Kenny De Meirleir’s research while affiliated with Pennington Biomedical Research Center and other places

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Publications (183)


Role of Mycoplasmal Infections in Fatigue Illnesses: Chronic Fatigue and Fibromyalgia Syndromes, Gulf War Illness and Rheumatoid Arthritis
  • Chapter
  • Full-text available

October 2024

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76 Reads

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A.R. Franco

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J. Haier

Bacterial and viral infections are associated with several fatigue illnesses, including Chronic Fatigue Syndrome (CFS), Fibromyalgia Syndrome (FMS), Gulf War Illnesses (GWI) and Rheumatoid Arthritis (RA), as causative agents, cofactors or opportunistic infections. We and others have looked for the presence of invasive pathogenic mycoplasmal infections in patients with CFS, FMS, GWI and RA and have found significantly more mycoplasmal infections in CFS, FMS, GWI and RA patients than in healthy controls. Most patients had multiple mycoplasmal infections (more than one species). Patients with chronic fatigue as a major sign often have different clinical diagnoses but display overlapping signs/symptoms similar to many of those found in CFS/FMS. When a chronic fatigue illness, such as GWI, spreads to immediate family members, they present with similar signs/symptoms and mycoplasmal infections. CFS/FMS/GWI patients with mycoplasmal infections generally respond to particular antibiotics (doxycycline, minocycline, ciprofloxacin, azithromycin and clarithromycin), and their long-term administration plus nutritional support, immune enhancement and other supplements appear to be necessary for recovery. Examination of the efficacy of antibiotics in recovery of chronic illness patients reveals that the majority of mycoplasma-positive patients respond and many eventually recover. Other chronic infections, such as viral infections, may also be involved in various chronic fatigue illnesses with or without mycoplasmal and other bacterial infections, and these multiple infections could be important in causing patient morbidity and difficulties in treating these illnesses.

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Figure 4. Secretory IgA promotes GI homeostasis through immune exclusion. Dysbioticbacterial metabolites promote cell-mediated immune responses (1). Activation of these responses promotes the production of dimeric IgA by plasma cells (2). Dimeric IgA covalently binds to the polymeric immunoglobin receptor (pIgR) and is transported from the basolateral side of the gut epithelium to the apical side, where it is released by luminal proteases and subsequently binds to commensal bacteria (3), promoting GI homeostasis (4) [105].
Mucosal Immunity and the Gut-Microbiota-Brain-Axis in Neuroimmune Disease

November 2022

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265 Reads

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17 Citations

International Journal of Molecular Sciences

Recent advances in next-generation sequencing (NGS) technologies have opened the door to a wellspring of information regarding the composition of the gut microbiota. Leveraging NGS technology, early metagenomic studies revealed that several diseases, such as Alzheimer’s disease, Parkinson’s disease, autism, and myalgic encephalomyelitis, are characterized by alterations in the diversity of gut-associated microbes. More recently, interest has shifted toward understanding how these microbes impact their host, with a special emphasis on their interactions with the brain. Such interactions typically occur either systemically, through the production of small molecules in the gut that are released into circulation, or through signaling via the vagus nerves which directly connect the enteric nervous system to the central nervous system. Collectively, this system of communication is now commonly referred to as the gut-microbiota-brain axis. While equally important, little attention has focused on the causes of the alterations in the composition of gut microbiota. Although several factors can contribute, mucosal immunity plays a significant role in shaping the microbiota in both healthy individuals and in association with several diseases. The purpose of this review is to provide a brief overview of the components of mucosal immunity that impact the gut microbiota and then discuss how altered immunological conditions may shape the gut microbiota and consequently affect neuroimmune diseases, using a select group of common neuroimmune diseases as examples.


Figure 1. Manhattan plot of genome-wide association raw p-values. The horizontal line corresponds to single SNP associations with p-values of p=1×10 −5 .
Figure 3. A genotypic organization of 32 controls (first 32 columns) and 38 MHO cases (last 38 columns) on chromosome 8 between 115,612,652 and 115,613,480 containing the TRPS1 gene. The distinct genotypic pattern shared by the ten cases is seen in only three controls.
Figure 4. A genotypic organization of 32 controls (first 32 columns) and 38 MHO cases (last 38 columns) on chromosome 20 between 44,045,208 and 44,042,793, containing the TOX2 gene. The genotypic pattern shared by the three MHO cases at the top left of the second panel does not occur in any of the controls.
A genotypic organization of 32 controls (first 32 columns) and 38 MHO cases (last 38 columns) on chromosome 6 between 163,712,118 and 163,772,486, containing the LOC107986666 gene. This region contains seven SNPs found to be statistically significantly associated with the MHO cohort. The first seven cases show a haplotypic pattern not shared by the control cohort: the red cells represent the homozygous genotype of the minor allele and the light blue cells denote the homozygous genotype of the major allele. Also, of note, is the rather distinct region that the last eight control samples share. These are relatively large haplotypic regions not typically shared between many individuals. The color bar, directly to the left of the heatmap, shows the intragenic and near-gene nature of most of the SNPs in the region
Single-nucleotide polymorphisms in a cohort of significantly obese women without cardiometabolic diseases

