Chronic Inflammatory Response Research Articles

Hypotensive drugs mitigate the high-sodium diet-induced pro-inflammatory activation of mouse macrophages in vivo

Nowadays, there is an increasing emphasis on the need to alleviate the chronic inflammatory response to effectively treat hypertension. However, there are still gaps in our understanding on how to achieve this. Therefore, research on interaction of antihypertensive drugs with the immune system is extremely interesting, since their therapeutic effect could partly result from amelioration of hypertension-related inflammation, in which macrophages seem to play a pivotal role. Thus, current comprehensive studies have investigated the impact of repeatedly administered hypotensive drugs (captopril, olmesartan, propranolol, carvedilol, amlodipine, verapamil) on macrophage functions in the innate and adaptive immunity, as well as if drug-induced effects are affected by a high-sodium diet (HSD), one of the key environmental risk factors of hypertension. Although the assayed medications increased the generation of reactive oxygen and nitrogen intermediates by macrophages from standard fed donors, they reversed HSD-induced enhancing effects on macrophage oxidative burst and secretion of pro-inflammatory cytokines. On the other hand, some drugs increased macrophage phagocytic activity and the expression of surface markers involved in antigen presentation, which translated into enhanced macrophage ability to activate B cells for antibody production. Moreover, the assayed medications augmented macrophage function and the effector phase of contact hypersensitivity reaction, but suppressed the sensitization phase of cell-mediated hypersensitivity under HSD conditions. Our current findings contribute to the recognition of mechanisms, by which excessive sodium intake affects macrophage immune activity in hypertensive individuals, and provide evidence that the assayed medications mitigate most of the HSD-induced adverse effects, suggesting their additional protective therapeutic activity.

Trained Immunity and Trained Tolerance: The Case of Helicobacter pylori Infection

Trained immunity is a concept in immunology in which innate immune cells, such as monocytes and macrophages, exhibit enhanced responsiveness and memory-like characteristics following initial contact with a pathogenic stimulus that may promote a more effective immune defense following subsequent contact with the same pathogen. Helicobacter pylori, a bacterium that colonizes the stomach lining, is etiologically associated with various gastrointestinal diseases, including gastritis, peptic ulcer, gastric adenocarcinoma, MALT lymphoma, and extra gastric disorders. It has been demonstrated that repeated exposure to H. pylori can induce trained immunity in the innate immune cells of the gastric mucosa, which become more responsive and better able to respond to subsequent H. pylori infections. However, interactions between H. pylori and trained immunity are intricate and produce both beneficial and detrimental effects. H. pylori infection is characterized histologically as the presence of both an acute and chronic inflammatory response called acute-on-chronic inflammation, or gastritis. The clinical outcomes of ongoing inflammation include intestinal metaplasia, gastric atrophy, and dysplasia. These same mechanisms may also reduce immunotolerance and trigger autoimmune pathologies in the host. This review focuses on the relationship between trained immunity and H. pylori and underscores the dynamic interplay between the immune system and the pathogen in the context of gastric colonization and inflammation.

