Alterations In Immune System Research Articles

P0516 Chronic Rhinosinusitis and Inflammatory Bowel Disease: discovering the gut-lung axis- preliminary results from a single-center pilot study

Abstract Background Inflammatory Bowel Diseases (IBD) are multifactorial and debilitating diseases that significantly impact patients’ quality of life. As it is known, they involve an altered immune system. For this reason, patients with IBD have an increased risk of developing other chronic immune disorders, including chronic rhinosinusitis (CRS). The coexistence of these two conditions can undoubtedly affect patients’ life and disease history. This study aims to define the prevalence of CRS in IBD patients and assess how it affects their quality of life. Methods We conducted a prospective, observational, monocentric pilot study. in which we enrolled consecutive IBD under biological therapy. We collected clinical, demographic, and disease history data. Four questionnaires were administered to the patients: the Short Inflammatory Bowel Disease Questionnaire (SIBDQ), EuroQol 5 Dimension 5 Level (EQ-5D-5L), the Short-Form- 36 (SF-36), and the SNOT-22 questionnaire to identify subjective symptoms of CRS. According to the SNOT-22 score, patients were divided into two groups: patients without/mild CRS (group 1, SNOT-22 <30 points) and patients with moderate/severe CRS (group 2, SNOT-22>30 points). Results We enrolled 50 IBD patients, of which 48% were affected by ulcerative colitis (UC) and 52% were affected by Crohn’s Disease (CD). Among them, 42% (n=21) of patients were naive to biological therapy, while 48% had failed at least two lines of biological therapy. We observed no statistically significant differences in the mean values of the score of SNOT-22 between naive and multi-failure patients (30.1 and 28.5, respectively, p=0.76). Dividing patients based on the SNOT-22 score, 42% were part of group 1 (absent or mild CRS), and 58% were part of group 2 (moderate/severe CRS).CD patients of group 2 had a significantly higher disease activity, defined according to the Harvey-Bradshaw Index (HBI), compared to group 1 (mean value of 2.3 vs 0.48, p=0.008).We did not observe statistically significant differences in Full Mayo Score between group 1 and group 2 UC patients. The median VAS EQ-5D-5L was compared between Groups 1 and 2 showing a lower score in patients with moderate/severe CRS (66.6 vs. 81.3, p = 0.0019). Conclusion CRS is frequent in IBD patients. Those with both conditions have reduced quality of life, more severe symptoms, and worse disease characteristics than those without CRS. Level of some cytokines can induce alterations of gastrointestinal motility in gastrointestinal disorders, due to increased intestinal barrier damage. However, our findings are preliminary, and further studies, clinical evaluations, and specialized laboratory investigations are needed to better understand the gut-lung axis.

Changes and Long-Term Effects of the Immune System after COVID-19 Infection

Following the pandemic in 2020, physical health has generally declined. All of this is brought on by modifications to the body's immune system and the consequences of sequelae. The current research gap is caused by the neglect of COVID-19's after effects. In this paper, the relationship between immune system changes, complications and their physical conditions was studied, and preliminary results on the harm and prevention of the sequelae were obtained. The immune system's alterations during the epidemic infection and its consequences are the main topics of this article, including cytokine storms, inflammatory responses, and changes in immune cells. At the same time, the article explores the relationship between complications and underlying health conditions, such as chronic diseases and autoimmune diseases, and the harm they cause. Through observation and analysis in the later stages of the epidemic, the article explores the reasons for the general decline in people's physical fitness and changes in the immune system. In the future, it is hoped that there will be improvements in disease analysis and prevention measures after pandemic diseases.

