Research progress on relationship between intestinal flora and anxiety as well as depression in patients with rheumatism

ZHENG Huajin; JI Wei

doi:10.7619/jcmp.20200403

Journal of Clinical Medicine in Practice > 2021 > 25(1): 104-108. > DOI: 10.7619/jcmp.20200403

ZHENG Huajin, JI Wei. Research progress on relationship between intestinal flora and anxiety as well as depression in patients with rheumatism[J]. Journal of Clinical Medicine in Practice, 2021, 25(1): 104-108. DOI: 10.7619/jcmp.20200403

Citation:

PDF (657 KB)

Research progress on relationship between intestinal flora and anxiety as well as depression in patients with rheumatism

ZHENG Huajin,
JI Wei^,

Affiliated Hospital of Nanjing University of Traditional Chinese Medicine, Nanjing, Jiangsu, 210019

More Information

Received Date: July 31, 2020
Available Online: January 17, 2021
Published Date: January 14, 2021

Graphical Abstract

Abstract

Abstract

Severity of anxiety and depression in patients with rheumatism is obviously greater than that in patients with other internal diseases. Intestinal flora imbalance may lead to a variety of autoimmune diseases. The imbalance of intestinal flora can affect the bi-directional communication between mucosal immune system and gut-brain axis. Therefore, anxiety and depression of patients with rheumatism are also closely related to the imbalance of intestinal flora, which are mainly manifested in the following three aspects: the influence of intestinal flora and intestinal peptide on the bi-directional communication of gut-brain axis, the relationship between intestinal autonomic nerve and vagus nerve and central nervous system, and the relationship between intestinal flora imbalance and autoimmunity. Based on the analysis in the above factors, the imbalance of intestinal flora has a negative superimposed effect on anxiety and depression in patients with rheumatism.
- intestinal flora,
- anxiety,
- depression,
- gut-brain axis,
- rheumatism,
- intestinal peptide,
- short-chain fatty acids

FullText(HTML)

References (48)

