neurological abnormalities occur in the context of systemic inflammatory conditions, such as acute pancreatitis, it is crucial to take PRES into account.

Complete Blood Cell Count-Derived Inflammation Biomarkers in Patients with Xanthelasma Palpebrarum.

Xanthelasma palpebrarum (XP) is the most common type of cutaneous xanthoma, characterized by yellowish cutaneous plaques commonly located near the medial canthus of the eyelid. Although dyslipidemia significantly contributes to its development, inflammation is also believed to be another element in the pathogenesis, especially in normolipidemic patients. Recently, cell counts derived from complete blood counts have been identified as indicators of systemic inflammatory conditions and have also been under discussion concerning their relevance to ocular diseases. This study aimed to assess inflammation indices derived from complete blood cell counts (CBC) in XP patients with normal lipid levels. Patients who had been referred to the oculoplasty department with the diagnosis of XP between January 2020 and January 2023 and age-matched control subjects were retrospectively reviewed. Patients who had abnormal lipid profiles and systemic diseases such as diabetes mellitus, hypertension, malignancy, cardiovascular diseases, systemic infections, and inflammatory diseases were not included in the study. CBC parameters were analyzed and compared between the groups. The study comprised 27 normolipidemic patients with XP and 27 age-matched healthy individuals as the control group. There were no statistically significant differences between the two groups in terms of age (p=0.143). The mean hemoglobin, neutrophil, monocyte, lymphocyte, platelet, neutrophil-to-lymphocyte ratio, monocyte-to-lymphocyte ratio, systemic immune-inflammation index, and aggregate index of systemic inflammation values were higher in the patient group, but the differences were not statistically significant (p>0.05). The mean red cell distribution width and platelet-to-lymphocyte ratio appeared to be lower in the patient group compared to the control group; however, no significant differences were observed between the two groups (p=0.272, p=0.387, respectively). This study might offer insights into the pathogenesis of XP, yet numerous questions remain unanswered, awaiting further investigation in future studies.

Aseptic Liver Abscess in a Patient With Diversion Colitis

ABSTRACT Aseptic abscess syndrome is a rare clinical entity mainly associated with systemic inflammatory conditions, particularly inflammatory bowel disease. The syndrome is characterized by an inflammatory infiltrate predominantly consisting of neutrophils, most commonly in the liver and spleen. We present a case of a patient with symptomatic diversion colitis diagnosed with a clinical and histological presentation consistent with aseptic abscess syndrome of the liver. Treatment and resolution of the inflamed colon was associated with complete disappearance of the liver lesions and normalization of liver enzymes. To the best of our knowledge, this is the first report suggesting the unique link between diversion colitis and aseptic liver abscess.

Efficacy and Safety of CD19-Specific CAR-T Cell Therapy Following Immunochemotherapy in Newly Diagnosed B-Cell Lymphoma Associated Hemophagocytic Lymphohistiocytosis