Transitioning from NAFLD to MAFLD and MASLD: the toxic relationship with alcohol consumption

Alcohol is a well-known toxic etiologic factor for liver injury. Metabolic substrates of alcohol (especially acetaldehyde) have a major responsibility and genetic susceptibility, alterations in microbiota and immune system are important co-factors for this injury. Major injury in liver is hepatocellular lipid accumulation. Therefore the relationship between non-alcoholic and alcoholic fatty liver diseases should have been defined clearly. Recently two major liver committees adopted new terminologies such as metabolic-associated fatty liver disease (MAFLD), metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction and alcohol-related liver disease (MetALD), and alcoholic liver disease (ALD) instead of non-alcoholic fatty liver disease (NAFLD). These terminologies were based on the effects of metabolic syndrome on liver. Alcohol consumption was defined differently according to these nomenclatures. MAFLD defined alcohol intake (regardless of amount) as “dual etiology fatty liver disease” and the Delphi consensus defined MASLD, MetALD, or ALD according to daily consumption of alcohol amount.

Role of Immunization in Adults with Diabetes in India: An Overview

Vaccination is one of the most cost-effective public health strategies. Millions of adults globally suffer from diseases preventable by vaccines. Vaccination in persons with diabetes mellitus is crucial for enhancing immunity, protecting against new infectious agents, and boosting the efficacy of childhood vaccines. It also reduces the community spread of infectious diseases. People with diabetes (PWD) are particularly vulnerable to infections such as Streptococcus pneumoniae, influenza, hepatitis B, and COVID-19 due to hyperglycemia-induced immune system alterations. As diabetes prevalence rises, so does the susceptibility of large populations to infectious diseases, resulting in serious complications and high mortality rates among PWD. Increasing vaccination coverage can significantly reduce mortality and improve health outcomes in PWD. Studies reveal a significant lack of awareness and knowledge about vaccines among PWD, with barriers including fear of complications, financial constraints, and lack of information. Healthcare providers should educate patients about the benefits of vaccinations, integrate vaccination recommendations into routine care, and address barriers through consistent guidance and support.

An untargeted metabolomic analysis of acute AFB1 treatment in liver, breast, and lung cells.

Aflatoxin B1 (AFB1) is a class 1 carcinogen and mycotoxin known to contribute to the development of hepatocellular carcinoma (HCC), growth impairment, altered immune system modulation, and malnutrition. AFB1 is synthesized by Aspergillus flavus and is known to widely contaminate foodstuffs, particularly maize, wheat, and groundnuts. The mechanism in which AFB1 causes genetic mutations has been well studied, however its metabolomic effects remained largely unknown. A better understanding of how AFB1 disrupts metabolism would provide insight into how this mycotoxin leads to carcinogenesis, growth impairment, and/or immunomodulation, and may reveal potential targets for pharmacological or nutritional interventions to protect against these effects. The current study evaluated the metabolomic effects of various doses (2.5 μM, 5 μM, 10uM) of AFB1 treatment to HepG2 (liver), MDA-MB-231 (breast), and A549 (lung) cells. Treated and control cells' metabolomic profiles were evaluated via ultra-high performance liquid chromatography-high resolution mass spectrometry (UHPLC-HRMS). Univariate and multivariate analyses revealed significant alterations in metabolite concentrations from each dose of AFB1 treatment in each cell type. Pathway analysis was then used to understand broader biochemical functions affected by AFB1 treatment in each cell type. HepG2 cell pathway analyses revealed significant pathway perturbations in lipid metabolism, carnitine synthesis, catecholamine biosynthesis, purine metabolism, and spermidine and spermine biosynthesis. Analysis of A549 cells found a greater emphasis of perturbations on various amino acids along with lipid synthesis-related pathways, and catecholamine biosynthesis. Finally, analysis of treated MDA-MB-231 cells found spermidine and spermine biosynthesis, carnitine synthesis, plasma membrane-related pathways (phosphatidylcholine synthesis and alpha linolenic acid and linoleic acid metabolism), and various amino acid metabolism pathways to be most affected. These highlighted pathways should be targeted in future investigations to evaluate their potential in mitigating or preventing the development of negative health effects associated with AFB1 exposure.

Decoding senescence of aging single cells at the nexus of biomaterials, microfluidics, and spatial omics.

