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International Journal of Frontiers in Medicine, 2023, 5(6); doi: 10.25236/IJFM.2023.050614.

Research progress on the effect of intestinal flora changes on liver and kidney function in AIDS patients


Ma Mingjun1, Chen Panpan2, Xiao Shaotan2, Xin Xin2

Corresponding Author:
Xin Xin

1School of Public Health, Dali University, Dali, Yunnan, 671000, China

2Shanghai Pudong New Area Center for Disease Control and Prevention, Pudong Institute of Preventive Medicine, Fudan University, Shanghai, 200136, China


HIV, also known as HIV, infects the body's immune cells, causing immune deficiencies. The intestine is not only the immune organ of the human body, but also includes a large number of intestinal flora, and the intestinal microecology composed of these flora is closely related to immunity. HIV infection itself and its infection caused by intestinal flora imbalance, intestinal mucosal barrier destruction, causing the body's systemic inflammatory cascade reaction, the production of various inflammatory cytokines and metabolites, and eventually cause certain damage to liver and kidney function. This article reviews the mechanism and relationship between the effects of intestinal microbiota changes on liver and kidney function in AIDS patients, and changes the regulation of intestinal microbiota disorders on the microinflammatory state of the body, thereby providing a new entry point for the improvement of liver and kidney function in AIDS patients.


HIV; Intestinal Flora; Inflammatory Cytokine; Gut-Liver Axis; Gut-Kidney Axis

Cite This Paper

Ma Mingjun, Chen Panpan, Xiao Shaotan, Xin Xin. Research progress on the effect of intestinal flora changes on liver and kidney function in AIDS patients. International Journal of Frontiers in Medicine (2023), Vol. 5, Issue 6: 89-96. https://doi.org/10.25236/IJFM.2023.050614.


[1] Chinese Medical Association, Infectious Diseases Branch, Hepatitis C AIDS Group, Chinese Center for Disease Control and Prevention. Chinese guidelines for the diagnosis and treatment of AIDS (2021 edition) [J]. Concord Medical Journal, 2022, 13(02):203-226. 

[2] Jones RM, Neish AS. Gut Microbiota in Intestinal and Liver Disease[J]. Annu Rev Pathol, 2021, 16: 251-275. 

[3] Jandhyala SM, Talukdar R, Subramanyam C, et al. Role of the normal gut microbiota [J]. World J Gastroenterol, 2015, 21(29):8787-803. 

[4] Ramakrishna B, Krishnan S. The normal bacterial flora of the human intestine and its regulation [J]. Clin Gastroenterol, 2007, 41: S2-S6. 

[5] Frank DN, St Amand AL, Feldman RA et al. Molecular-phylogenetic characterization of microbial community imbalances in human inflammatory bowel diseases[J]. Proc Natl Acad Sci U S A, 2007, 104(34): 13780-5. 

[6] Backhed F, Roswall J, Peng Y, et al. Dynamics and Stabilization of the Human Gut Microbiome during the First Year of Life[J]. Cell Host Microbe, 2015, 17(5):690-703. 

[7] Landman C, Quévrain E. Le microbiote intestinal: description, rôle et implication physiopathologique [Gut microbiota: Description, role and pathophysiologic implications][J]. Rev Med Interne, 2016, 37(6):418-23. 

[8] Wang Lamei, Kong Xiangyang, Wang Kunhua. Research progress on the relationship between intestinal flora and AIDS [J]. Journal of Cellular and Molecular Immunology, 2016, 32(06):859-862. 

[9] Pei Z, Bini EJ, Y ang L, et al. Bacterial biota in the human distal esophagus[J]. Proc Natl Acad Sci USA, 2004, 101: 4250-4255. 

[10] Justesen T, Nielsen OH, Jacobsen IE et al. The normal cultivable microflora in upper jejunal fluid in healthy adults [J]. Scandinavian journal of gastroenterology, 1984, 19(2):279-82. 

[11] Ley RE, Turnbaugh PJ, Klein S et al. Microbial ecology: human gut microbes associated with obesity [J]. Nature, 2006, 444(7122):1022-3. 

[12] Faust K, Sathirapongsasuti JF, Izard J, et al. Microbial co-occurrence relationships in the human microbiome [J]. PLoS Comput Biol, 2012, 8(7):e1002606. 

[13] Gillespie JJ, Wattam AR, Cammer SA, et al. PATRIC: the comprehensive bacterial bioinformatics resource with a focus on human pathogenic species[J]. Infection and immunity, 2011, 79(11):4286-98. 

[14] Swidsinski A, Loening-Baucke V, Lochs H, et al. Spatial organization of bacterial flora in normal and inflamed intestine: a fluorescence in situ hybridization study in mice[J]. World J Gastroenterol, 2005, 11:1131-1140. 