Bioactive peptides as alternative treatment for Helicobacter pylori infection

The infection and chronic inflammatory response generated by Helicobacter pylori is a global health concern. This pathogen is characterized as a major risk factor in the development of gastric cancer and other diseases. Conventional eradication therapies are based on antibiotic regimens and as a consequence there is an increase in antimicrobial resistance of the pathogen strains, besides other potential side effects for the host. Therefore, it is necessary to explore new alternatives. This review delves into the realm of antimicrobial peptides, exploring their efficacy against H. pylori sourced from diverse origins. Furthermore, it sheds light on food-derived peptides exhibiting remarkable biological activity. These peptides exhibit promising effects on biomarkers associated with H. pylori infection, demonstrating anti-inflammatory and antioxidant properties validated through rigorous testing in both cell and animal models. Regarding the anti-inflammatory activity, the peptide VPY derived from soybean and the peptides derived from animal sources such as meat (β-Ala-His), egg (DEDTQAMPFR, DEDTQAMPF, MLGATSL, MSYSAGF, CR, FL, HC, LL, MK) and milk (IPAV) have reported a reduction of the cytokine IL-8, biomarker directly related to H. infection. For the antioxidant activity, peptides derived from milk (EAMAPK, AVPYPQ) and from Spirulina maxima (LDAVNR, MMLDF) have reduced ROS levels and could have a positive effect on the control of H. infection. Food-derived bioactive peptides with an anti-adhesive effect were also discussed. They derive from vegetable sources (corn, pea and wheat) and are capable of interacting with the host cells, interfering the adherence of H. pylori. Food-derived bioactive peptides have potential to avoid and/or mitigate undesired outcomes of infectious diseases due to the possibility of its application in nutraceuticals and food products, resulting in a preventive approach. Keywords: Helicobacter pylori, antibiotic resistance, bioactive peptides, antimicrobial peptides

The Effects of Smoking on Telomere Length, Induction of Oncogenic Stress, and Chronic Inflammatory Responses Leading to Aging

Telomeres, potential biomarkers of aging, are known to shorten with continued cigarette smoke exposure. In order to further investigate this process and its impact on cellular stress and inflammation, we used an in vitro model with cigarette smoke extract (CSE) and observed the downregulation of telomere stabilizing TRF2 and POT1 genes after CSE treatment. hTERT is a subunit of telomerase and a well-known oncogenic marker, which is overexpressed in over 85% of cancers and may contribute to lung cancer development in smokers. We also observed an increase in hTERT and ISG15 expression levels after CSE treatment, as well as increased protein levels revealed by immunohistochemical staining in smokers’ lung tissue samples compared to non-smokers. The effects of ISG15 overexpression were further studied by quantifying IFN-γ, an inflammatory protein induced by ISG15, which showed greater upregulation in smokers compared to non-smokers. Similar changes in gene expression patterns for TRF2, POT1, hTERT, and ISG15 were observed in blood and buccal swab samples from smokers compared to non-smokers. The results from this study provide insight into the mechanisms behind smoking causing telomere shortening and how this may contribute to the induction of inflammation and/or tumorigenesis, which may lead to comorbidities in smokers.

The footprint of gut microbiota in gallbladder cancer: a mechanistic review.

Gallbladder cancer (GBC) is the most common malignant tumor of the biliary system with the worst prognosis. Even after radical surgery, the majority of patients with GBC have difficulty achieving a clinical cure. The risk of tumor recurrence remains more than 65%, and the overall 5-year survival rate is less than 5%. The gut microbiota refers to a variety of microorganisms living in the human intestine, including bacteria, viruses and fungi, which profoundly affect the host state of general health, disease and even cancer. Over the past few decades, substantial evidence has supported that gut microbiota plays a critical role in promoting the progression of GBC. In this review, we summarize the functions, molecular mechanisms and recent advances of the intestinal microbiota in GBC. We focus on the driving role of bacteria in pivotal pathways, such as virulence factors, metabolites derived from intestinal bacteria, chronic inflammatory responses and ecological niche remodeling. Additionally, we emphasize the high level of correlation between viruses and fungi, especially EBV and Candida spp., with GBC. In general, this review not only provides a solid theoretical basis for the close relationship between gut microbiota and GBC but also highlights more potential research directions for further research in the future.