Aging has profound effects on the body, most notably an increase in the prevalence of several diseases. An important aging hallmark is the presence of senescent cells that no longer multiply nor die off properly. Another characteristic is an altered immune system that fails to properly self-surveil. In this multi-player aging process, cellular senescence induces a change in the secretory phenotype, known as senescence-associated secretory phenotype (SASP), of many cells with the intention of recruiting immune cells to accelerate the clearance of these damaged senescent cells. However, the SASP phenotype results in inducing secondary senescence of nearby cells, resulting in those cells becoming senescent, and improper immune activation resulting in a state of chronic inflammation, called inflammaging, in many diseases. Senescence in immune cells, termed immunosenescence, results in further dysregulation of the immune system. An interdisciplinary approach is needed to physiologically assess aging changes of the immune system at the cellular and tissue level. Thus, the intersection of biomaterials, microfluidics, and spatial omics has great potential to collectively model aging and immunosenescence. Each of these approaches mimics unique aspects of the body undergoes as a part of aging. This perspective highlights the key aspects of how biomaterials provide non-cellular cues to cell aging, microfluidics recapitulate flow-induced and multi-cellular dynamics, and spatial omics analyses dissect the coordination of several biomarkers of senescence as a function of cell interactions in distinct tissue environments. An overview of how senescence and immune dysregulation play a role in organ aging, cancer, wound healing, Alzheimer's, and osteoporosis is included. To illuminate the societal impact of aging, an increasing trend in anti-senescence and anti-aging interventions, including pharmacological interventions, medical procedures, and lifestyle changes is discussed, including further context of senescence.

Engineered exosomes in service of tumor immunotherapy: From optimizing tumor-derived exosomes to delivering CRISPR/Cas9 system.

Exosomes can be modified and designed for various therapeutic goals because of their unique physical and chemical characteristics. Researchers have identified tumor-derived exosomes (TEXs) as significant players in cancer by influencing tumor growth, immune response evasion, angiogeneis, and drug resistance. TEXs promote the production of specific proteins important for cancer progression. Due to their easy accessibility, TEXs are being modified through genetic, drug delivery, membrane, immune system, and chemical alterations to be repurposed as vehicles for delivering drugs to improve cancer treatment outcomes. In the complex in vivo environment, the clustered regularly interspaced short palindromic repeats and CRISPR-associated protein 9 (CRISPR/Cas9) system encounters challenges from degradation, neutralization, and immune responses, emphasizing the need for strategic distribution strategies for effective genome editing. Engineered exosomes present a promising avenue for delivering CRISPR/Cas9 in vivo. In this review, we will explore different techniques for enhancing TEXs using various engineering strategies. Additionally, we will discuss how these exosomes can be incorporated into advanced genetic engineering systems like CRISPR/Cas9 for possible therapeutic uses.

Unexplained Recurrent Pregnancy Loss: Clinical Application of Immunophenotyping.

Recurrent pregnancy loss (RPL) is defined as the failure of two or more pregnancies and affects approximately 5% of couples, often without a clear cause. The etiologies of RPL include factors such as maternal age, endocrine dysfunction, uterine abnormalities, chromosomal abnormalities, thrombophilias, infections, and autoimmune disorders. However, these conditions account for only 50%-60% of RPL cases. Research has explored whether an altered immune system, compared to the physiological state, may be linked to RPL. This review aims to determine whether specific immunophenotypes are associated with unexplained Recurrent Pregnancy Loss (uRPL) and whether targeted therapies addressing specific immunophenotypic alterations can improve pregnancy outcomes. A literature review was conducted using Pubmed/Medline, Scopus, and Embase databases, analyzing data from 95 articles published between 2001 and 2023. The roles of various cells of the immune system (B lymphocytes, T lymphocytes, natural killer cells, macrophages) in different tissues (peripheral blood, menstrual blood) were specifically investigated in women with uRPL. Specific immunophenotypes have been demonstrated to be associated with this condition. However, there is a need to standardize immunophenotyping assays and conduct more trials to stratify RPL risk and improve potential therapeutic strategies.

The effects of stress on gut virome: Implications on infectious disease and systemic disorders.