February 2019

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85 Reads

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17 Citations

International Journal of Obesity

Background/objectives: Obesity is an important risk factor for the development of diseases such as diabetes mellitus, hypertension, and dyslipidemia; however, a small number of individuals with long-standing obesity do not present with these cardiometabolic diseases. Such individuals are referred to as metabolically healthy obese (MHO) and potentially represent a subgroup of the general population with a protective genetic predisposition to obesity-related diseases. We hypothesized that individuals who were metabolically healthy, but significantly obese (BMI ≥ 35 kg/m2) would represent a highly homogenous subgroup, with which to investigate potential genetic associations to obesity. We further hypothesized that such a cohort may lend itself well to investigate potential genotypes that are protective with respect to the development of cardiometabolic disease. Subjects/methods: In the present study, we implemented this novel selection strategy by screening 892 individuals diagnosed as Class 2 or Class 3 obese and identified 38 who presented no manifestations of cardiometabolic disease. We then assessed these subjects for single-nucleotide polymorphisms (SNPs) that associated with this phenotype. Results: Our analysis identified 89 SNPs that reach statistical significance (p < 1 × 10-5), some of which are associated with genes of biological pathways that influences dietary behavior; others are associated with genes previously linked to obesity and cardiometabolic disease as well as neuroimmune disease. This study, to the best of our knowledge, represents the first genetic screening of a cardiometabolically healthy, but significantly obese population.





Decision tree produced using CART analysis. Each node represents a split value of the independent variable, which determines the optimal number cases or controls predicted by the analysis. Colored boxes represent the terminal point of the decision metric. Blue boxes represent cases and red boxes represent controls. A comprehensive version of the decision tree, which defines the predictive algorithm, is presented as Additional file 1: Figure S1
Evaluation of four clinical laboratory parameters for the diagnosis of myalgic encephalomyelitis

November 2018

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220 Reads

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3 Citations

Journal of Translational Medicine

Background Myalgic encephalomyelitis (ME) is a complex and debilitating disease that often initially presents with flu-like symptoms, accompanied by incapacitating fatigue. Currently, there are no objective biomarkers or laboratory tests that can be used to unequivocally diagnosis ME; therefore, a diagnosis is made when a patient meets series of a costly and subjective inclusion and exclusion criteria. The purpose of the present study was to evaluate the utility of four clinical parameters in diagnosing ME. Methods In the present study, we utilized logistic regression and classification and regression tree analysis to conduct a retrospective investigation of four clinical laboratory in 140 ME cases and 140 healthy controls. Results Correlations between the covariates ranged between [− 0.26, 0.61]. The best model included the serum levels of the soluble form of CD14 (sCD14), serum levels of prostaglandin E2 (PGE2), and serum levels of interleukin 8, with coefficients 0.002, 0.249, and 0.005, respectively, and p-values of 3 × 10⁻⁷, 1 × 10⁻⁵, and 3 × 10⁻³, respectively. Conclusions Our findings show that these parameters may help physicians in their diagnosis of ME and may additionally shed light on the pathophysiology of this disease. Electronic supplementary material The online version of this article (10.1186/s12967-018-1696-z) contains supplementary material, which is available to authorized users.




Biomedical approach in autism spectrum disorders—the importance of assessing inflammation

July 2018

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204 Reads

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7 Citations

Autism spectrum disorders (ASD) are severe heterogeneous neurodevelopmental disorders characterized by dysfunctions in social interaction and communication skills, repetitive and stereotypic verbal and nonverbal behaviors. Published findings have identified widespread changes in the immune systems of children with autism, at the systemic and cellular levels, suggesting that autism may, in fact, be a systemic disorder with connections to abnormal immune responses. Evaluating autism is hindered by a lack of specific biomarkers, making these pathologies difficult to diagnose. A critical priority for the future of ASD management is the identification of potential targets for the development of diagnostic and therapeutic strategies. The purpose of this brief report is to raise awareness regarding the involvement of different inflammatory processes in ASD and the need to assess them as a part of a biomedical evaluation. An extensive analysis of biomarkers relating to inflammation, immune dysfunctions, intestinal dysfunctions and infections will assist in the management of the autistic patient through a more personalized therapy.


Citations (73)


... 77 The intestinal epithelium consists of a monolayer of intestinal epithelial cells (IEC), primarily made up of enterocytes and specialized cells, which serve as the primary point of contact between the host and microbes. 78,79 Enteroendocrine cells (EEC) produce hormones, goblet cells produce mucus, paneth cells secrete antimicrobial peptides and microfold cells secrete immunoglobulins A (IgA) into the inner mucus, providing protection against bacterial invasion. 80 Transmembrane protein complexes, such as tight junctions and adherens junctions, that regulate intestinal permeability interconnect IEC. ...

