The immune-related adverse events resulting from the therapy of immune checkpoint inhibitors could cause kidney injury. Inflammatory reprogramming of regulatory T helper (Treg) cells or type 17 T helper (Th17) cells might be involved in the pathogenesis of nephropathy. Accumulating evidence confirms a connection between the diversity of gut microbiota and kidney diseases, suggesting that successful modification of gut microbiota could attenuate kidney injury. In other words, certain gut microbiota could contribute to the protection of kidneys via the gut-kidney axis. It has been shown that the dysbiosis of gut microbiota might affect the gut-kidney axis, leading to nephrotoxicity. On the contrary, altered levels of D-amino acids, ROS, and SCFAs through the adjustment of gut microbiota might be relevant to the reduction of nephrotoxicity. Here, we have discussed and suggested the beneficial roles of gut microbiota in the prevention of the kidney injury induced during immune-checkpoint therapy.
Citation: Sayuri Yoshikawa, Kurumi Taniguchi, Haruka Sawamura, Yuka Ikeda, Ai Tsuji, Satoru Matsuda. Promising probiotics for the treatment of nephrotoxicity induced during immune-checkpoint therapy against cancers[J]. AIMS Bioengineering, 2022, 9(3): 283-292. doi: 10.3934/bioeng.2022019
[1] | Kurumi Taniguchi, Yuka Ikeda, Nozomi Nagase, Ai Tsuji, Yasuko Kitagishi, Satoru Matsuda . Implications of Gut-Brain axis in the pathogenesis of Psychiatric disorders. AIMS Bioengineering, 2021, 8(4): 243-256. doi: 10.3934/bioeng.2021021 |
[2] | Liwei Chen, Jaslyn Lee, Wei Ning Chen . The use of metabolic engineering to produce fatty acid-derived biofuel and chemicals in Saccharomyces cerevisiae: a review. AIMS Bioengineering, 2016, 3(4): 468-492. doi: 10.3934/bioeng.2016.4.468 |
[3] | Benlong Ma, Yifang Zhang, Wenbo Yuan, Nan Hu, Shanshan Li . Gut microbiota differences between sports and non-sports major students: a population-controlled trial. AIMS Bioengineering, 2024, 11(3): 478-488. doi: 10.3934/bioeng.2024021 |
[4] | Eduardo Federighi Baisi Chagas, Piero Biteli, Bruno Moreira Candeloro, Miguel Angelo Rodrigues, Pedro Henrique Rodrigues . Physical exercise and COVID-19: a summary of the recommendations. AIMS Bioengineering, 2020, 7(4): 236-241. doi: 10.3934/bioeng.2020020 |
[5] | Xiao-Li Gu, Li Yu, Yu Du, Xiu-Peng Yang, Yong-Gang Xu . Identification and validation of aging-related genes and their classification models based on myelodysplastic syndromes. AIMS Bioengineering, 2023, 10(4): 440-465. doi: 10.3934/bioeng.2023026 |
[6] | Mayra A. Mendez-Encinas, Dora E. Valencia-Rivera, Elizabeth Carvajal-Millan, Humberto Astiazaran-Garcia, Agustín Rascón-Chu, Francisco Brown-Bojorquez . Electrosprayed highly cross-linked arabinoxylan particles: effect of partly fermentation on the inhibition of Caco-2 cells proliferation. AIMS Bioengineering, 2021, 8(1): 52-70. doi: 10.3934/bioeng.2021006 |
[7] | Shaoyung Chen, Hsinyi Mao, Pinhua Tu, Naichen Cheng, Jiashing Yu . Fabrication of decellularized adipose tissue/alginate composite microspheres with pASCs encapsulation for tissue engineering. AIMS Bioengineering, 2017, 4(3): 351-365. doi: 10.3934/bioeng.2017.3.351 |
[8] | Siseon Lee, Robert J. Mitchell . Perspectives on the use of transcriptomics to advance biofuels. AIMS Bioengineering, 2015, 2(4): 487-506. doi: 10.3934/bioeng.2015.4.487 |
[9] | Mark Warburton, Hossam Omar Ali, Wai Choon Liong, Arona Martin Othusitse, Amir Zaki Abdullah Zubir, Steve Maddock, Tuck Seng Wong . OneClick: A Program for Designing Focused Mutagenesis Experiments. AIMS Bioengineering, 2015, 2(3): 126-143. doi: 10.3934/bioeng.2015.3.126 |