Trefoil factor 3 can stimulate Th17 cell response in the development of type 2 diabetes mellitus

This study aims to evaluate the role of trefoil factor 3 (TFF3) peptides in type 2 diabetes mellitus (T2DM) from an inflammatory perspective. The focus was on exploring how TFF3 affects the function of T cells. TFF3 overexpression model was constructed using lentivirus in Jurkat cell lines. We evaluated the impact of TFF3 on the proliferation, apoptosis, and IL-17A levels of Jurkat cells cultured in high glucose. The T2DM model was induced in TFF3 knockout (KO) mice through streptozotocin combined with high-fat diet. The measurements included glucose tolerance, insulin tolerance, inflammation markers, Th17 cell proportion, and pancreatic pathological changes. The T2DM modeling led to splenomegaly in mice, and increased expression of TFF3 in their spleens. Overexpression of TFF3 increased the proportion of IL-17+ T cells and the levels of Th17-related cytokines in Jurkat cells. There was no difference in body weight and blood glucose levels between wild-type and TFF3 KO mice. However, T2DM mice lacking the TFF3 gene showed improved glucose utilization, ameliorated pancreatic pathology, decreased inflammation levels, and reduced Th17 cell ratio. TFF3 may be involved in the chronic inflammatory immune response in T2DM. Its mechanism may be related to the regulation of the RORγt/IL-17 signaling pathway and its impact on T cell proliferation and apoptosis.

The Role of Inflammasome in Abdominal Aortic Aneurysm and Its Potential Drugs.

Abdominal aortic aneurysm (AAA) has been recognized as a serious chronic inflammatory degenerative aortic disease in recent years. At present, there is no other effective intervention except surgical treatment for AAA. With the aging of the human population, its incidence is increasing year by year, posing a serious threat to human health. Modern studies suggest that vascular chronic inflammatory response is the core process in AAA occurrence and development. Inflammasome, a multiprotein complex located in the cytoplasm, mediates the expression of various inflammatory cytokines like interleukin (IL)-1β and IL-18, and thus plays a pivotal role in inflammation regulation. Therefore, inflammasome may exert a crucial influence on the progression of AAA. This article reviews some mechanism studies to investigate the role of inflammasome in AAA and then summarizes several potential drugs targeting inflammasome for the treatment of AAA, aiming to provide new ideas for the clinical prevention and treatment of AAA beyond surgical methods.

The chronic leukocyte and inflammatory cytokine responses of older adults to resistance training in normobaric hypoxia; a randomized controlled trial

Trial designOlder adults experience chronic dysregulation of leukocytes and inflammatory cytokines, both at rest and in response to resistance training. Systemic hypoxia modulates leukocytes and cytokines, therefore this study characterized the effects of normobaric hypoxia on the leukocyte and cytokine responses of older adults to resistance training.Methods20 adults aged 60–70 years performed eight weeks of moderate-intensity resistance training in either normoxia or normobaric hypoxia (14.4% O2), consisting of two lower body and two upper body exercises. Venous blood was drawn before and after the training intervention and flow cytometry was used to quantify resting neutrophils, lymphocytes, monocytes, eosinophils and basophils, in addition to the subsets of lymphocytes (T, B and natural killer (NK) cells). Inflammatory cytokines were also quantified; interleukin 1 beta (IL-1β), IL-4, IL-6, IL-8, IL-10 and tumor necrosis factor alpha (TNF-α). Acute changes in leukocytes and cytokines were also measured in the 24 h following the last training session.ResultsAfter the intervention there was a greater concentration of resting white blood cells (p = 0.03; 20.3% higher) T cells (p = 0.008; 25.4% higher), B cells (p = 0.004; 32.6% higher), NK cells (p = 0.012; 43.9% higher) and eosinophils (p = 0.025; 30.8% higher) in hypoxia compared to normoxia, though the cytokines were unchanged. No acute effect of hypoxia was detected in the 24 h following the last training session for any leukocyte population or inflammatory cytokine (p < 0.05).ConclusionsHypoxic training caused higher concentrations of resting lymphocytes and eosinophils, when compared to normoxic training. Hypoxia may have an additional beneficial effect on the immunological status of older adults.Trial registrationAustralian New Zealand Clinical Trials Registry (ANZCTR). Trial number: ACTRN12623001046695. Registered 27/9/2023. Retrospectively registered. All protocols adhere to the COSORT guidelines.

Potential role of oxidative stress in pathogenesis of benign prostatic hyperplasia in male dogs.