The role of gut microbiota in health and disease is being thoroughly examined in various contexts, with a specific focus on the bacterial fraction due to its significant abundance. However, despite their lower abundance, viruses within the gut microbiota are gaining recognition for their crucial role in shaping the structure and function of the intestinal microbiota, with significant effects on the host as a whole, particularly the immune system. Similarly, environmental factors such as stress are key in modulating the host immune system, which in turn influences the composition of the gut virome and neurological functions through the bidirectional communication of the gut-brain axis. In this context, alterations in the host immune system due to stress and/or dysbiosis of the gut virome are critical factors in the development of both infectious and noninfectious diseases. The molecular mechanisms and correlation patterns between microbial species are not yet fully understood. This literature review seeks to explore the interconnected relationship between stress and the gut virome, with a focus on how this interaction is influenced by the host's immune system. We also discuss how disturbances in this finely balanced system can lead to the onset and/or progression of diseases.

Effects of Schistosoma haematobium infection and treatment on the systemic and mucosal immune phenotype, gene expression and microbiome: A systematic review.

Urogenital schistosomiasis caused by Schistosoma haematobium affects approximately 110 million people globally, with the majority of cases in low- and middle-income countries. Schistosome infections have been shown to impact the host immune system, gene expression, and microbiome composition. Studies have demonstrated variations in pathology between schistosome subspecies. In the case of S. haematobium, infection has been associated with HIV acquisition and bladder cancer. However, the underlying pathophysiology has been understudied compared to other schistosome species. This systematic review comprehensively investigates and assimilates the effects of S. haematobium infection on systemic and local host mucosal immunity, cellular gene expression and microbiome. We conducted a systematic review assessing the reported effects of S. haematobium infections and anthelmintic treatment on the immune system, gene expression and microbiome in humans and animal models. This review followed PRISMA guidelines and was registered prospectively in PROSPERO (CRD42022372607). Randomized clinical trials, cohort, cross-sectional, case-control, experimental ex vivo, and animal studies were included. Two reviewers performed screening independently. We screened 3,177 studies and included 94. S. haematobium was reported to lead to: (i) a mixed immune response with a predominant type 2 immune phenotype, increased T and B regulatory cells, and select pro-inflammatory cytokines; (ii) distinct molecular alterations that would compromise epithelial integrity, such as increased metalloproteinase expression, and promote immunological changes and cellular transformation, specifically upregulation of genes p53 and Bcl-2; and (iii) microbiome dysbiosis in the urinary, intestinal, and genital tracts. S. haematobium induces distinct alterations in the host's immune system, molecular profile, and microbiome. This leads to a diverse range of inflammatory and anti-inflammatory responses and impaired integrity of the local mucosal epithelial barrier, elevating the risks of secondary infections. Further, S. haematobium promotes cellular transformation with oncogenic potential and disrupts the microbiome, further influencing the immune system and genetic makeup. Understanding the pathophysiology of these interactions can improve outcomes for the sequelae of this devastating parasitic infection.

A Transcriptomic Analysis of Laryngeal Dysplasia.

This article describes how the transcriptional alterations of the innate immune system divide dysplasias into aggressive forms that, despite the treatment, relapse quickly and more easily, and others where the progression is slow and more treatable. It elaborates on how the immune system can change the extracellular matrix, favoring neoplastic progression, and how infections can enhance disease progression by increasing epithelial damage due to the loss of surface immunoglobulin and amplifying the inflammatory response. We investigated whether these dysregulated genes were linked to disease progression, delay, or recovery. These transcriptional alterations were observed using the RNA-based next-generation sequencing (NGS) panel Oncomine Immune Response Research Assay (OIRRA) to measure the expression of genes associated with lymphocyte regulation, cytokine signaling, lymphocyte markers, and checkpoint pathways. During the analysis, it became apparent that certain alterations divide dysplasia into two categories: progressive or not. In the future, these biological alterations are the first step to provide new treatment modalities with different classes of drugs currently in use in a systemic or local approach, including classical chemotherapy drugs such as cisplatin and fluorouracile, older drugs like fenretinide, and new checkpoint inhibitor drugs such as nivolumab and pembrolizumab, as well as newer options like T cell therapy (CAR-T). Following these observed alterations, it is possible to differentiate which dysplasias progress or not or relapse quickly. This information could, in the future, be the basis for determining a close follow-up, minimizing surgical interventions, planning a correct and personalized treatment protocol for each patient and, after specific clinical trials, tailoring new drug treatments.