[10] | Tutuka Dlume, Nonso E. Nnolim, Uchechukwu U. Nwodo . Exiguobacterium acetylicum transformed poultry feathers into amino acids through an extracellular secretion of keratinolytic enzymes. AIMS Bioengineering, 2024, 11(4): 489-505. doi: 10.3934/bioeng.2024022 |
The immune-related adverse events resulting from the therapy of immune checkpoint inhibitors could cause kidney injury. Inflammatory reprogramming of regulatory T helper (Treg) cells or type 17 T helper (Th17) cells might be involved in the pathogenesis of nephropathy. Accumulating evidence confirms a connection between the diversity of gut microbiota and kidney diseases, suggesting that successful modification of gut microbiota could attenuate kidney injury. In other words, certain gut microbiota could contribute to the protection of kidneys via the gut-kidney axis. It has been shown that the dysbiosis of gut microbiota might affect the gut-kidney axis, leading to nephrotoxicity. On the contrary, altered levels of D-amino acids, ROS, and SCFAs through the adjustment of gut microbiota might be relevant to the reduction of nephrotoxicity. Here, we have discussed and suggested the beneficial roles of gut microbiota in the prevention of the kidney injury induced during immune-checkpoint therapy.
adenosine triphosphate;
cytotoxic T lymphocyte-associated protein 4;
chronic kidney disease;
deoxyribonucleic acid;
fecal microbiota transplantation;
graft-versus-host disease;
histone deacetylase;
programmed cell death protein 1;
programmed cell death ligand 1;
reactive oxygen species;
superoxide dismutase;
type 1 T helper;
type 17 T helper;
regulatory T
The immune checkpoint inhibitors targeting programmed cell death protein-1 (PD-1) or its ligand (PD-L1) are among the most effective immunotherapy agents, which are now given to increasing numbers of patients with advanced cancers. Consequently, a considerable number of immune-related adverse events have been reported, predicting that such events will become important [1]. The immune-related adverse events which may result from the therapy of immune checkpoint inhibitors could affect various organs, including the kidneys [2]. Now, the number of immune-related adverse events have grown noticeably, and it has become a major focus of current investigation. The most common kidney side effect associated with immune-related nephrotoxicity is acute kidney injury, which is usually caused by acute tubule-interstitial nephritis, with severity ranging from mild to life-threatening; it is also imitating the acute T-cell-mediated kidney injury of graft-versus-host disease (GVHD) in hematopoietic stem cell transplantation [3]. In addition, it has been reported that the use of the immune checkpoint inhibitors in patients with a preexisting autoimmune disease might be related to the increased occurrence of overall adverse events [4]. Recently, probiotics and/or prebiotics were shown to attenuate the severity of the disease condition within acute kidney injury [5], GVHD [6] and autoimmune disease [7], suggesting that gut microbiota might have considerable protective effects on the host against the above-mentioned immunological disorders. In addition, the uses of probiotics and/or prebiotics have shown potential positive effects, even against the production of uremic toxins in kidneys, with minimal risk of hyperkalemia and/or cachexia [8]. An increasing number of studies are also suggesting the effects of gut microbiota on the alleviation of acute kidney injury. In fact, plant-based diets and prebiotic, probiotic and symbiotic supplementation may lead to favorable alterations in the gut microbiota [9], suggesting that probiotics and/or prebiotics have potential benefits for the primary prevention of immune-related adverse events. Therefore, probiotics may therefore be a promising strategy to reduce the severity of acute kidney injury [5].
