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1.
Am J Med Sci ; 364(6): 695-705, 2022 12.
Article in English | MEDLINE | ID: mdl-35870511

ABSTRACT

Glomerular injury is the major cause of chronic kidney diseases (CKD) worldwide and is characterized by proteinuria. Glomerulonephritis (GN) has a wide spectrum of etiologies, the intensity of glomerular damage, histopathology, and clinical outcomes that can be associated with the landscape of the nephritogenic immune response. Beyond impaired immune responses and genetic factors, recent evidence indicates that microbiota can be contributed to the pathogenesis of GN and patients' outcomes by impacting many aspects of the innate and adaptive immune systems. It is still unknown whether dysbiosis induces GN or it is a secondary effect of the disease. Several factors such as drugs and nutritional problems can lead to dysbiosis in GN patients. It has been postulated that gut dysbiosis activates immune responses, promotes a state of systemic inflammation, and produces uremic toxins contributing to kidney tissue inflammation, apoptosis, and subsequent proteinuric nephropathy. In this review, the impact of gastrointestinal tract (GI) microbiota on the pathogenesis of the primary GN will be highlighted. The application of therapeutic interventions based on the manipulation of gut microbiota with special diets and probiotic supplementation can be effective in GN.


Subject(s)
Glomerulonephritis , Microbiota , Renal Insufficiency, Chronic , Humans , Dysbiosis/complications , Glomerulonephritis/etiology , Renal Insufficiency, Chronic/complications , Inflammation/complications
2.
Pharmacol Res ; 155: 104692, 2020 05.
Article in English | MEDLINE | ID: mdl-32070720

ABSTRACT

Pre-eclampsia (PE) is a complication of pregnancy that is associated with mortality and morbidity in mothers and fetuses worldwide. Oxygen dysregulation in the placenta, abnormal remodeling of the spiral artery, defective placentation, oxidative stress at the fetal-maternal border, inflammation and angiogenic impairment in the maternal circulation are the main causes of this syndrome. These events result in a systemic and diffuse endothelial cell dysfunction, an essential pathophysiological feature of PE. The impact of bacteria on the multifactorial pathway of PE is the recent focus of scientific inquiry since microbes may cause each of the aforementioned features. Microbes and their derivatives by producing antigens and other inflammatory factors may trigger infection and inflammatory responses. A mother's bacterial communities in the oral cavity, gut, vagina, cervix and uterine along with the placenta and amniotic fluid microbiota may be involved in the development of PE. Here, we review the mechanistic and pathogenic role of bacteria in the development of PE. Then, we highlight the impact of alterations in a set of maternal microbiota (dysbiosis) on the pathogenesis of PE.


Subject(s)
Microbiota , Pre-Eclampsia/microbiology , Animals , Bacterial Infections/microbiology , Female , Humans , Hypertension/microbiology , Pregnancy
3.
Life Sci ; 233: 116680, 2019 Sep 15.
Article in English | MEDLINE | ID: mdl-31344431

ABSTRACT

Cancer is a globally challenging health problem threatening mankind. Despite therapeutic advances in dealing with this malignancy, heterogeneous response and resistance to chemotherapeutic agents remain the hallmarks of cancer therapy. On the other hand, the involvement of the microbiota in affecting human health is well defined. An ever-growing body of evidence implicates the potential link between the microbiome and the efficacy of cancer therapies. Gut microbiota can modulate the metabolism of drugs in a number of ways. The presence of bacteria within the tumor environment can also impact the responses to cancer therapies; changing the chemical structure of chemotherapeutic drugs, affecting their activity, and local concentration. However, the underlying mechanisms by which gut and tumor microbial communities affect the response to cancer therapy are poorly understood and deciphering these mechanisms is of paramount importance. This review provides an overview of how gut and tumor microbiota might affect the efficacy of chemotherapy, radiotherapy, and immunotherapy and alleviate the adverse side effects of these therapies for the development of personalized and effective anticancer therapy.


Subject(s)
Antineoplastic Agents/therapeutic use , Gastrointestinal Microbiome , Immunotherapy , Neoplasms/microbiology , Neoplasms/therapy , Radiotherapy , Humans , Neoplasms/immunology , Treatment Outcome
4.
Biochimie ; 158: 156-164, 2019 Mar.
Article in English | MEDLINE | ID: mdl-30629975

ABSTRACT

From the halophilic bacteria to human, cells have to survive under the stresses of harsh environments. Hyperosmotic stress is a process that triggers cell shrinkage, oxidative stress, DNA damage, and apoptosis and it potentially contributes to a number of human diseases. Remarkably, by high salts and organic solutes concentrations, a variety of organisms struggle with these conditions. Different strategies have been developed for cellular osmotic adaptations among which organic osmolyte synthesis/accumulation is a conserved once. Osmolytes are naturally occurring solutes used by cells of several halophilic (micro) organisms to preserve cell volume and function. In this review, the osmolytes diversity and their protective roles in harsh hyperosmolar environments from bacteria to human cells are highlighted. Moreover, it provides a close look at mammalian kidney osmoregulation at a molecular level. This review provides a concise view on the recent developments and advancements on the applications of osmolytes. Identification of disease-related osmolytes and their targeted-delivery may be used as a therapeutic measurement for treatment of the pathological conditions and the inherited diseases related to protein misfolding and aggregation. The molecular and cellular aspects of cell adaptation against harsh environmental osmolarity will benefit the development of effective drugs for many diseases.


Subject(s)
Osmoregulation , Osmotic Pressure , Protein Aggregation, Pathological/metabolism , Proteostasis Deficiencies/metabolism , Animals , Bacteria , Humans , Protein Aggregation, Pathological/pathology , Proteostasis Deficiencies/pathology
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