Reference:

Effects of gastric bypass bariatric surgery on gut microbiota in patients with morbid obesity
Mucosal Immunity and the Gut-Microbiota-Brain-Axis in Neuroimmune Disease

International Journal of Molecular Sciences

... Our data are in keeping with studies identifying two distinct clusters of long COVID patients in a large UK cohort of 500,000, with fatigue predominating in one and respiratory symptoms in the other [36]. Importantly, changes in prostaglandin E2 levels (generated by COX-2 from conversion of arachidonic acid) have been associated with chronic fatigue syndrome [38] and targeting this eicosanoid pathway may be therapeutic benefit. Our data demonstrating low levels of CXCR2 associated with severe disease during acute COVID-19 and ongoing fatigue during convalescence support a protective role for CXCR2 in inflammation, in keeping with CXCR2 deficiency inducing an exaggerated inflammatory response associated with increased macrophage accumulation at inflamed sites [39]. ...

Evaluation of four clinical laboratory parameters for the diagnosis of myalgic encephalomyelitis

Journal of Translational Medicine

... This polymorphism has three alleles, namely, T, A, and G; the G allele is the dominant or wildtype allele, while the T and A alleles are the recessive alleles or single nucleotide polymorphisms (SNPs) (13). The genotype frequency of this SNP has been investigated in various diseases, including obesity (14). In SNPs, there is a difference in one nucleotide unit compared to a similar position in the DNA sequence (15). ...

Single-nucleotide polymorphisms in a cohort of significantly obese women without cardiometabolic diseases

International Journal of Obesity

... Рецепторы к окситоцину OXTR-V3, как оказалось, эксрпессируются на всех субпопуляциях Т-лифмоцитов и макрофагах, эпителиальных и эндотелиальных, стволовых клетках, в тимусе, поджелудочной железе, адпиоцитах. Периферическая поддержка синтеза окситоцина индуцируется бактериями: Лактобациллы reuteri и Lactobacillus plantarum PS128 [10,11,12]. В 2021 году в крупном рандомизированном плацебо-контролируемом исследовании было продемонстрировано, что одновременный прием интраназального окситоцина и пробиотиков Lactobacillus plantarum могут уменьшить основные социально-поведенческие симптомы у людей с РАС [9]. ...

Nutritional Modulation of the Intestinal Microbiota; Future Opportunities for the Prevention and Treatment of Neuroimmune and Neuroinflammatory Disease
  • Citing Article
  • April 2018

The Journal of Nutritional Biochemistry

... This finding implies that, at least in theory, one could explore the binding profile of a polyclonal response by sparsely and evenly sampling the entire binding space with randomly generated peptide libraries and obtain relevant information about the circulating Ab repertoire. This hypothesis is supported by previous studies directed at Ab binding profiling using solid-phase planar PMs in sera of patients diagnosed with a number of different infectious diseases to robustly distinguish circulating Ab repertoires elicited by the humoral immune response to various pathogens (30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43). In contrast to this study, these efforts used a purely statistical basis to distinguish Ab binding profiles, without taking into account the sequence information contained in the library peptides the antibodies bound to. ...

Humoral Immunity Profiling of Subjects with Myalgic Encephalomyelitis Using a Random Peptide Microarray Differentiates Cases from Controls with High Specificity and Sensitivity

Molecular Neurobiology

... Two prior studies [44,45] found that autistic people had larger absolute numbers of NK cells in their peripheral blood. While another study found that a large number of people with ASD had a decrease in their NK cell count [46], our study discovered that increasing the fraction of CD3-lymphocytes reduced the incidence of ASD. The selection and quantification of NK cells were based only on the use of CD56 and CD3 markers. ...

Decreased Numbers of CD57+CD3- Cells Identify Potential Innate Immune Differences in Patients with Autism Spectrum Disorder

In vivo (Athens, Greece)

... Other studies have found that the number of circulating NK cells is lower in children with ASD compared to typically developing children. In addition, studies have suggested that alterations in NK cell function may be related to abnormalities in cytokine signaling and oxidative stress in individuals with ASD [93,94] . Dysregulation of cytokine signaling has been implicated in the pathogenesis of ASD, and some studies have suggested that alterations in cytokine production and signaling may contribute to the altered NK cell function observed in ASD. ...

Decreased Numbers of CD57+CD3- Cells Identify Potential Innate Immune Differences in Patients with Autism Spectrum Disorder
  • Citing Article
  • February 2016

In vivo (Athens, Greece)

... Enhanced sensitivity to light and noise in ME/CFS is assumed to be due to low GABA levels. Noteworthy, a single nucleotide variant in SRRM3 was found to be associated with ME/CFS (41). In multiple sclerosis, autoantibodies to SRRM3 were found already years before the disease outbreak (42). ...

Genome-wide association analysis identifies genetic variations in subjects with myalgic encephalomyelitis/chronic fatigue syndrome

Translational Psychiatry

... Serum samples and clinical data from 121 PCS patients suffering from moderate-tosevere fatigue and exertion intolerance following mostly mild COVID-19 were collected between October 2020 and January 2024 at the ME/CFS outpatient clinic of the Institute of Medical Immunology, Charité, Berlin. From these, 72 met the CCC for diagnosis of ME/CFS [25,26]. Relevant cardiac, respiratory, neurological, or psychiatric comorbidities were excluded. ...

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Journal of Chronic Fatigue Syndrome