PD-1-blocking antibody therapy may rapidly result in the depletion of circulating PD-1 positive T regulatory (Treg) cells [10], which plays an important role in the effective anti-tumor responses in the tumor microenvironment [11]. Treg cells can facilitate immune-avoidance by tumor cells via diminishing anti-tumor immunity [12]. Similarly, the role of PD-L1 is overriding in type 1 T helper (Th1) and type 17 T helper (Th17) cell immunity [13]. Functional T cells, including the subsets of Th17 cells and Treg cells, play significant roles in determining the inflammatory microenvironment [14]. Therefore, anti-PD-1 therapies often trigger T cell-mediated adverse events that mimic Th17-mediated inflammatory diseases [15]. The reprogramming of immune cells might be a feature of GVHD, which is associated with the differentiation of CD4 positive Th1 cells into Th17 cells, along with the dysfunction of Treg cells [16]. In addition, Th17 cells are more prevalent in immune-related enterocolitis than Th1 cells [17]. Arthritis, after combined CTLA-4 and PD-1 inhibitor therapy, has favorably enhanced Th17 and transient Th1 or Th17 cell signatures [18]. Treg cells and/or Th17 cells are important in the immunopathology of lupus nephritis [19]. A high ratio of Th17/Treg cells was observed in lupus nephritis [20]. A potential role of the Th17 cells was also indicated in renal inflammation in glomerulonephritis [21]. In the setting of inflammatory responses with pathogenic Th17 cells, mesenchymal stem cells may suppress the differentiation of Th17 cells and the related inflammation in the kidneys [22]. In addition, it has been suggested that an imbalance of Th17/Treg cells seems to be an immunological basis of nephritic syndrome [23]. Accordingly, inflammatory reprogramming of Treg cells and/or Th17 cells might be a feature of the nephropathy in immunotherapy-induced immune-related adverse events [24].
Accumulating evidence confirms a connection between the diversity of gut microbiota and host diseases. In other words, the potential of gut microbiota has been recognized as a contributing factor in the development of various diseases, including obesity, diabetes, kidney disease and hypertension [25],[26]. Gut microbiota can affect the systemic levels of reactive oxygen species (ROS) that play vital roles in inflammatory diseases [27]. Generally, living cells reluctantly release ROS for indispensable ATP synthesis, which may cause DNA damage in cells [28]. However, some important physiological roles of ROS include the regulation of enzymes involved in autophagy, whose signaling could affect the balance of Th17/Treg cells [29]. ROS are defined as oxygen-hugging active molecules capable of reacting with various host molecules or organs, which also result from inflammatory reactions [30]. Gut microbiota may manage the production of ROS, which eventually protect some organs against oxidative stress [31]. Therefore, understanding the redox regulation of physiological processes seems to be important for developing a therapeutic approach with the modification of gut microbiota. The pathogenic connection between the gut microbiome and kidney diseases is termed the gut–kidney axis [32], which is often implicated in IgA nephropathy and/or in chronic kidney disease (CKD) (Figure 1). In the cases of both diseases, an apparent reduction of the tight junction proteins may be possibly be attributed to the production of uremic toxins [33],[34]. In addition, gut bacteria could activate a Th17/Th1 T-cell response, which may increase the production of inflammatory cytokines, triggering inflammation and/or immune response in the kidneys [35]. In fact, changes in the composition of the gut microbiota can promote an inflammatory status that is relevant to the pathogenesis of nephropathy [36]. For example, patients with renal failure have a low abundance of the genus Lactobacillus, whereas the proportion of the family Enterobacteriaceae are increased in the patients [37].
A beneficial role of gut microbiota in the progression of kidney diseases has been suggested. For example, probiotics such as Akkermansia and Lactobacillus could alleviate renal metabolism in CKD through the gut-kidney axis [38]. The reversal of gut dysbiosis using fecal microbiota transplantation (FMT) may be a promising therapy for CKD [39]. Successful modification or remodeling of the composition of gut microbiota could attenuate kidney inflammation [40]. In the development and/or prevention of diabetic nephropathy, the microbiota in the gut-kidney axis might play a key role [36], suggesting potential efficacy of the gut microbiota in the nephrotoxicity induced during immune-checkpoint therapy. For example, Salvia miltiorrhiza could alleviate the renal metabolism caused by cyclosporine-induced chronic nephrotoxicity through the gut-kidney axis [38] (Figure 1).