The pathogenesis of benign prostatic hyperplasia (BPH) in dogs is still not fully understood. Some studies suggest that oxidative stress may have a potential role in the pathogenesis of BPH in dogs. Age-related hormonal changes may activate a chronic inflammatory response in the prostate. This causes the generation of reactive oxygen species (ROS) and results in oxidative stress. Excessive production of ROS results in DNA damage and hyperplastic transformation of prostatic cells. The use of antioxidants for improvement of treatment outcomes for canine PBH has been discussed. Further research is needed on the importance of oxidative stress in the development of BPH in dogs and the usefulness of antioxidants in the supportive treatment of this condition.

White spots amidst the gold: ultrastructural and histological aspects of the chronic inflammatory response of goldfish with ichthyophthiriasis

Ichthyophthirius multifiliis, the causative agent of white spot disease, is a ciliated protozoan parasite that infects freshwater fish and induces high mortality. Outbreaks occur both in natural and production sites. The aim of the present study was to describe the lesions caused by chronic infection by I. multifiliis in goldfish (Carassius auratus) from an ornamental fish farm, highlighting important ultrastructural aspects of this protozoan. Damaged skin and gills, collected from fish with white or ulcerative skin lesions, were routinely processed for histological analysis and transmission electron microscopy. The parasitic forms present in the skin were associated with an inflammatory infiltrate consisting of macrophages, lymphocytes and other polymorphonuclear cells. The lesions associated with the presence of the parasite were organized in the form of granulomas, with macrophages in the layers closest to the parasites. A trophont-thickened membrane and induction of granulomatous inflammation were identified in this study as mechanisms for evasion of the immune response. We concluded that the presence of I. multifiliis trophonts resulted in the formation of granulomatous inflammation, whether associated or not with pathogen lysis, suggesting that the parasite can use an inflammatory response to evade the immune response.

Yantiao Formula intervention in Rats with Sepsis: Network Pharmacology and Experimental Analysis.

Traditional Chinese Medicine prescribes Yantiao Formula (YTF; peach kernel, mirabilite, Angelica sinensis, Radix Scrophulariae, raw rhubarb, Radix Paeoniae, Flos Lonicerae, Forsythia, and Ophiopogon japonicus) to treat sepsis. Clinically, it reduced the inflammatory response of sepsis. It also reduced lung damage by decreasing the level of TNF-α in septic rats' serum. Using network pharmacology analysis, we investigated the efficacy network and mechanism of YTF in treating sepsis. We used the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and a Bioinformatics Analysis Tool for Molecular Mechanisms of Traditional Chinese Medicine (BATMAN-TCM) combined with literature to collect the main components in YTF and their targets. DisGeNET and GENECARDS databases were used for sepsis-related targets. Cytoscape 3.7.1 software was used to construct the herbcomponent- target and ingredient-target-disease interaction protein-protein interaction networks of YTF. The jvenn was used to perform the intersection of YTF targets and sepsis targets. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed． We also created a sepsis rat model using cecal ligation and perforation and stimulated alveolar macrophages (NR8383) with endotoxin to investigate the mechanisms of YTF. GO, and KEGG enrichment analysis revealed that these targets involved mineralocorticoid secretion, aldosterone secretion, active regulation of chronic inflammatory response, the exogenous coagulation pathway, and other pathophysiology. It was linked to various inflammatory factors and the MAPK pathway. YTF inhibits the p38MAPK pathway and decreases TNF- α, IL-6, and CXCL8 levels. YTF has a multi-component, multi-target, and multi-channel role in treating sepsis. The primary mechanisms may involve inhibiting the p38MAPK pathway to reduce the inflammatory response.

The economic and societal impact of periodontal and peri-implant diseases.