Level of selected exponents of the kynurenine pathway in patients diagnosed with depression and selected cancers

Altered immune system activity is one of the common pathomechanisms of depressive disorders and cancer. The aim of this study is to evaluate level of selected elements of the kynurenine pathway in groups of depressed and oncological patients. The study included 156 individuals, aged 19–65 years (M = 43.46, SD = 13.99), divided into three groups, namely depressive disorders (DD), oncology patients (OG), and a comparison group of healthy subjects (CG). A sociodemographic questionnaire and the Hamilton Depression Rating Scale (HDRS) were used in the study to assess the intensity of depressive symptoms. Level of TDO2, L-KYN, HK, AA and QA was significantly higher in patients from OG and DD groups than in the comparison group. TDO2 level in the OG group was positively correlated with the severity of depressive symptoms. When the OG and DD groups were analyzed together, level of TDO2, 3-HKYN, AA, QA correlated positively with the severity of depressive symptoms. Thus, kynurenine pathway might play an integral role in the pathogenesis of depression.

T-Cell Senescence in Human Metabolic Diseases.

Immunosenescence denotes a state of dysregulated immune cell function characterized by a confluence of factors, including arrested cell cycle, telomere shortening, markers of cellular stress, mitochondrial dysfunction, loss of proteostasis, epigenetic reprogramming, and secretion of proinflammatory mediators. This state primarily manifests during the aging process but can also be induced in various pathological conditions, encompassing chronic viral infections, autoimmune diseases, and metabolic disorders. Age-associated immune system alterations extend to innate and adaptive immune cells, with T-cells exhibiting heightened susceptibility to immunosenescence. In particular, senescent T-cells have been identified in the context of metabolic disorders such as obesity, diabetes, and cardiovascular diseases. Recent investigations suggest a direct link between T-cell senescence, inflammation, and insulin resistance. The perturbation of biological homeostasis by senescent T-cells appears intricately linked to the initiation and progression of metabolic diseases, particularly through inflammation-mediated insulin resistance. Consequently, senescent T-cells are emerging as a noteworthy therapeutic target. This review aims to elucidate the intricate relationship between metabolic diseases and T-cell senescence, providing insights into the potential roles of senescent T-cells in the pathogenesis of metabolic disorders. Through a comprehensive examination of current research findings, this review seeks to contribute to a deeper understanding of the complex interplay between immunosenescence and metabolic health.

Long COVID Syndrome: A Narrative Review on Burden of Age and Vaccination.

Background/Objective: The COVID-19 pandemic has led to the emergence of post-acute COVID-19 syndrome, also known as long COVID, which presents a significant challenge due to its varied symptoms and unpredictable course, particularly in older adults. Similar to COVID-19 infections, factors such as age, pre-existing health conditions, and vaccination status may influence the occurrence and severity of long COVID. The objective is to analyze the role of aging in the context of long COVID and to investigate prevalence rates and vaccination efficacy to improve prevention strategies and treatment in this age group. Methods: Four researchers independently conducted a literature search of the PubMed database to trace studies published between July 2020 and July 2024. Results: Aging influences both the likelihood of developing long COVID and the recovery process, due to age-related physiological changes, immune system alterations, and the presence of comorbidities. Vaccination plays a key role in reducing the risk of long COVID by attenuating the inflammatory responses associated with its symptoms. Conclusions: Despite the protection vaccines offer against severe infection, hospitalization, and post-infection sequelae, vaccine hesitancy remains a major obstacle, worsening the impact of long COVID. Promising treatments for this condition include antivirals although further research is needed.

Anti-ulcerogenic Potential of Kalanchoë gastonis-bonnieri Extracts in Male ICR Mice Model of Ethanol-induced Gastric Ulcers.