[15] Dominguez-Bello MG, Blaser MJ, Ley RE, et al. Development of the Human Gastrointestinal Microbiota and Insights From High-Throughput Sequencing[J]. Gastroenterology, 2011, 140: 1713-1719. 

[16] Sonnenburg JL, Xu J, Leip DD, et al. Glycan foraging in vivo by an intestine-adapted bacterial symbiont[J]. Science, 2005, 307: 1955-1959. 

[17] Kang Y, Cai Y. Altered Gut Microbiota in HIV Infection: Future Perspective of Fecal Microbiota Transplantation Therapy[J]. AIDS Res Hum Retroviruses, 2019, 35(3):229-235. 

[18] Xie MH, Wang Z, Sun YY et al. Research progress on small molecule inhibitors of HIV-1 envelope glycoprotein gp120 [J/OL]. Journal of Pharmacology:1-23 [2023-03-03]. http: // kns. cnki. net/ kcms/ detail/ 11. 2163. r. 20221123. 1610. 008. html. 

[19] Jette CA, Barnes CO, Kirk SM, et al. Cryo-EM structures of HIV-1 trimer bound to CD4-mimetics BNM-III-170 and M48U1 adopt a CD4-bound open conformation [J]. Nat Commun, 2021, 12(1):1950. 

[20] Campbell DJ, Koch MA. Phenotypical and functional specialization of FOXP3+ regulatory T cells [J]. Nat Rev Immunol, 2011, 11(2):119-30. 

[21] Elhed A, Unutmaz D. Th17 cells and HIV infection[J]. Curr Opin HIV AIDS, 2010, 5(2):146-50. 

[22] Wynn TA. T (H)-17: a giant step from T(H)1 and T(H)2 [J]. Nat Immunol, 2005(11):1069-70. 

[23] Bettelli E, Korn T, Kuchroo VK. Th17: the third member of the effector T cell trilogy[J]. Curr Opin Immunol, 2007, 19(6):652-7. 

[24] Korn T, Oukka M, Kuchroo V, et al. Th17 cells: effector T cells with inflammatory properties[J]. Semin Immunol, 2007, 19(6):362-71. 

[25] Stockinger B, Veldhoen M. Differentiation and function of Th17 T cells[J]. Curr Opin Immunol, 2007, 19(3):281-6. 

[26] Stockinger B, Veldhoen M, Martin B. Th17 T cells: linking innate and adaptive immunity[J]. Semin Immunol, 2007, 19(6):353-61. 

[27] Weaver CT, Hatton RD, Mangan PR, et al. IL-17 family cytokines and the expanding diversity of effector T cell lineages [J]. Annu Rev Immunol, 2007, 25:821-52. 

[28] Lee JS, Tato CM, Joyce-Shaikh B, et al. Interleukin-23-Independent IL-17 Production Regulates Intestinal Epithelial Permeability [J]. Immunity, 2015, 43(4):727-38. 

[29] Maxwell JR, Zhang Y, Brown WA, et al. Differential roles for interleukin-23 and interleukin-17 in intestinal immunoregulation [J]. Immunity, 2015, 43, 739-750. 

[30] Wacleche VS, Landay A, Routy JP, et al. The Th17 Lineage: From Barrier Surfaces Homeostasis to Autoimmunity, Cancer, and HIV-1 Pathogenesis[J]. Viruses, 2017, 9(10):303. 

[31] Huber S, Gagliani N, Flavell RA. life, death, and miracles:Th17 cells in the intestine[J]. Eur. J. Immunol, 2012, 42, 2238-2245. 

[32] O'Connor W Jr, Zenewicz LA, Flavell RA. The dual nature of T(H)17 cells: shifting the focus to function [J]. Nat Immunol, 2010, 11(6):471-6. 

[33] Rocafort M, Noguera-Julian M, Rivera J, et al. Evolution of the gut microbiome following acute HIV-1 infection [J]. Microbiome, 2019, 7(1):73. 

[34] Li S, Su B, Zhu JP, He QWS, Zhang T. Progress in the study of intestinal flora and immune activation and inflammation associated with HIV infection[J]. Chinese Journal of Viral Diseases, 2020, 10(04): 313-317. 

[35] Shin NR, Whon TW, Bae JW. Proteobacteria: microbial signature of dysbiosis in gut microbiota [J]. Trends Biotechnol, 2015, 33(9):496-503. 

[36] McGuckin MA, Linden SK, Sutton P, et al. Mucin dynamics and enteric pathogens[J]. Nat Rev Microbiol, 2011, 9(4):265-278. 

[37] Rey FE, Gonzalez MD, Cheng J, et al. Metabolic niche of a prominent sulfate-reducing human gut bacterium [J]. ProcNatl Acad Sci USA, 2013, 110(33):13582-13587. 

[38] March C, Regueiro V, Llobet E, et al. Dissection of host cell signal transduction during Acinetobacter baumannii-triggered inflammatory response [J]. PLoS One, 2010, 5(4):e10033. 