As a vital regulator of gut microbiota, the role of the linkage between nutrition and the gut microbiota in conserving the host health has been widely discussed [41]. Therefore, researchers have increasingly turned their attention to gut microbiota and its derived metabolites as a potential target for various therapeutics [42]. In clinical practice, the most largely used gut microbiota-targeted therapies are probiotics and prebiotics. Probiotics are alive bacteria that have health benefits when administered [43]. Prebiotics can promote the growth and/or activity of beneficial bacteria [43]. Synbiotics denote a mixture comprising probiotic and prebiotics, and they also present a health benefit. Also, the use of substances produced through metabolism of the gut microbes has also shown an encouraging effect on the host as postbiotics [44]. The gut microbiota may produce various D-amino acids that are beneficial for the protection of kidneys. For example, D-Ala inhibits ROS production and/or improves the potential of mitochondria [45]. Some Enterobacteriaceae, including Escherichia coli and/or Klebsiella oxytoca, could generate D-Ala in the gut, which might ameliorate kidney injury in mice, suggesting that D-Ala could be a promising therapeutic target [45]. In addition, it has been demonstrated the protective effects of gut-derived D-serine on kidney injury as another potential therapeutic target [46]. Several studies highlighted the relationship among the gut microbiota and oxidative stresses in various diseases [47]. ROS might be strictly controlled by the various signaling processes for appropriate gut immunity [48]. Some microbial products could upregulate the activity of superoxide dismutase, which results in a lower level of systemic ROS [49]. Nephrotoxicity rapidly weakens kidney function due to exposure to ROS, leading to inflammatory responses [50], which could be affected by alterations in the redox conditions of the gut. Carbohydrates are fermented to generate short-chain fatty acids (SCFAs), which are fatty acids with fewer than six carbon atoms, and they may work as an inhibitor for histone deacetylase (HDAC) [51]. HDAC inhibitors can attenuate acute kidney injury-mediated damage in the animal models of kidney diseases [52]. In addition, certain levels of SCFAs produced by healthy gut microbiota have been shown to possess anti-inflammatory properties with the regulation of T cell proliferation [53]. Furthermore, it has been shown that SCFAs can improve kidney function through the modulation of the inflammatory process via the expression levels of the enzymes involved in chromatin epigenetic modification [54]. In other words, SCFAs can improve kidney function after an injury, most likely via the epigenetic modification occurring as a result of a dual relationship between gut and kidneys [54]. Altering the composition of the gut microbiota has been shown to systematically alleviate the immunopathology of the CTLA-4 blockade in a Treg-dependent manner in mice [55]. The gut microbiota might also impact host cell metabolism [55]. Consequently, levels of D-amino acids, ROS and SCFAs that have been altered via the modification of gut microbiota could be relevant to the reduction of nephrotoxicity and/or the protection of kidneys. Recent relevant research showing promising effects of probiotics, prebiotics and FMT against kidney injury, including nephropathy, are shown in Table 1.
Method | Reference No. |
Probiotics | 5,36,42,43,44 |
Prebiotics | 42,43,44 |
FMT | 36,39 |
It has been shown that cisplatin causes the dysbiosis of gut microbiota, which might change the microbiota-derived metabolites and affect the gut–kidney axis, leading to nephrotoxicity [56]. Therefore, potential mechanisms for kidney protection should include several changes in the structure of commensal bacteria, such as increasing butyrate-producing bacteria, decreasing pathogenic bacteria and modulating the levels of microbiota-dependent metabolites, such as those affected by SCFAs, endotoxins and uremic toxins. As for immune-related adverse events, the gut-immune axis might affect the pathogenesis of the events. As an interesting example, it has been shown that high salt-intake may induce Th17 cells via the gut-immune axis, affecting autoimmunity and/or cardiovascular disease [57]. In a dose-dependent manner, sodium chloride was shown to be a driving factor for autoimmune diseases, including rheumatoid arthritis, through the induction of pathogenic Th17 cells [58]. Furthermore, it has been reported that a diet rich in sodium chloride may affect gut microbiota and increase intestinal Th17 cells, indicating the harmful effects of salt consumption on the gut-immune axis in multiple sclerosis [59]. Prospective clinical trials will be mandatory to investigate the effects of gut microbiota as a potential supportive therapeutic intervention against the nephropathy in human immune-related adverse events. In the end, the application of microorganisms could transmit antibiotic-resistance actors to the other microorganisms in the gut, which could result in important infections to the host [60]. Therefore, more studies should also be compulsory for identifying promising strategies to evade antibiotic resistance spread to pathogens in the gut.