Periodontal and peri-implant diseases result from a chronic inflammatory response to dysbiotic microbial communities and are characterized by inflammation in the soft tissue and the ensuing progressive destruction of supporting bone, resulting in tooth or implant loss. These diseases' high prevalence, multifactorial etiology, extensive treatment costs, and significant detriment to patients' quality-of-life underscore their status as a critical public health burden. This review delineates the economic and sociocultural ramifications of periodontal and peri-implant diseases on patient welfare and healthcare economics. We delve into the implications of diagnosis, treatment, supportive care, and managing destructive tissue consequences, contrasting these aspects with healthy patients.

Comparative analysis of endometrial, vaginal, and gut microbiota in patients with and without adenomyosis.

Alterations in microbiota composition have been implicated in a variety of human diseases. Patients with adenomyosis present immune dysregulation leading to a persistent chronic inflammatory response. In this context, the hypothesis that alterations in the microbiota may be involved in the pathogenesis of adenomyosis, by affecting the epigenetic, immunologic, and biochemical functions of the host, has recently been postulated. The aim of the present study was to compare the microbiota composition in the vagina, endometrium, and gut of individuals with and without adenomyosis. Cross-sectional study including 38 adenomyosis patients and 46 controls, performed between September 2021 and October 2022 in a university hospital-based research center. The diagnosis of adenomyosis was based on sonographic criteria. Fecal, vaginal, and endometrial samples were collected. Study of the microbiota using 16S rRNA gene sequencing. Patients with adenomyosis exhibited a significant reduction in the gut microbial alpha diversity compared with healthy controls (Chao1 p = 0.012, Fisher p = 0.005, Observed species p = 0.005). Beta-diversity analysis showed significant differences in the compositions of both gut and vaginal microbiota between adenomyosis patients and the control group (Adonis p-value = 0.001; R2 = 0.03 and Adonis p-value = 0.034; R2 = 0.04 respectively). Specific bacterial taxa were found to be either overrepresented (Rhodospirillales, Ruminococcus gauvreauii group, Ruminococcaceae, and Actinomyces) or underrepresented in the gut and endometrial microbiota of adenomyosis patients compared with controls. Distinct microbiota profiles were identified among patients with internal and external adenomyosis phenotypes. The study revealed reduced gut microbiota diversity in adenomyosis patients, accompanied by distinct compositions in gut and vaginal microbiota compared with controls. Overrepresented or underrepresented bacterial taxa were noted in the gut and endometrial microbiota of adenomyosis patients, with variations in microbiota profiles among those with internal and external adenomyosis phenotypes. These findings suggest a potential association between microbiota and adenomyosis, indicating the need for further research to comprehensively understand the implications of these differences.

Identification and experimental validation of PYCARD as a crucial PANoptosis-related gene for immune response and inflammation in COPD.

Chronic inflammatory and immune responses play key roles in the development and progression of chronic obstructive pulmonary disease (COPD). PANoptosis, as a unique inflammatory cell death modality, is involved in the pathogenesis of many inflammatory diseases. We aim to identify critical PANoptosis-related biomarkers and explore their potential effects on respiratory tract diseases and immune infiltration landscapes in COPD. Total microarray data consisting of peripheral blood and lung tissue datasets associated with COPD were obtained from the GEO database. PANoptosis-associated genes in COPD were identified by intersecting differentially expressed genes (DEGs) with genes involved in pyroptosis, apoptosis, and necroptosis after normalizing and removing the batch effect. Furthermore, GO, KEGG, PPI network, WGCNA, LASSO-COX, and ROC curves analysis were conducted to screen and verify hub genes, and the correlation between PYCARD and infiltrated immune cells was analyzed. The effect of PYCARD on respiratory tract diseases and the potential small-molecule agents for the treatment of COPD were identified. PYCARD expression was verified in the lung tissue of CS/LPS-induced COPD mice. PYCARD was a critical PANoptosis-related gene in all COPD patients. PYCARD was positively related to NOD-like receptor signaling pathway and promoted immune cell infiltration. Moreover, PYCARD was significantly activated in COPD mice mainly by targeting PANoptosis. PANoptosis-related gene PYCARD is a potential biomarker for COPD diagnosis and treatment.