Hemophagocytic lymphohistiocytosis (HLH) represents a grave and potentially fatal systemic inflammatory condition. Lymphoma associated hemophagocytic lymphohistiocytosis (LAHS), as a common type in secondary HLH, suffers the worst outcome among sHLH. B cell Lymphoma associated hemophagocytic lymphohistiocytosis (B-LAHS) typically presents as high-risk lymphoma and is associated with a poorer prognosis compared to B cell lymphoma without HLH with standard first-line chemoimmunotherapy. As a result, there is an urgent need for more effective therapeutic strategies. Recent advancements in chimeric antigen receptor (CAR) T-cell therapy have demonstrated remarkable responses in relapsed or refractory B-cell non-Hodgkin lymphoma (B-NHL), as well as in some high-risk newly diagnosed B-cell lymphoma. However, There have been no clinical reports regarding the application of CAR-T cell treatment as part of first-line therapy in B-LAHS. We assessed the effectiveness and safety of autologous anti-CD19 CAR-T cell therapy following an immunochemotherapeutic regimen based on R-DEP (Rituximab-doxorubicin-etoposide-methylprednisolone) as a first-line treatment option for patients with B-LAHS. As of 1 July 2023, a cohort of 13 patients diagnosed with B-LAHS（with 3 cases enrolled before registration for clinical trials）was recruited for evaluation and met the criteria for assessing treatment efficacy at our institution. The overall response rate (ORR) for HLH was 100% (with 7 cases achieving complete response and 6 cases achieving partial response) prior to infuse CAR-T cells and the ORR for lymphoma also was 100% (with 10 cases achieving complete response and 3 cases achieving partial response) on the time of a month after CAR-T cell infusion. As of the follow-up date on 1 July 2023 (with a median follow-up time of 14 months), all 13 patients were still alive, 12 cases maintained sustained remission, while 1 case experienced relapse at 16 months after CAR-T cell infusion. The median overall survival (OS) has not been reached, and the median progression-free survival (PFS) was 31.5 months. To provide comparison, we included a group of 26 patients diagnosed with B-LAHS who did not receive CAR-T cell therapy during the same period. The non-CAR-T group demonstrated a significantly lower median OS of 5.93 months and a median PFS of 4.43 months, highlighting the superior prognosis of the CAR-T group (p &amp;lt; 0.001). Regarding adverse events, the CAR-T group exhibited a cytokine release syndrome (CRS) incidence of 53.8% (7/13) and an immune effector cell-associated neurotoxicity syndrome (ICANS) incidence of 30.7% (4 /13), all of which were classified as grade 1. None of the patients experienced non-hematologic toxicity of grade ≥3. While all 13 patients developed cytopenias, hematologic toxicity reactions ≥ grade 3 were observed in 76.9% (10 /13) of patients, but blood cell counts recovered within 3 weeks. Robust expansion of CAR T-cells occurred in all patients, with a median time to peak expansion of 8 days. Importantly, no exacerbation of hemophagocytic syndrome occurred following CAR-T cell infusion, and no patients succumbed to adverse events. In conclusion, our findings suggest that CD19 CAR-T cell treatment exhibits high efficacy as part of first-line therapy for B-LAHS, with a manageable safety profile.

Acute interstitial nephritis secondary to sarcoid-like reaction after autologous bone marrow transplantation: Case report

Sarcoid-Like Reaction is a systemic inflammatory granulomatous condition that does not meet the criteria for systemic Sarcoidosis—it is triggered by a known underlying factor, such as immunosuppression. Here we report a case of acute interstitial nephritis without granuloma in the context of a Sarcoid-Like systemic disease in the three-year period after an autologous stem cell transplant. The patient presented with a suspected relapse, associated with hemolytic anemia and an increase of serum creatinine. The investigation showed non-caseating epithelioid cell granuloma in a chest lymph node and in bone marrow, associated with combined hypogammaglobulinemia. Evaluation of the kidney tissue demonstrated acute interstitial nephritis.

Big Data Analysis of Inflammatory Conditions Associated With Optic Neuritis.

Previous studies in the United States established multiple sclerosis (MS) as the most common cause of optic neuritis (ON). ON can be associated with other systemic inflammatory conditions including sarcoidosis, neuromyelitis optica spectrum disorder (NMOSD), myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), and lupus; however, prospective studies to establish risk of ON associated with these diseases are lacking. Furthermore, appropriate workup for ON is still debated. A deidentified electronic medical record of a tertiary care academic center was searched for ON and rheumatologic/neuro-inflammatory diseases in the medical history, diagnoses, and laboratory results; followed by the intersection of ON with each condition. We calculated frequency of systemic conditions among patients with ON and prevalence of ON in those conditions. We also calculated relative risk (RR) of underlying systemic conditions among patients with ON compared with the study patient population. In 6.7 million charts, 5,344 cases of ON were identified. Among those, MS occurred most commonly (20.6%), followed by NMOSD (10.5%). Conversely, ON occurred in 98.4% of NMOSD cases, 53.3% of MOGAD, and 10.0% of MS. NMOSD (RR = 1,233), MOGAD (RR = 688), and MS (RR = 126) had the highest RR among the conditions we evaluated. The subset analysis showed similar findings. The high RR for ON among patients with NMOSD and MOGAD suggests that clinical suspicion for ON should be high among patients with these conditions presenting with vision changes. Conversely, MS and NMOSD should initially be high on the differential diagnosis for any patient presenting with optic neuritis.