[39] Epeldegui M, Magpantay L, Guo Y, et al. A prospective study of serum microbial translocation biomarkers and risk of AIDS-related non-Hodgkin lymphoma[J]. AIDS, 2018;32(7):945-954. 

[40] Mingjun Z, Fei M, Zhousong X, et al. 16S rDNA sequencing analyzes differences in intestinal flora of human immunodeficiency virus (HIV) patients and association with immune activation[J]. Bioengineered, 2022, 13(2):4085-4099. 

[41] Liu RT, Rowan-Nash AD, Sheehan AE, et al. Reductions in anti-inflammatory gut bacteria are associated with depression in a sample of young adults[J]. . Brain Behav Immun, 2020, 88:308-324. 

[42] Seki E, De Minicis S, Osterreicher CH, et al. TLR4 enhances TGF-beta signaling and hepatic fibrosis [J]. Nat Med, 2007, 13(11):1324-32. 

[43] Chassaing B, Etienne-Mesmin L, Gewirtz AT. Microbiota-liver axis in hepatic disease [J]. Hepatology, 2014, 59(1):328-39. 

[44] Cheng Z, Yang L, Chu H. The Gut Microbiota: A Novel Player in Autoimmune Hepatitis [J]. Front Cell Infect Microbiol, 2022, 12:947382. 

[45] Meijers BK, Evenepoel P. The gut-kidney axis: indoxyl sulfate, p-cresyl sulfate and CKD progression [J]. Nephrol Dial Transplant, 2011, 26(3):759-61. 

[46] Mariathasan S, Monack DM. Inflammasome adaptors and sensors: intracellular regulators of infection and inflammation [J]. Nat Rev Immunol, 2007, 7:31-40. 

[47] Wang J, Wang Y, Zhang X, et al. Gut Microbial Dysbiosis Is Associated with Altered Hepatic Functions and Serum Metabolites in Chronic Hepatitis B Patients [J]. Front Microbiol, 2017, 8:2222. 

[48] Yiu JH, Dorweiler B, Woo CW. Interaction between gut microbiota and toll-like receptor: from immunity to metabolism [J]. J Mol Med (Berl), 2017, 95(1):13-20. 

[49] Sim JH, Mukerji SS, Russo SC, et al. Gastrointestinal Dysfunction and HIV Comorbidities [J]. Curr HIV/AIDS Rep, 2021, 18(1):57-62. 

[50] Meyer TW, Hostetter TH. Uremia [J]. N Engl J Med, 2007, 357(13):1316-25. 

[51] Jankowski J, van der Giet M, Jankowski V, et al. Increased plasma phenylacetic acid in patients with end-stage renal failure inhibits iNOS expression [J]. J Clin Invest, 2003, 112(2):256-64. 

[52] Wikoff WR, Anfora AT, Liu J, et al. Metabolomics analysis reveals large effects of gut microflora on mammalian blood metabolites[J]. Proc Natl Acad Sci U S A, 2009, 106(10):3698-703. 

[53] Evenepoel P, Meijers BK, Bammens BR, et al. Uremic toxins originating from colonic microbial metabolism [J]. Kidney Int Suppl, 2009, (114):S12-9. 

[54] Fukagawa M, Watanabe Y. Role of uremic toxins and oxidative stress in chronic kidney disease[J]. Ther Apher Dial, 2011, 15(2):119. 

[55] Meijers BK, Claes K, Bammens B, et al. P-Cresol and cardiovascular risk in mild-to-moderate kidney disease[J]. Clin J Am Soc Nephrol, 2010, 5(7):1182-9. 

[56] Bammens B, Evenepoel P, Keuleers H, et al. Free serum concentrations of the protein-bound retention solute p-cresol predict mortality in hemodialysis patients[J]. Kidney Int, 2006, 69(6):1081-7. 

[57] Missailidis C, Hällqvist J, Qureshi AR, et al. Serum Trimethylamine-N-Oxide Is Strongly Related to Renal Function and Predicts Outcome in Chronic Kidney Disease[J]. PLoS One, 2016, 11(1):e0141738. 

[58] Tang WH, Wang Z, Kennedy DJ, et al. Gut microbiota-dependent trimethylamine N-oxide (TMAO) pathway contributes to both development of renal insufficiency and mortality risk in chronic kidney disease[J]. Circ Res, 2015, 116(3):448-55. 

[59] Milosevic I, Vujovic A, Barac A, et al. Gut-Liver Axis, Gut Microbiota, and Its Modulation in the Management of Liver Diseases: a Review of the Literature [J]. Int J Mol Sci, 2019, 20(2):395. 

[60] Gentric G, Maillet V, Paradis V, et al. Oxidative stress promotes pathologic polyploidization in nonalcoholic fatty liver disease [J]. J Clin Invest, 2015, 125(3):981-92.