[1] | Min JW, Lim JU (2022) Immune checkpoint inhibitors in patients with chronic kidney disease: Assessing their ability to cause acute kidney injury and informing their proper use. Semin Oncol 49: 141-147. https://doi.org/10.1053/j.seminoncol.2022.01.012 |
[2] | Seethapathy H, Herrmann SM, Sise ME (2021) Immune checkpoint inhibitors and kidney toxicity: advances in diagnosis and management. Kidney Med 3: 1074-1081. https://doi.org/10.1016/j.xkme.2021.08.008 |
[3] | Di Giacomo AM, Guarnieri A, Tripodi SA, et al. (2022) Brief communication PD1-related nephrotoxicity: optimizing its clinical management through histopathologic features. J Immunother 45: 217-221. https://doi.org/10.1097/CJI.0000000000000412 |
[4] | Chang CY, Park H, Malone DC, et al. (2020) Immune checkpoint inhibitors and immune-related adverse events in patients with advanced melanoma: a systematic review and network meta-analysis. JAMA Netw Open 3: e201611. https://doi.org/10.1001/jamanetworkopen.2020.1611 |
[5] | Yang J, Ji GE, Park MS, et al. (2021) Probiotics partially attenuate the severity of acute kidney injury through an immunomodulatory effect. Kidney Res Clin Pract 40: 620-633. https://doi.org/10.23876/j.krcp.20.265 |
[6] | Lin D, Hu B, Li P, et al. (2021) Roles of the intestinal microbiota and microbial metabolites in acute GVHD. Exp Hematol Oncol 10: 49. https://doi.org/10.1186/s40164-021-00240-3 |
[7] | Fan Z, Ross RP, Stanton C, et al. (2021) Lactobacillus casei CCFM1074 alleviates collagen-induced arthritis in rats via balancing Treg/Th17 and modulating the metabolites and gut microbiota. Front Immunol 12: 680073. https://doi.org/10.3389/fimmu.2021.680073 |
[8] | Sumida K, Lau WL, Kovesdy CP, et al. (2021) Microbiome modulation as a novel therapeutic approach in chronic kidney disease. Curr Opin Nephrol Hypertens 30: 75-84. https://doi.org/10.1097/MNH.0000000000000661 |
[9] | Lapaquette P, Bizeau JB, Acar N, et al. (2021) Reciprocal interactions between gut microbiota and autophagy. World J Gastroenterol 27: 8283-8301. https://doi.org/10.3748/wjg.v27.i48.8283 |
[10] | Gambichler T, Schröter U, Höxtermann S, et al. (2020) Decline of programmed death-1-positive circulating T regulatory cells predicts more favourable clinical outcome of patients with melanoma under immune checkpoint blockade. Br J Dermatol 182: 1214-1220. https://doi.org/10.1111/bjd.18379 |
[11] | Sandin LC, Eriksson F, Ellmark P, et al. (2014) Local CTLA4 blockade effectively restrains experimental pancreatic adenocarcinoma growth in vivo. Oncoimmunology 3: e27614. https://doi.org/10.4161/onci.27614 |
[12] | Kumar P, Saini S, Prabhakar BS (2020) Cancer immunotherapy with check point inhibitor can cause autoimmune adverse events due to loss of Treg homeostasis. Semin Cancer Biol 64: 29-35. https://doi.org/10.1016/j.semcancer.2019.01.006 |
[13] | Okiyama N, Tanaka R (2022) Immune-related adverse events in various organs caused by immune checkpoint inhibitors. Allergol Int 71: 169-178. https://doi.org/10.1016/j.alit.2022.01.001 |
[14] | Sun S, Wang F (2020) Molecular events behind adverse effects. Adv Exp Med Biol 1248: 119-141. https://doi.org/10.1007/978-981-15-3266-5_6 |
[15] | Maillard A, Pastor D, Merat R (2021) Anti-PD-1-Induced hidradenitis suppurativa. Dermatopathology 8: 37-39. https://doi.org/10.3390/dermatopathology8010007 |
