Adverse health effects of emerging contaminants on inflammatory bowel disease

Chen, Xuejie; Wang, Sidan; Mao, Xueyi; Xiang, Xin; Ye, Shuyu; Chen, Jie; Zhu, Angran; Meng, Yunlong; Yang, Xiya; Peng, Shuyu; Deng, Minzi; Wang, Xiaoyan

doi:10.3389/fpubh.2023.1140786

Cited by 12 publications

(6 citation statements)

References 198 publications

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“…This is not surprising because the gastrointestinal tract harbors the most abundant lymphoid tissues and microbial community ( 163 , 164 ). The microbial community and gut homeostasis are constantly subject to various environmental challenges ( 165 , 166 ), including pathogen intruders ( 167 – 170 ), chemical damage ( 171 , 172 ), drug exposure ( 173 – 175 ), and nutrient delivery ( 176 – 178 ). Harmful challenges can compromise the integrity of the intestinal epithelium, induce dysfunction, cause dysbiosis, and trigger gut inflammatory disorders; these can occur not only by injuring diseased segments but also by affecting other segments through disruption of microbial ecology ( 179 – 181 ).…”

Section: Contribution Of Inflammatory Stressors To Autoimmune Diseasesmentioning

confidence: 99%

When inflammatory stressors dramatically change, disease phenotypes may transform between autoimmune hematopoietic failure and myeloid neoplasms

Zhao,

Ju,

Xiu

et al. 2024

Front. Immunol.

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Aplastic anemia (AA) and hypoplastic myelodysplastic syndrome are paradigms of autoimmune hematopoietic failure (AHF). Myelodysplastic syndrome and acute myeloid leukemia are unequivocal myeloid neoplasms (MNs). Currently, AA is also known to be a clonal hematological disease. Genetic aberrations typically observed in MNs are detected in approximately one-third of AA patients. In AA patients harboring MN-related genetic aberrations, a poor response to immunosuppressive therapy (IST) and an increased risk of transformation to MNs occurring either naturally or after IST are predicted. Approximately 10%–15% of patients with severe AA transform the disease phenotype to MNs following IST, and in some patients, leukemic transformation emerges during or shortly after IST. Phenotypic transformations between AHF and MNs can occur reciprocally. A fraction of advanced MN patients experience an aplastic crisis during which leukemic blasts are repressed. The switch that shapes the disease phenotype is a change in the strength of extramedullary inflammation. Both AHF and MNs have an immune-active bone marrow (BM) environment (BME). In AHF patients, an inflamed BME can be evoked by infiltrated immune cells targeting neoplastic molecules, which contributes to the BM-specific autoimmune impairment. Autoimmune responses in AHF may represent an antileukemic mechanism, and inflammatory stressors strengthen antileukemic immunity, at least in a significant proportion of patients who have MN-related genetic aberrations. During active inflammatory episodes, normal and leukemic hematopoieses are suppressed, which leads to the occurrence of aplastic cytopenia and leukemic cell regression. The successful treatment of underlying infections mitigates inflammatory stress-related antileukemic activities and promotes the penetration of leukemic hematopoiesis. The effect of IST is similar to that of treating underlying infections. Investigating inflammatory stress-powered antileukemic immunity is highly important in theoretical studies and clinical practice, especially given the wide application of immune-activating agents and immune checkpoint inhibitors in the treatment of hematological neoplasms.

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Section: Contribution Of Inflammatory Stressors To Autoimmune Diseasesmentioning

confidence: 99%

When inflammatory stressors dramatically change, disease phenotypes may transform between autoimmune hematopoietic failure and myeloid neoplasms

Zhao,

Ju,

Xiu

et al. 2024

Front. Immunol.

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“…Emerging contaminants closely linked with daily human life can be categorized as biological (e.g., resistant genes, algal toxins), chemical (e.g., novel pesticides, endocrine disruptors, flame retardants, antibiotics, perfluorinated compounds), and physical (e.g., microplastics, nanomaterials) [ 22 , 30 , 31 ]. Based on publicly available regional or site-specific monitoring data, typical emerging pollutants in China mainly include endocrine disruptors, perfluorinated compounds, microplastics, and antibiotics, all of which are causing severe pollution issues in the air, water, and soil environments [ 22 , 30 ]. Numerous published articles have indicated that the presence of emerging pollutants in the environment increases the risk of diabetes in exposed populations and accelerates the onset and progression of the disease.…”