Peptic ulcers (PU) are a breach in the mucosa of the digestive tract and are related to several factors including an altered immune system and an unbalanced diet. Current treatment carries to long-term complications; therefore, the use of medicinal plants is an alternative for several inflammatory diseases including ulcerative lesions. Kalanchoë gastonis-bonnieri, is a succulent plant and, has been used in traditional medicine against gastric ulcers, inflammation, and cancer among others. The main goal of this work was to analyze the anti-ulcerogenic potential of extracts from leaves of K. gastonis-bonnieri in an assay of ethanol-induced gastric ulcers. An ethanolic extract was obtained by maceration from fresh leaves of K. gastonis-bonnieri, and fractions were obtained through bipartition and chemical fractioning. The chemical characterization of the extract was made through HPLC, GC-MS, and NMR. Total extract and fractions showed an anti-ulcerogenic effect in specimens of male ICR mice with a gastric ulcer index (UI) of 3.27-5.47. The recorded effect is attributed to the presence of terpenoid compounds such as β-Amyrin acetate, which showed antioxidant properties and lessened formations of ulcers induced by ethanol administration in mice stomach.

Association between cardiovascular inflammation and alterations in immune system induced by HIV infection detected on [18F]FDG PET/MRI

ObjectiveTo assess by [18F]FDG PET/MR the biomarkers of HIV-induced inflammation at baseline and 1 year post-antiretroviral therapy (ART). MethodsProspective study, 14 patients, newly diagnosed HIV-positive, asymptomatic.[18F]FDG PET/MRI (PET/MR-3.0T, Signa.GE) whole body and heart was performed, baseline and 1 year post-ART.Qualitative vascular assessment (hepatic reference). Quantitative assessment (SUVmax) of the whole body. T1 and T2 value estimation in 16 myocardial segments. ResultsBaseline CMR showed in 3 (21.4%) a decreased LVEF, normalising post-TAR. Fibrosis was ruled out (T1), with no signs of myocardial oedema (T2) at baseline or post-TAR.Four (28.6%) showed baseline vascular [18F]FDG uptake, two in ascending thoracic aorta and two in ascending and descending thoracic aorta, normalising post-TAR.All (100%) showed basal lymph-nodes activity; supra (n:14) and infradiaphragmatic (n:13), laterocervical (n:14) and inguinal (n:13), with variable number of territories (9 patients >6;64.3%). Post-ART, 7 patients (50%) showed resolution and the other 7 reduction in extension (0 patients >5): 7 supra (100%) and 2 infradiaphragmatic (28.6%), 5 in the axilla and 2 in the groin.All (100%) had persistent basal adenoid uptake post-ART, 9 (64.3%) splenic all resolved post-ART and 7 (50.5%) gastric, persistent 3 post-ART. ConclusionsCardiovascular biomarkers by [18F]FDG PET/MR have shown baseline 28.6% of patients with large vessel activity and 21.4% with low LVEF, normalising post-ART.Inflammatory/immune biomarkers showed baseline activity in 100% of lymph-nodes, 100% adenoids, 64.3% splenic and 50.5% gastric. Post-TAR the reduction was 50% lymph-nodes, 0% adenoid, 100% splenic and 57.1% gastric.

Necroptosis in recurrent implantation failure: A bioinformatics analysis of key genes and therapeutic targets.

Recurrent implantation failure (RIF), a major issue in assisted reproductive technology (ART), may be influenced by necroptosis, a form of cell death linked to several diseases. This study was aimed at investigating the involvement of necroptosis in RIF. Using RNA-sequencing data from the Gene Expression Omnibus database, we identified differentially expressed necroptosis-related genes (DENRGs) in RIF patients compared with those in controls. Functional enrichment, protein-protein interaction (PPI) networks, and transcription factor (TF) regulatory networks were analyzed to identify key genes. Immune cell infiltration was analyzed using the single-sample gene set enrichment analysis (ssGSEA) algorithm. Finally, potential therapeutic drugs targeting key genes were explored using a Drug Gene Interaction Database. In total, 20 DENRGs associated with RIF were identified, with a focus on 6 key genes (MLKL, FASLG, XIAP, CASP1, BIRC3, and TLR3) implicated in necroptosis and immune processes. These genes were used to develop a predictive model for RIF, which was validated in 2 datasets. The model and TF network analysis underscored the importance of TLR3. Immune infiltration analysis showed reduced levels of 16 immune cells in RIF patients, highlighting immune system alterations. Several drugs targeting CASP1, such as nivocasan and emricasan, were identified as potential treatments. The study sheds light on the role of necroptosis in RIF, identifying key genes and immune alterations that could serve as biomarkers and therapeutic targets. These findings pave the way for future experimental research and clinical applications targeting necroptosis in RIF treatment.