Is SARS-CoV-2-induced disease a decisive factor influencing testosterone in males? Findings from a case-control ex post facto study.

Whether the observed lower total testosterone (tT) levels in male patients with COVID-19 are caused by a direct impact of SARS-CoV-2 infection or are collateral phenomena shared by other systemic inflammatory conditions has not yet been clarified. To investigate the independent role of COVID-19 in reducing circulating tT levels in men. We compared demographic, clinical, and hormonal values of patients with laboratory confirmed COVID-19 admitted during the first wave of the pandemic with a cohort of consecutive male patients admitted to the intensive care unit (ICU) of the same academic center because of severe acute respiratory distress syndrome (ARDS) but without SARS-CoV-2 infection and no previous history of COVID-19. Linear regression model tested the independent impact of COVID-19 on circulating tT levels. Logistic regression model was used to test predictors of death in the entire cohort. Of 286 patients with COVID-19, 70 men had been admitted to the ICU ( =cases) and were compared to 79 patients equally admitted to ICU because of severe ARDS but negative for SARS-CoV-2 infection and without previous history of COVID-19 ( =controls). Controls were further grouped into noninfective (n=49) and infective-ARDS (n=30) patients. At baseline, controls were older (p=0.01) and had more comorbidities (p<0.0001). Overall, cases admitted to ICU had significantly lower circulating tT levels compared to controls (0.9nmol/L vs. 2.1nmol/L; vs. 1.2nmol/L; p=0.03). At linear regression, being negative for COVID-19 was associated with higher tT levels (Coeff: 2.13; 95% confidence interval - CI 0.71-3.56; p=0.004) after adjusting for age, BMI, comorbidities and IL-6 levels. Only age and IL-6 levels emerged to be associated with higher risk of death regardless of COVID-19 status. This case-control ex post facto study showed lower tT levels in men with COVID-19 compared to those without COVID-19 despite both groups have been equally admitted to ICU for severe ARDS, thus suggesting a possible direct impact of SARS-CoV-2 infection toward circulating tT levels and a consequent more severe clinical outcome.

Platelet to albumin ratio: A risk factor related to prognosis in patients with non-ST-segment elevation acute coronary syndrome undergoing percutaneous coronary intervention

BackgroundAtherosclerotic cardiovascular disease (ASCAD) is recognized as a chronic subclinical systemic inflammatory condition. The platelet-albumin ratio (PAR) has shown promise in prognosticating various inflammation-related disorders. Our study aimed to assess the connection between PAR and major adverse cardiovascular events (MACE) in percutaneous coronary intervention (PCI)-treated patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS). MethodsPAR, derived from platelet and albumin counts, categorized participants into four quartiles. The primary outcome was composite MACE, encompassing all-cause mortality, non-fatal myocardial infarction (MI), and ischemia-driven revascularization. Secondary outcomes comprised individual MACE components. Multivariate Cox regression evaluated PAR's independent impact on adverse events. The non-linear relationship between the PAR value and MACE was explored using a restricted cubic spline (RCS). Receiver operating characteristic (ROC) analysis was conducted and the area under the curve (AUC) was calculated. Subgroup analysis was used to determine the effect of PAR on MACE in different subgroups. ResultsEnrolling 1391 NSTE-ACS patients, high PAR quartiles were correlated with elevated MACE rates (quartile 4 vs. quartile 1: 33.5% vs. 10.2%, p < 0.001). PAR was revealed to be independently related to an increased risk of MACE (quartile 4 vs. quartile 1: HR, 2.04 [95% CI, 1.34–3.08], p = 0.001). RCS indicated a positive PAR-MACE relationship. The AUC of PAR for the 3-year MACE was 0.659 (95% CI: 0.626–0.677, P<0.001). Subgroup analysis showed no significant interactions across subsets. ConclusionPAR independently predicted MACE risk in PCI-treated NSTE-ACS patients.