References

[1]	DALILE B, VAN OUDENHOVE L, VERVLIET B, et al. The role of short-chain fatty acids in microbiota-gut-brain communication[J]. Nat Rev Gastroenterol Hepatol, 2019, 16(8): 461-478. doi: 10.1038/s41575-019-0157-3
[2]	HOWREN A, AVIÑA-ZUBIETA J A, PUYAT J H, et al. Defining depression and anxiety in individuals with rheumatic diseases using administrative health databases: a systematic review[J]. Arthritis Care Res, 2020, 72(2): 243-255. doi: 10.1002/acr.24048
[3]	NASERIBAFROUEI A, HESTAD K, AVERSHINA E, et al. Correlation between the human fecal microbiota and depression[J]. Neurogastroenterol Motil, 2014, 26(8): 1155-1162. doi: 10.1111/nmo.12378
[4]	BUTLER M I, CRYAN J F, DINAN T G. Man and the microbiome: a new theory of everything[J]. Annu Rev Clin Psychol, 2019, 15: 371-398. doi: 10.1146/annurev-clinpsy-050718-095432
[5]	RUSSO R, CRISTIANO C, AVAGLIANO C, et al. Gut-brain axis: role of lipids in the regulation of inflammation, pain and CNS diseases[J]. Curr Med Chem, 2018, 25(32): 3930-3952. doi: 10.2174/0929867324666170216113756
[6]	SODERHOLM A T, PEDICORD V A. Intestinal epithelial cells: at the interface of the microbiota and mucosal immunity[J]. Immunology, 2019, 158(4): 267-280. doi: 10.1111/imm.13117
[7]	HOLZER P, REICHMANN F, FARZI A. Neuropeptide Y, peptide YY and pancreatic polypeptide in the gut-brain axis[J]. Neuropeptides, 2012, 46(6): 261-274. doi: 10.1016/j.npep.2012.08.005
[8]	JOHNSON P J, BORNSTEIN J C. Neurokinin-1 and-3 receptor blockade inhibits slow excitatory synaptic transmission in myenteric neurons and reveals slow inhibitory input[J]. Neuroscience, 2004, 126(1): 137-147. doi: 10.1016/j.neuroscience.2004.03.021
[9]	LATORRE R, STERNINI C, DE GIORGIO R, et al. Enteroendocrine cells: a review of their role in brain-gut communication[J]. Neurogastroenterol Motil, 2016, 28(5): 620-630. doi: 10.1111/nmo.12754
[10]	BANKS W A, TSCHÖP M, ROBINSON S M, et al. Extent and direction of ghrelin transport across the blood-brain barrier is determined by its unique primary structure[J]. J Pharmacol Exp Ther, 2002, 302(2): 822-827. doi: 10.1124/jpet.102.034827
[11]	SINGH J, ABALLAY A. Microbial colonization activates an immune fight-and-flight response via neuroendocrine signaling[J]. Dev Cell, 2019, 49(1): 89-99. doi: 10.1016/j.devcel.2019.02.001
[12]	JOGENDER S, ALEJANDRO A. Intestinal infection regulates behavior and learning via neuroendocrine signaling[J]. eLife, 2019(8): e50033. http://www.ncbi.nlm.nih.gov/pubmed/31674907
[13]	VERMA D, WOOD J, LACH G, et al. Hunger promotes fear extinction by activation of an amygdala microcircuit[J]. Neuropsychopharmacology, 2016, 41(2): 431-439. doi: 10.1038/npp.2015.163
[14]	EL-SALHY M, HAUSKEN T. The role of the neuropeptide Y(NPY)family in the pathophysiology of inflammatory bowel disease(IBD)[J]. Neuropeptides, 2016, 55: 137-144. doi: 10.1016/j.npep.2015.09.005
[15]	FRÖHLICH E E, FARZI A, MAYERHOFER R, et al. Cognitive impairment by antibiotic-induced gut dysbiosis: Analysis of gut microbiota-brain communication[J]. Brain Behav Immun, 2016, 56: 140-155. doi: 10.1016/j.bbi.2016.02.020
[16]	FEUILLOLEY M G J. Antidromic neurogenic activity and cutaneous bacterial flora[J]. Semin Immunopathol, 2018, 40(3): 281-289. doi: 10.1007/s00281-018-0671-3
[17]	DEEHAN E C, YANG C, PEREZ-MUÑOZ M E, et al. Precision microbiome modulation with discrete dietary fiber structures directs short-chain fatty acid production[J]. Cell Host Microbe, 2020, 27(3): 389-404. doi: 10.1016/j.chom.2020.01.006
[18]	SPENCER S P, FRAGIADAKIS G K, SONNENBURG J L. Pursuing human-relevant gut microbiota-immune interactions[J]. Immunity, 2019, 51(2): 225-239. doi: 10.1016/j.immuni.2019.08.002
[19]	OBATA Y, CASTAÑO Á, BOEING S, et al. Neuronal programming by microbiota regulates intestinal physiology[J]. Nature, 2020, 578(7794): 284-289. doi: 10.1038/s41586-020-1975-8
[20]	PENNISI E. Gut bacteria linked to mental well-being and depression[J]. Science, 2019, 363(6427): 569. doi: 10.1126/science.363.6427.569
[21]	KAJI I, KARAKI S, KUWAHARA A. Short-chain fatty acid receptor and its contribution to glucagon-like peptide-1 release[J]. Digestion, 2014, 89(1): 31-36. doi: 10.1159/000356211
[22]	KOOPMAN M, EL AIDY S, MID trauma consortium. Depressed gut The microbiota-diet-inflammation trialogue in depression[J]. Curr Opin Psychiatry, 2017, 30(5): 369-377. doi: 10.1097/YCO.0000000000000350
[23]	CRYAN J F, DINAN T G. Mind-altering microorganisms: the impact of the gut microbiota on brain and behaviour[J]. Nat Rev Neurosci, 2012, 13(10): 701-712. doi: 10.1038/nrn3346
[24]	MILLER T L, WOLIN M J. Pathways of acetate, propionate, and butyrate formation by the human fecal microbial flora[J]. Appl Environ Microbiol, 1996, 62(5): 1589-1592. doi: 10.1128/AEM.62.5.1589-1592.1996
[25]	STILLING R M, VAN DE WOUW M, CLARKE G, et al. The neuropharmacology of butyrate: The bread and butter of the microbiota-gut-brain axis?[J]. Neurochem Int, 2016, 99: 110-132. doi: 10.1016/j.neuint.2016.06.011