Maternal Malaria and the Risk of Subsequent Pregnancy Complications

Maternal malaria, primarily caused by Plasmodium falciparum, has well-documented immediate effects on pregnancy, including preterm birth, low birth weight, and placental dysfunction. However, its impact extends beyond the current pregnancy, potentially influencing outcomes in subsequent pregnancies. This review examines how maternal malaria affects future pregnancies, focusing on the mechanisms through which previous malaria infections contribute to subsequent complications. Key mechanisms include chronic placental damage, immune system alterations, and persistent inflammation, which can disrupt placental function and increase the risk of adverse outcomes such as preterm labor and placental abruption in future pregnancies. The review highlights evidence that women with a history of maternal malaria are at an elevated risk for complications in subsequent pregnancies, including an increased likelihood of preterm birth and low birth weight. Persistent placental damage and immune dysregulation resulting from past malaria infections contribute to these risks. Understanding these long-term effects is crucial for developing effective public health strategies and interventions aimed at mitigating the risks of adverse pregnancy outcomes in malaria-endemic regions. Keywords: Maternal malaria, Plasmodium falciparum, pregnancy complications, placental damage, immune dysregulation, chronic inflammation, preterm birth

The Influence of Premature Birth on the Development of Pulmonary Diseases: Focus on the Microbiome.

Globally, around 11% of neonates are born prematurely, comprising a highly vulnerable population with a myriad of health problems. Premature births are often accompanied by an underdeveloped immune system biased towards a Th2 phenotype and microbiota dysbiosis. Typically, a healthy gut microbiota interacts with the host, driving the proper maturation of the host immunity. However, factors like cesarean section, formula milk feeding, hospitalization in neonatal intensive care units (NICU), and routine antibiotic treatments compromise microbial colonization and increase the risk of developing related diseases. This, along with alterations in the innate immune system, could predispose the neonates to the development of respiratory diseases later in life. Currently, therapeutic strategies are mainly focused on restoring gut microbiota composition using probiotics and prebiotics. Understanding the interactions between the gut microbiota and the immature immune system in premature neonates could help to develop novel therapeutic strategies for treating or preventing gut-lung axis disorders.

Transcriptome profiling reveals distinct alterations in the B-cell signature and dysregulation of peripheral B-cell subsets in sickle cell anemia patients

Sickle cell anemia (SCA) is characterized by immune system activation and heightened susceptibility to infections. We hypothesized that SCA patients exhibit transcriptional alterations in B-cell-related genes, impacting their peripheral B-cell compartment and leading to dysregulated humoral immunity and increased infection susceptibility. Our objective was to conduct an in silico analysis of whole blood transcriptomes from SCA patients and healthy controls obtained from public repositories. We aimed to identify alterations in the adaptive immune system and validate these findings in our own SCA patient cohort. Bioinformatic analyses unveiled significant transcriptional alterations in B-cell signatures, developmental pathways, and signaling pathways. These results were validated in peripheral blood mononuclear cells from our SCA patient cohort and controls using real-time polymerase chain reaction and flow cytometry. Ninety genes exhibited differential expression, with 70 upregulated and 20 downregulated. Dysregulation in the B-cell compartment of SCA patients was evident, characterized by increased frequencies of immature and naive B-cells, and decreased percentages of memory B-cell subsets compared with healthy controls. Our findings highlight previously unexplored transcriptional and quantitative alterations in peripheral B-cells among SCA patients. Understanding these changes sheds light on the mechanisms contributing to the heightened infection risk in this population. Future studies should delve deeper into these molecular changes to develop targeted interventions and therapeutic strategies aimed at mitigating infection susceptibility in individuals with SCA.