Type I interferon signature and cycling lymphocytes in macrophage activation syndrome.

BACKGROUNDMacrophage activation syndrome (MAS) is a life-threatening complication of Still's disease (SD) characterized by overt immune cell activation and cytokine storm. We aimed to further understand the immunologic landscape of SD and MAS.METHODWe profiled PBMCs from people in a healthy control group and patients with SD with or without MAS using bulk RNA-Seq and single-cell RNA-Seq (scRNA-Seq). We validated and expanded the findings by mass cytometry, flow cytometry, and in vitro studies.RESULTSBulk RNA-Seq of PBMCs from patients with SD-associated MAS revealed strong expression of genes associated with type I interferon (IFN-I) signaling and cell proliferation, in addition to the expected IFN-γ signal, compared with people in the healthy control group and patients with SD without MAS. scRNA-Seq analysis of more than 65,000 total PBMCs confirmed IFN-I and IFN-γ signatures and localized the cell proliferation signature to cycling CD38+HLA-DR+ cells within CD4+ T cell, CD8+ T cell, and NK cell populations. CD38+HLA-DR+ lymphocytes exhibited prominent IFN-γ production, glycolysis, and mTOR signaling. Cell-cell interaction modeling suggested a network linking CD38+HLA-DR+ lymphocytes with monocytes through IFN-γ signaling. Notably, the expansion of CD38+HLA-DR+ lymphocytes in MAS was greater than in other systemic inflammatory conditions in children. In vitro stimulation of PBMCs demonstrated that IFN-I and IL-15 - both elevated in MAS patients - synergistically augmented the generation of CD38+HLA-DR+ lymphocytes, while Janus kinase inhibition mitigated this response.CONCLUSIONMAS associated with SD is characterized by overproduction of IFN-I, which may act in synergy with IL-15 to generate CD38+HLA-DR+ cycling lymphocytes that produce IFN-γ.

Pharmacotherapy follow-up of patients under treatment with biologic agents for chronic inflammatory systemic conditions: an agreement among hospital pharmacists for the standardized collection of a minimum set of data

Background and objectiveThe objective of this study was to reach a consensus on the minimum set of data that would allow to optimize the pharmacotherapy follow-up of patients on biologic agents for chronic systemic inflammatory conditions, through structured and standardized collection with an electronic tool in the hospital pharmacy. Materials and methodA scientific committee was formed (n = 5 hospital pharmacists). The Delphi Technique was used, 2 rounds of consultation by e-mail for hospital pharmacists. A structured questionnaire was used, based on a bibliographic review and recommendations by the scientific committee; 37 statements were assessed with the Likert 5-point scale (1= „Strongly Disagree“; 5= „Strongly Agree“). Consensus was reached when 75% or more of panel members assigned a score of 1-2 (rejection consensus) or 4-5 (agreement consensus) to the matter reviewed. Descriptive statistical analyses were conducted. ResultsThe study included 21 hospital pharmacists (70 were invited, there was 70% response). Consensus was reached for 100% of statements. The minimum set of data was agreed upon, as well as the recommendations that the pharmacist had to collect and make during visits: to document the health status, health-related quality of life, changes In treatment compliance and In patient autonomy, as well as the conditions to make feasible the systematic collection of the minimum data set. ConclusionsThere Is consensus among hospital pharmacists about a minimum data set to be collected, through an electronic tool, which will order, standardize and structure the pharmacotherapy follow-up of patients with chronic Inflammatory conditions on treatment with biologic agents In the Spanish public health system.

Gut Bacterial Community Determines the Therapeutic Effect of Ginsenoside on Canine Inflammatory Bowel Disease by Modulating the Colonic Mucosal Barrier.