[16] | Gao Y, Shan W, Gu T, et al. (2021) Daratumumab prevents experimental xenogeneic graft-versus-host disease by skewing proportions of T Cell functional subsets and inhibiting T Cell activation and migration. Front Immunol 12: 785774. https://doi.org/10.3389/fimmu.2021.785774 |
[17] | Hailemichael Y, Johnson DH, Abdel-Wahab N, et al. (2022) Interleukin-6 blockade abrogates immunotherapy toxicity and promotes tumor immunity. Cancer Cell 40: 509-523.E6. https://doi.org/10.1016/j.ccell.2022.04.004 |
[18] | Kim ST, Chu Y, Misoi M, et al. (2022) Distinct molecular and immune hallmarks of inflammatory arthritis induced by immune checkpoint inhibitors for cancer therapy. Nat Commun 13: 1970. https://doi.org/10.1038/s41467-022-29539-3 |
[19] | Li Y, Tang D, Yin L, et al. (2022) New insights for regulatory T cell in lupus nephritis. Autoimmun Rev 21: 103134. https://doi.org/10.1016/j.autrev.2022.103134 |
[20] | Wang B, Jiang X, Li Y, et al. (2022) YY1 alleviates lupus nephritis-induced renal injury by reducing the Th17/Treg cell ratio via the IFN-γ/Fra2 axis. Lab Invest 102: 872-884. https://doi.org/10.1038/s41374-022-00777-9 |
[21] | Turner JE, Paust HJ, Steinmetz OM, et al. (2010) The Th17 immune response in renal inflammation. Kidney Int 77: 1070-1075. https://doi.org/10.1038/ki.2010.102 |
[22] | Duffy MM, McNicholas BA, Monaghan DA, et al. (2014) Mesenchymal stem cells and a vitamin D receptor agonist additively suppress T helper 17 cells and the related inflammatory response in the kidney. Am J Physiol Renal Physiol 307: F1412-F1426. https://doi.org/10.1152/ajprenal.00024.2014 |
[23] | Li YY, Wei SG, Zhao X, et al. (2016) Th17/Treg cell expression in children with primary nephritic syndrome and the effects of ox-LDL on Th17/Treg cells. Genet Mol Res 15: gmr.15027669. https://doi.org/10.4238/gmr.15027669 |
[24] | Grigoriou M, Banos A, Hatzioannou A, et al. (2021) Regulatory T-cell transcriptomic reprogramming characterizes adverse events by checkpoint inhibitors in solid tumors. Cancer Immunol Res 9: 726-734. https://doi.org/10.1158/2326-6066.CIR-20-0969 |
[25] | Kitai T, Tang WHW (2018) Gut microbiota in cardiovascular disease and heart failure. Clin Sci (Lond) 132: 85-91. https://doi.org/10.1042/CS20171090 |
[26] | Sata Y, Marques FZ, Kaye DM (2020) The emerging role of gut dysbiosis in cardio-metabolic risk factors for heart failure. Curr Hypertens Rep 22: 38. https://doi.org/10.1007/s11906-020-01046-0 |
[27] | Ballard JWO, Towarnicki SG (2020) Mitochondria, the gut microbiome and ROS. Cell Signal 75: 109737. https://doi.org/10.1016/j.cellsig.2020.109737 |
[28] | Espinosa A, Henríquez-Olguín C, Jaimovich E (2016) Reactive oxygen species and calcium signals in skeletal muscle: A crosstalk involved in both normal signaling and disease. Cell Calcium 60: 172-179. https://doi.org/10.1016/j.ceca.2016.02.010 |
[29] | Gao L, Luo D, Wu D, et al. (2022) Effects of mammalian target of rapamycin and aryl hydrocarbon receptor-mediating autophagy signaling on the balance of Th17/Treg cells during perinatal bisphenol a exposure in female offspring mice. Environ Toxicol 37: 1781-1789. https://doi.org/10.1002/tox.23525 |
[30] | Fernández-Sánchez A, Madrigal-Santillán E, Bautista M, et al. (2011) Inflammation, oxidative stress, and obesity. Int J Mol Sci 12: 3117-3132. https://doi.org/10.3390/ijms12053117 |