[26]	CORRÊA-OLIVEIRA R, FACHI J L, VIEIRA A, et al. Regulation of immune cell function by short-chain fatty acids[J]. Clin Transl Immunol, 2016, 5(4): e73-e84. doi: 10.1038/cti.2016.17
[27]	LEWIS K, LUTGENDORFF F, PHAN V, et al. Enhanced translocation of bacteria across metabolically stressed epithelia is reduced by butyrate[J]. Inflamm Bowel Dis, 2010, 16(7): 1138-1148. doi: 10.1002/ibd.21177
[28]	FRICK L R, WILLIAMS K, PITTENGER C. Microglial dysregulation in psychiatric disease[J]. Clin Dev Immunol, 2013, 2013: 1-10. http://pubmedcentralcanada.ca/pmcc/articles/pmid/23690824
[29]	O'KEEFE S J D. Diet, microorganisms and their metabolites, and colon cancer[J]. Nat Rev Gastroenterol Hepatol, 2016, 13(12): 691-706. doi: 10.1038/nrgastro.2016.165
[30]	LEGOUX F, BELLET D, DAVIAUD C, et al. Microbial metabolites control the thymic development of mucosal-associated invariant T cells[J]. Science, 2019, 366(6464): 494-499. doi: 10.1126/science.aaw2719
[31]	VILLEDA S A, LUO J, MOSHER K I, et al. The ageing systemic milieu negatively regulates neurogenesis and cognitive function[J]. Nature, 2011, 477(7362): 90-103. doi: 10.1038/nature10357
[32]	HIIPPALA K, JOUHTEN H, RONKAINEN A, et al. The potential of gut commensals in reinforcing intestinal barrier function and alleviating inflammation[J]. Nutrients, 2018, 10(8): 186-196. http://www.ncbi.nlm.nih.gov/pubmed/?term=30060606[uid]
[33]	PATANKAR J V, BECKER C. Cell death in the gut epithelium and implications for chronic inflammation[J]. Nat Rev Gastroenterol Hepatol, 2020, 17(9): 543-556. doi: 10.1038/s41575-020-0326-4
[34]	CAMILLERI M. Leaky gut: mechanisms, measurement and clinical implications in humans[J]. Gut, 2019, 68(8): 1516-1526. doi: 10.1136/gutjnl-2019-318427
[35]	BERTHELOT J M, WENDLING D. Translocation of dead or alive bacteria from mucosa to joints and epiphyseal bone-marrow: facts and hypotheses[J]. Joint Bone Spine, 2020, 87(1): 31-36. doi: 10.1016/j.jbspin.2019.01.004
[36]	WENDLING D, PRATI C. Spondyloarthritis: an expanding cast of cellular actors[J]. Joint Bone Spine, 2018, 85(1): 1-3. doi: 10.1016/j.jbspin.2017.05.001
[37]	BERTHELOT J M, LE GOFF B, MARTIN J, et al. Essential role for CD103⁺ cells in the pathogenesis of spondyloarthritides[J]. Jo Bone Spine, 2015, 82(1): 8-12. doi: 10.1016/j.jbspin.2014.07.011
[38]	DODD D, SPITZER M H, VAN TREUREN W, et al. A gut bacterial pathway metabolizes aromatic amino acids into nine circulating metabolites[J]. Nature, 2017, 551(7682): 648-652. doi: 10.1038/nature24661
[39]	DEHNER C, FINE R, KRIEGEL M A. The microbiome in systemic autoimmune disease: mechanistic insights from recent studies[J]. Curr Opin Rheumatol, 2019, 31(2): 201-207. doi: 10.1097/BOR.0000000000000574
[40]	ARBUCKLE M R, MCCLAIN M T, RUBERTONE M V, et al. Development of autoantibodies before the clinical onset of systemic lupus erythematosus[J]. N Engl J Med, 2003, 349(16): 1526-1533. doi: 10.1056/NEJMoa021933
[41]	乌日力嘎, 穆荣. 系统性硬化症与肠道菌群的关系[J]. 协和医学杂志, 2019, 10(3): 263-267. doi: 10.3969/j.issn.1674-9081.2019.03.013
[42]	DUSCHA A, GISEVIUS B, HIRSCHBERG S, et al. Propionic acid shapes the multiple sclerosis disease course by an immunomodulatory mechanism[J]. Cell, 2020, 180(6): 1067-1080. doi: 10.1016/j.cell.2020.02.035
[43]	O'MALLEY D, JULIO-PIEPER M, GIBNEY S M, et al. Distinct alterations in colonic morphology and physiology in two rat models of enhanced stress-induced anxiety and depression-like behaviour[J]. Stress, 2010, 13(2): 114-122. doi: 10.3109/10253890903067418
[44]	LISITSYNA T A, VELTISHCHEV D Y, SERAVINA O F, et al. Comparative analysis of anxiety-depressive spectrum disorders in patients with rheumatic diseases[J]. Ter Arkh, 2018, 90(5): 30-37.
[45]	BEIRLI A, ALPTEKIN J Ö, KAYMAK D, et al. The relationship between anxiety, depression, suicidal ideation and quality of life in patients with rheumatoid arthritis[J]. Psychiatr Q, 2020, 91(1): 53-64. doi: 10.1007/s11126-019-09680-x
[46]	笪茅敏. 从中医证候表现及证型分布探讨干燥综合征与中医肝生理病理的关系[D]. 南京: 南京中医药大学, 2017.
[47]	FRAGOULIS G E, CAVANAGH J, DERAKHSHAN M H, et al. OP0350 Depression and anxiety in an early rheumatoid arthritis inception cohort. associations with epidemiological, socioeconomic and disease features[C]. SATURDAY, 16 JUNE 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018: 350-359.
[48]	VAN DER HEIJDE D, DAIKH D I, BETTERIDGE N, et al. Common language description of the term rheumatic and musculoskeletal diseases(RMDs)for use in communication with the lay public, healthcare providers, and other stakeholders endorsed by the European league against rheumatism(EULAR)and the American college of rheumatology(ACR)[J]. Arthritis Rheumatol, 2018, 70(6): 826-831. doi: 10.1002/art.40448

Cited By

Get Citation

PDF

XML

Article views (420) PDF downloads (23)

Turn off MathJax

Article Contents

Abstract

References

Research progress on relationship between intestinal flora and anxiety as well as depression in patients with rheumatism

Abstract

References

Catalog

Export File

Citation

Format

Content