Section: Emerging Contaminants (Ecs)mentioning

confidence: 99%

Emerging Contaminants: An Emerging Risk Factor for Diabetes Mellitus

Niu,

Xu,

et al. 2024

Toxics

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Emerging contaminants have been increasingly recognized as critical determinants in global public health outcomes. However, the intricate relationship between these contaminants and glucose metabolism remains to be fully elucidated. The paucity of comprehensive clinical data, coupled with the need for in-depth mechanistic investigations, underscores the urgency to decipher the precise molecular and cellular pathways through which these contaminants potentially mediate the initiation and progression of diabetes mellitus. A profound understanding of the epidemiological impact of these emerging contaminants, as well as the elucidation of the underlying mechanistic pathways, is indispensable for the formulation of evidence-based policy and preventive interventions. This review systematically aggregates contemporary findings from epidemiological investigations and delves into the mechanistic correlates that tether exposure to emerging contaminants, including endocrine disruptors, perfluorinated compounds, microplastics, and antibiotics, to glycemic dysregulation. A nuanced exploration is undertaken focusing on potential dietary sources and the consequential role of the gut microbiome in their toxic effects. This review endeavors to provide a foundational reference for future investigations into the complex interplay between emerging contaminants and diabetes mellitus.

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“…The prevalence of inflammatory bowel disease (IBD) has increased over time closely in step with the rise in glyphosate usage on core crops [57]. Glyphosate was one of the toxic chemicals identified as a contributor to IBD in a recent publication by Chen et al [58]. Children with autism are at a significant increased risk to IBD, with an odds ratio (OR) of 1.66 (p < 0.001) [59].…”

Section: Glyphosate and Autismmentioning

confidence: 99%

Is Autism a PIN1 Deficiency Syndrome? A Proposed Etiological Role for Glyphosate

Seneff,

Kyriakopoulos,

Nigh

2024

Preprint

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Autism is a neurodevelopmental disorder whose prevalence has increased dramatically in the United States over the past two decades. It is characterized by stereotyped behaviors and impairments in social interaction and communication. In this paper, we present evidence that autism can be viewed as a PIN1 deficiency syndrome. PIN1 (Peptidylprolyl Cis/Trans Isomerase, NIMA-Interacting 1) is a peptidylprolyl cis/trans isomerase, and it has widespread influences in biological organisms. Broadly speaking, PIN1 deficiency is linked to many neurodegenerative diseases, whereas PIN1 overexpression is linked to cancer. Death associated protein kinase 1 (DAPK1) strongly inhibits PIN1, and the hormone melatonin inhibits DAPK1. Melatonin deficiency is strongly linked to autism. It has recently been shown that glyphosate exposure to rats inhibits melatonin synthesis due to increased glutamate release from glial cells and increased expression of metabotropic glutamate receptors. Glyphosate's inhibition of melatonin leads to a reduction in PIN1 availability in neurons. In this paper, we show that PIN1 deficiency can explain many of the unique morphological features of autism, including increased dendritic spine density, missing or thin corpus callosum and reduced bone density. We show how PIN1 deficiency disrupts the functioning of powerful high level signaling molecules, such as nuclear factor erythroid 2-related factor 2 (NRF2) and p53. Dysregulation of both of these proteins has been linked to autism. Severe depletion of glutathione in the brain resulting from chronic exposure to oxidative stressors and extracellular glutamate leads to oxidation of the cysteine residue in PIN1, inactivating the protein and further contributing to PIN1 deficiency. Impaired autophagy leads to increased sensitivity of neurons to ferroptosis. Finally, we consider evidence of the potential toxic effects of the mRNA SARS-CoV-2 vaccines in the light of metabolic defects in autism, and we propose that children with autism would be especially sensitive to damage from the vaccines.

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Adverse health effects of emerging contaminants on inflammatory bowel disease

Cited by 12 publications

References 198 publications

When inflammatory stressors dramatically change, disease phenotypes may transform between autoimmune hematopoietic failure and myeloid neoplasms

When inflammatory stressors dramatically change, disease phenotypes may transform between autoimmune hematopoietic failure and myeloid neoplasms

Emerging Contaminants: An Emerging Risk Factor for Diabetes Mellitus

Is Autism a PIN1 Deficiency Syndrome? A Proposed Etiological Role for Glyphosate

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