[31] | Wada A, Higashiyama M, Kurihara C, et al. (2022) Protective effect of luminal uric acid against indomethacin-induced enteropathy: role of antioxidant effect and gut microbiota. Dig Dis Sci 67: 121-133. https://doi.org/10.1007/s10620-021-06848-z |
[32] | Yang T, Richards EM, Pepine CJ, et al. (2018) The gut microbiota and the brain-gut-kidney axis in hypertension and chronic kidney disease. Nat Rev Nephrol 14: 442-456. https://doi.org/10.1038/s41581-018-0018-2 |
[33] | Peng SN, Zeng HH, Fu AX, et al. (2013) Effects of rhein on intestinal epithelial tight junction in IgA nephropathy. World J Gastroenterol 19: 4137-4145. https://doi.org/10.3748/wjg.v19.i26.4137 |
[34] | Sol CM, Santos S, Asimakopoulos AG, et al. (2020) Associations of maternal phthalate and bisphenol urine concentrations during pregnancy with childhood blood pressure in a population-based prospective cohort study. Environ Int 138: 105677. https://doi.org/10.1016/j.envint.2020.105677 |
[35] | Andersen K, Kesper MS, Marschner JA, et al. (2017) Intestinal dysbiosis, barrier dysfunction, and bacterial translocation account for CKD-related systemic inflammation. J Am Soc Nephrol 28: 76-83. https://doi.org/10.1681/ASN.2015111285 |
[36] | Nagase N, Ikeda Y, Tsuji A, et al. (2022) Efficacy of probiotics on the modulation of gut microbiota in the treatment of diabetic nephropathy. World J Diabetes 13: 150-160. https://doi.org/10.4239/wjd.v13.i3.150 |
[37] | Zhao J, Ning X, Liu B, et al. (2021) Specific alterations in gut microbiota in patients with chronic kidney disease: an updated systematic review. Ren Fail 43: 102-112. https://doi.org/10.1080/0886022X.2020.1864404 |
[38] | Han C, Jiang YH, Li W, et al. (2021) Astragalus membranaceus and Salvia miltiorrhiza ameliorates cyclosporin a-induced chronic nephrotoxicity through the “gut-kidney axis”. J Ethnopharmacol 269: 113768. https://doi.org/10.1016/j.jep.2020.113768 |
[39] | Bian J, Liebert A, Bicknell B, et al. (2022) Faecal microbiota transplantation and chronic kidney disease. Nutrients 14: 2528. https://doi.org/10.3390/nu14122528 |
[40] | Feng Y, Li L, Guo F, et al. (2018) Protective effects of SKLB023 on a mouse model of unilateral ureteral obstruction by the modulation of gut microbiota. RSC Adv 8: 40232-40242. https://doi.org/10.1039/C8RA08049F |
[41] | Campaniello D, Corbo MR, Sinigaglia M, et al. (2022) How diet and physical activity modulate gut microbiota: evidence and perspectives. Nutrients 14: 2456. https://doi.org/10.3390/nu14122456 |
[42] | Zheng HJ, Guo J, Wang Q, et al. (2021) Probiotics, prebiotics, and synbiotics for the improvement of metabolic profiles in patients with chronic kidney disease: A systematic review and meta-analysis of randomized controlled trials. Crit Rev Food Sci Nutr 61: 577-598. https://doi.org/10.1080/10408398.2020.1740645 |
[43] | Pandey KR, Naik SR, Vakil BV (2015) Probiotics, prebiotics and synbiotics- a review. J Food Sci Technol 52: 7577-7587. https://doi.org/10.1007/s13197-015-1921-1 |
[44] | Żółkiewicz J, Marzec A, Ruszczyński M, et al. (2020) Postbiotics-a step beyond pre- and probiotics. Nutrients 12: 2189. https://doi.org/10.3390/nu12082189 |
[45] | Iwata Y, Nakade Y, Kitajima S, et al. (2022) Protective effect of d-alanine against acute kidney injury. Am J Physiol Renal Physiol 322: F667-F679. https://doi.org/10.1152/ajprenal.00198.2021 |
[46] | Nakade Y, Iwata Y, Furuichi K, et al. (2018) Gut microbiota-derived D-serine protects against acute kidney injury. JCI Insight 3: e97957. https://doi.org/10.1172/jci.insight.97957 |