Dynamics of CD44+ bovine nucleus pulposus cells with inflammation

Intervertebral Disc (IVD) degeneration has been associated with a chronic inflammatory response, but knowledge on the contribution of distinct IVD cells, namely CD44, to the progression of IVD degeneration remains elusive. Here, bovine nucleus pulposus (NP) CD44 cells were sorted and compared by gene expression and proteomics with the negative counterpart. NP cells were then stimulated with IL-1b (10 ng/ml) and dynamics of CD44 gene and protein expression was analyzed upon pro-inflammatory treatment. The results emphasize that CD44 has a multidimensional functional role in IVD metabolism, ECM synthesis and production of neuropermissive factors. CD44 widespread expression in NP was partially associated with CD14 and CD45, resulting in the identification of distinct cell subsets. In conclusion, this study points out CD44 and CD44-based cell subsets as relevant targets in the modulation of the IVD pro-inflammatory/degenerative cascade.

Effect of repeated post-resistance exercise cold or hot water immersion on in-season inflammatory responses in academy rugby players: a randomised controlled cross-over design.

Uncertainty exists if post-resistance exercise hydrotherapy attenuates chronic inflammatory and hormone responses. The effects of repeated post-resistance exercise water immersion on inflammatory and hormone responses in athletes were investigated. Male, academy Super Rugby players (n = 18, 19.9 ± 1.5 y, 1.85 ± 0.06m, 98.3 ± 10.7kg) participated in a 12-week programme divided into 3 4-week blocks of post-resistance exercise water immersion (either, no immersion control [CON]; cold [CWI]; or hot [HWI] water immersion), utilising a randomised cross-over pre-post design. Fasted, morning blood measures were collected prior to commencement of first intervention block, and every fourth week thereafter. Linear mixed-effects models were used to analyse main (treatment, time) and interaction effects. Repeated CWI (p = 0.025, g = 0.05) and HWI (p < 0.001, g = 0.62) reduced creatine kinase (CK), compared to CON. HWI decreased (p = 0.013, g = 0.59) interleukin (IL)-1ra, compared to CON. HWI increased (p < 0.001-0.026, g = 0.06-0.17) growth factors (PDGF-BB, IGF-1), compared to CON and CWI. CWI increased (p = 0.004, g = 0.46) heat shock protein-72 (HSP-72), compared to HWI. Post-resistance exercise CWI or HWI resulted in trivial and moderate reductions in CK, respectively, which may be partly due to hydrostatic effects of water immersion. Post-resistance exercise HWI moderately decreased IL-1ra, which may be associated with post-resistance exercise skeletal muscle inflammation influencing chronic resistance exercise adaptive responses. Following post-resistance exercise water immersion, CWI increased HSP-72 suggesting a thermoregulatory response indicating improved adaptive inflammatory responses to temperature changes, while HWI increased growth factors (PDGF-BB, IGF-1) indicating different systematic signalling pathway activation. Our data supports the continued use of post-resistance exercise water immersion recovery strategies of any temperature during in-season competition phases for improved inflammatory adaptive responses in athletes.

Keloid Cryotherapy: Experience in patients from Jutiapa, Guatemala

Keloid scars, result from a chronic inflammatory response after trauma to the reticular dermis. Although first line treatment in Guatemala is triamcinolone intralesional injections, I present 2 cases treated with cryotherapy. Cryotherapy has proved to be a good treatment option for patients suffering from keloid scars, since it induces an antifibrotic inflammatory response.

The Expression of MAFB Gene in Circulating Monocytes Is Related to Chronic Inflammatory Status in T2DM Patients.