Inflammatory bowel disease (IBD) comprises systemic inflammatory conditions primarily affecting the gastrointestinal tract, including Crohn's disease and ulcerative colitis. This research aims to analyze the clinical symptoms and pathogenesis of a Dextran sodium sulfate (DSS)-induced canine IBD model and evaluate the restorative effect of ginsenoside from a pathogenesis perspective. We established the DSS-induced canine IBD model and studied the pathological mechanisms. Additionally, we examined the therapeutic effect of ginsenosides by assessing the Canine Inflammatory Bowel Disease Activity Index (CIBDAI), C-reactive protein (CRP) levels, colonic tissue morphology, protein expression, and mucosal bacterial community analysis. Our findings revealed a total ginsenoside content of 22.7% in the ginsenoside extract. Animal experiments demonstrated that dogs with IBD exhibited decreased mental state, significantly increased CIBDAI and CRP levels, disrupted colonic epithelial tissue structure, decreased expression of mucin, tight junctions, and adherens junctions, as well as reduced diversity of the colonic mucosal bacterial community. Furthermore, correlation analysis highlighted a total of 38 bacterial strains correlated with physiological indices. Significantly, ginsenoside treatment could improve these symptoms and reverse the relative abundance of some bacterial communities. In conclusion, alterations in the properties of the colonic mucus layer or the reduction in MUC2, its core component, in dogs with IBD can lead to bacterial penetration of the mucus layer and subsequent contact with intestinal epithelial cells, resulting in inflammation. Remarkably, ginsenoside intervention showcased the capacity to positively influence the relative abundance of bacteria and impact the colonic mucus layer properties, thereby offering promising prospects for IBD management and recovery.

Immunosuppression causes dynamic changes in expression QTLs in psoriatic skin

Psoriasis is a chronic, systemic inflammatory condition primarily affecting skin. While the role of the immune compartment (e.g., T cells) is well established, the changes in the skin compartment are more poorly understood. Using longitudinal skin biopsies (n = 375) from the “Psoriasis Treatment with Abatacept and Ustekinumab: A Study of Efficacy”(PAUSE) clinical trial (n = 101), we report 953 expression quantitative trait loci (eQTLs). Of those, 116 eQTLs have effect sizes that were modulated by local skin inflammation (eQTL interactions). By examining these eQTL genes (eGenes), we find that most are expressed in the skin tissue compartment, and a subset overlap with the NRF2 pathway. Indeed, the strongest eQTL interaction signal – rs1491377616-LCE3C – links a psoriasis risk locus with a gene specifically expressed in the epidermis. This eQTL study highlights the potential to use biospecimens from clinical trials to discover in vivo eQTL interactions with therapeutically relevant environmental variables.

A Case Report on Adult - Onset Still’s Disease

Background: Adult-onset Still's disease (AOSD) is an uncommon systemic inflammatory condition with an unknown cause, presenting with a set of three main symptoms: recurrent high fevers, joint pain (sometimes accompanied by arthritis), and an evanescent skin rash.&#x0D; Case Report: We here describe a 38-year-old female patient who presented to the ER with complaints of fever on and off, body pain and swelling of multiple joints for 3 months, and a rash with itching all over the body for 1 month. Fever was associated with chills and rigors, negative rheumatological factors, and infections. Investigations of bone marrow analysis revealed a normal cell count and a slight increase in eosinophil precursors, without any abnormal cells or parasites. Based on the Yamaguchi criteria, the patient was diagnosed with AOSD.