[47] | Winiarska-Mieczan A, Tomaszewska E, Donaldson J, et al. (2022) The Role of nutritional factors in the modulation of the composition of the gut microbiota in people with autoimmune diabetes. Nutrients 14: 2498. https://doi.org/10.3390/nu14122498 |
[48] | Flores MV, Crawford KC, Pullin LM, et al. (2010) Dual oxidase in the intestinal epithelium of zebrafish larvae has anti-bacterial properties. Biochem Biophys Res Commun 400: 164-168. https://doi.org/10.1016/j.bbrc.2010.08.037 |
[49] | Wang T, Yang J, Lin G, et al. (2021) Effects of dietary mannan oligosaccharides on non-specific immunity, intestinal health, and antibiotic resistance genes in pacific white shrimp litopenaeus vannamei. Front Immunol 12: 772570. https://doi.org/10.3389/fimmu.2021.772570 |
[50] | Abdel-Fattah MM, Elgendy ANAM, Mohamed WR (2021) X anthenone, ACE2 activator, counteracted gentamicin-induced nephrotoxicity in rats: Impact on oxidative stress and ACE2/Ang-(1-7) signaling. Life Sci 275: 119387. https://doi.org/10.1016/j.lfs.2021.119387 |
[51] | Ratajczak W, Rył A, Mizerski A, et al. (2019) Immunomodulatory potential of gut microbiome-derived short-chain fatty acids (SCFAs). Acta Biochim Pol 66: 1-12. https://doi.org/10.18388/abp.2018_2648 |
[52] | Zhang H, Zhang W, Jiao F, et al. (2018) The nephroprotective effect of MS-275 on lipopolysaccharide (LPS)-induced acute kidney injury by inhibiting reactive oxygen species (ROS)-oxidative stress and endoplasmic reticulum stress. Med Sci Monit 24: 2620-2630. https://doi.org/10.12659/MSM.906362 |
[53] | D'Souza WN, Douangpanya J, Mu S, et al. (2017) Differing roles for short chain fatty acids and GPR43 agonism in the regulation of intestinal barrier function and immune responses. PLoS One 12: e0180190. https://doi.org/10.1371/journal.pone.0180190 |
[54] | Andrade-Oliveira V, Amano MT, Correa-Costa M, et al. (2015) Gut bacteria products prevent AKI induced by ischemia-reperfusion. J Am Soc Nephrol 26: 1877-1888. https://doi.org/10.1681/ASN.2014030288 |
[55] | Sun S, Luo L, Liang W, et al. (2020) Bifidobacterium alters the gut microbiota and modulates the functional metabolism of T regulatory cells in the context of immune checkpoint blockade. Proc Natl Acad Sci U S A 117: 27509-27515. https://doi.org/10.1073/pnas.1921223117 |
[56] | Zou YT, Zhou J, Zhu JH, et al. (2022) Gut microbiota mediates the protective effects of traditional chinese medicine formula Qiong-Yu-Gao against cisplatin-induced acute kidney injury. Microbiol Spectr 10: e0075922. https://doi.org/10.1128/spectrum.00759-22 |
[57] | Wilck N, Matus MG, Kearney SM, et al. (2017) Salt-responsive gut commensal modulates TH17 axis and disease. Nature 551: 585-589. https://doi.org/10.1038/nature24628 |
[58] | Jung SM, Kim Y, Kim J, et al. (2019) Sodium chloride aggravates arthritis via Th17 polarization. Yonsei Med J 60: 88-97. https://doi.org/10.3349/ymj.2019.60.1.88 |
[59] | Haase S, Wilck N, Kleinewietfeld M, et al. (2019) Sodium chloride triggers Th17 mediated autoimmunity. J Neuroimmunol 329: 9-13. https://doi.org/10.1016/j.jneuroim.2018.06.016 |
[60] | Devirgiliis C, Zinno P, Perozzi G (2013) Update on antibiotic resistance in foodborne Lactobacillus and Lactococcus species. Front Microbiol 4: 301. https://doi.org/10.3389/fmicb.2013.00301 |
Method | Reference No. |
Probiotics | 5,36,42,43,44 |
Prebiotics | 42,43,44 |
FMT | 36,39 |