Immune cell-mediated chronic inflammation is one of the causes of type 2 diabetes mellitus (T2DM). Therefore, identifying inflammatory markers in circulating immune cells is highly important for predicting insulin resistance (IR) and the occurrence of T2DM. In this study, we discovered that differentially expressed genes (DEGs) in peripheral blood mononuclear cells (PBMCs) from T2DM patients were associated with innate immunity and chronic inflammatory responses through bulk transcriptome sequencing (bulk RNA-seq). Gene integration analysis revealed that nine DEGs were upregulated, and receiver operating characteristic (ROC) curve analysis revealed that V-maf musculoaponeurotic fibrosarcoma oncogene homolog B (MAFB), a candidate biomarker, has a certain predictive value for T2DM. In population-based cohort studies, we found that MAFB expression was significantly upregulated in the PBMCs of T2DM patients and was significantly correlated with homeostasis model assessment of IR (HOMA-IR), tumor necrosis factor-α (TNF-α), adiponectin (Adipoq), etc. We further evaluated the sensitivity and specificity of MAFB and other clinical parameters for predicting and diagnosing T2DM and found that MAFB expression in PBMCs had a positive effect on the prediction and diagnosis of T2DM. Finally, single-cell RNA sequencing (scRNA-seq) analysis revealed that the increase in MAFB expression was mainly in nonclassical monocytes. Our results suggest that increased MAFB expression in circulating monocytes may mediate chronic inflammatory status in patients with T2DM. Therefore, MAFB gene expression in circulating monocytes has certain clinical significance for predicting and assisting in the diagnosis of T2DM.

Assessing Tuberculosis and Risk Factors: Population Study in Rivers State, Nigeria's Niger Delta Region, Nigeria

Mycobacterium tuberculosis (MTB), an infectious airborne bacterium primarily impacting the lungs and instigating a chronic inflammatory response, persists as an enduring menace. This study aims to evaluate the interplay between MTB infection and associated risk factors in Rivers State, Nigeria. The study involved 392 participants from three local government areas (LGAs): Eleme, Obio/Akpor, and PHALGA. Data collection involved a structured questionnaire covering socio-demographics variables and associated risk factors. A stratified random sampling method was employed. Statistical analysis, including descriptive statistics and Spearman's correlation coefficient, was performed using SPSS version 25. Correlation analysis of socio-demographic variables revealed no significant associations with MTB, as indicated by non-significant p-values of (p=0.27), (p=0.83), (p=0.42), (p=0.35), (p=0.49), (p=0.28) for age, sex, education, occupation, marital status and geographical area respectively. However, significant positive weak correlations emerged between MTB infection and cough (p=0.00), hepatitis (p=0.01), coughing blood (p=0.00), and fever (p=0.00). Conversely, family TB history (p=0.93), cough lasting 2 weeks (p=0.84), weight loss (p=0.19), contact with a person who has been coughing for 2 weeks (p=0.93), and alcohol consumption (p=0.55) did not show significant associations. While demographic characteristics alone may not be strong predictors of MTB infection, this study highlights the complex interplay between various risk factors Addressing these risk factors through targeted interventions and raising awareness can contribute to reducing the TB burden in Rivers State and the Niger Delta region.

Long COVID and its association with neurodegenerative diseases: pathogenesis, neuroimaging, and treatment.

Corona Virus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has presented unprecedented challenges to the world. Changes after acute COVID-19 have had a significant impact on patients with neurodegenerative diseases. This study aims to explore the mechanism of neurodegenerative diseases by examining the main pathways of central nervous system infection of SARS-CoV-2. Research has indicated that chronic inflammation and abnormal immune response are the primary factors leading to neuronal damage and long-term consequences of COVID-19. In some COVID-19 patients, the concurrent inflammatory response leads to increased release of pro-inflammatory cytokines, which may significantly impact the prognosis. Molecular imaging can accurately assess the severity of neurodegenerative diseases in patients with COVID-19 after the acute phase. Furthermore, the use of FDG-PET is advocated to quantify the relationship between neuroinflammation and psychiatric and cognitive symptoms in patients who have recovered from COVID-19. Future development should focus on aggressive post-infection control of inflammation and the development of targeted therapies that target ACE2 receptors, ERK1/2, and Ca2+.