Study on the Correlation of Elevated Neutrophil-To-Lymphocyte Ratio and Platelet-To-Lymphocyte Ratio With Covid-19 Mortality among Patients in a Hospital Isolation Ward in Baler, Aurora

Neutrophil-to-Lymphocyte Ratio (NLR) and Platelet-to-Lymphocyte Ratio (PLR) are inflammatory biomarkers known to assess several disease types effectively. With the surge of Coronavirus disease (COVID-19) cases, many patients manifested various systemic inflammatory conditions suggesting a possible relationship between the predictive values of NLR and PLR to COVID-19 mortality. The study aims to assess a correlation between elevated biomarker values of NLR and PLR with COVID-19 mortality. A single-center, cross-sectional study of COVID-19 patients, admitted to a hospital isolation ward in Baler, Aurora, between May to October 2021 was conducted. Secondary data, namely demographic profiles, complete blood count results, and comorbidities upon admission, were collected. The effect of NLR and PLR on the risk of mortality, along with the impact of covariate variables that may affect the study’s outcome, was determined using a multiple binary logistic regression model and the computation of the odds ratio. 264 COVID-19 patients were included in the study–202 were recovered and 62 were deceased. Multiple binary logistic regression demonstrated a higher mortality risk in patients with elevated NLR (OR=2.607; 95% CI: 1.276 to 5.324; p=.009). Other risk factors such as age (OR=1.053; 95% CI: 1.029 to 1.077; p&lt;.001) and diabetes mellitus (OR=3.537; 95% CI: 1.441 to 8.682; p=.006) are risk factors for COVID-19 mortality. Patients with elevated NLR values indicate poor clinical outcomes with a higher mortality risk compared to those with low NLR in COVID-19 patients. Moreover, age and diabetes must be considered in patient assessment upon admission due to their correlation to COVID-19 mortality. Keywords: COVID-19 mortality, inflammatory biomarker, Neutrophil-to-Lymphocyte Ratio (NLR), Platelet-to-Lymphocyte Ratio (PLR).

Inflammation in Cardiovascular Disease: A Comprehensive Review of Biomarkers and Therapeutic Targets.

Cardiovascular disorders (CVDs) represent a global challenge and are regarded as one of the leading causes of mortality. The role of inflammation as a risk factor in these disorders has been studied, with the accelerated atherosclerotic process being a crucial factor in the pathogenesis. Several inflammatory biomarkers such as C-reactive protein (CRP), Interleukins (ILs), Tumor Necrosis Factor-alpha (TNF-α), and others have been identified that play a role in the atherosclerotic process, thus linking systemic inflammatory conditions with CVDs, including acute myocardial infarction (AMI), chronic heart failure (CHF), venous thromboembolism (VTE) and others. These markers could be used to predict the risk of CVDs. Understanding the precise mechanisms can lead to therapeutic strategies targeted at pro-inflammatory processes. We aim to provide an overview of the existing literature on the role of inflammation in various cardiovascular disorders and identify different inflammatory biomarkers and therapeutic targets in this comprehensive literature review. We reviewed 190 references published between 2013 and August 3, 2023, in well-reputed journals and analyzed eight selected papers in-depth. We describe the pathophysiologic pathways that lead to atherosclerosis and other cardiovascular pathologies. Several inflammatory cytokines encompassing various groups were identified to be causing endothelial dysfunction, leading to an increased risk for CVDs. Polymorphisms in the genes for different cytokines also led to different levels of susceptibility to CVDs. Nevertheless, future research detailing the inflammatory pathways and their link with CVDs would lead to better outcomes for patients with preexisting and new onset of CVDs as well as chronic inflammatory disorders.

Imaging Carotid Plaque Inflammation Using Positron Emission Tomography: Emerging Role in Clinical Stroke Care, Research Applications, and Future Directions.

Atherosclerosis is a chronic systemic inflammatory condition of the vasculature and a leading cause of stroke. Luminal stenosis severity is an important factor in determining vascular risk. Conventional imaging modalities, such as angiography or duplex ultrasonography, are used to quantify stenosis severity and inform clinical care but provide limited information on plaque biology. Inflammatory processes are central to atherosclerotic plaque progression and destabilization. 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) is a validated technique for quantifying plaque inflammation. In this review, we discuss the evolution of FDG-PET as an imaging modality to quantify plaque vulnerability, challenges in standardization of image acquisition and analysis, its potential application to routine clinical care after stroke, and the possible role it will play in future drug discovery.