Bieżący numer
Archiwum
Online first
O czasopiśmie
Redakcja
Rada Naukowa
Wydawca
Standardy etyczne i procedury
Bazy indeksacyjne
Recenzenci
Recenzenci Honorowi
Prenumerata
Kontakt
Najczęściej czytane artykuły
Dla autorów
Opłata za przetwarzanie artykułu (APC)
Książki i Konferencje
Książki
Konferencje
SARS CoV-2/COVID-19
PRACA PRZEGLĄDOWA
Dysbiosis, gut-blood barrier rupture and autoimmune response in rheumatoid arthritis and schizophrenia
1
Early Arthritis Clinic, National Institute of Geriatrics, Rheumatology and Rehabilitation, Warsaw, Poland
2
Department and Clinic of Psychiatric Rehabilitation, Department of Psychiatry and Psychotherapy, Faculty of Medical Sciences,
Medical University of Silesia in Katowice, Poland
Data nadesłania: 08-03-2021
Data ostatniej rewizji: 12-06-2021
Data akceptacji: 17-06-2021
Data publikacji online: 11-07-2021
Data publikacji: 16-07-2021
Reumatologia 2021;59(3):180-187
SŁOWA KLUCZOWE
rheumatoid arthritisschizophreniamicrobiome dysbiosisautoimmune modulationgastrointestinal-blood barrier
DZIEDZINY
Reumatoidalne zapalenie stawów - etiologia, patogeneza, obraz kliniczny i leczeniePowiązane z infekcją choroby reumatyczne
STRESZCZENIE
The primary cause of chronic autoimmune diseases is elusive both in somatic medicine and psychiatry. Examples of such conditions are rheumatoid arthritis and schizophrenic disorders. Immune disturbances occur in both diseases, but it is difficult to combine them into a meaningful pathogenetic model. The immunological hypothesis of schizophrenia is based on non-specific changes in the cytokine system and exponents of chronic inflammation in some patients. In rheumatoid arthritis the cytokine network is much better known than in schizophrenia, and interleukin-6, tumor necrosis factor or Janus kinases became a target of treatment. Microbiome dysbiosis and disturbances of the blood–gut barrier may be a new hypothesis of the pathogenesis of somatic and psychiatric diseases. The purpose of this narrative review was to show, using the example of two chronic diseases – rheumatoid arthritis and schizophrenic disorders – that disturbances in the blood barrier of the intestine can be a common mechanism of somatic and mental disorders.
The paper presents the current state of knowledge on the hypothetical relationship between microbiome dysbiosis and the pathogenesis of schizophrenia and rheumatoid arthritis. In conclusion, in the light of discoveries regarding the microbiome–gut–brain axis the immunological model of rheumatoid arthritis and schizophrenia formation may gain importance and contribute to the creation of new strategies for causal treatment of these still incurable diseases.
The paper presents the current state of knowledge on the hypothetical relationship between microbiome dysbiosis and the pathogenesis of schizophrenia and rheumatoid arthritis. In conclusion, in the light of discoveries regarding the microbiome–gut–brain axis the immunological model of rheumatoid arthritis and schizophrenia formation may gain importance and contribute to the creation of new strategies for causal treatment of these still incurable diseases.
REFERENCJE (54)
1.
Deane KD, Demoruelle MK, Kelmenson LB, et al. Genetic and environmental risk factors for rheumatoid arthritis. Best Pract Res Clin Rheumatol 2017; 31: 3–18, DOI: 10.1016/j.berh. 2017.08.003.
2.
Lundberg K, Wegner N, Yucel-Lindberg T, Venables PJ. Periodontitis in RA-the citrullinated enolase connection. Nat Rev Rheumatol 2010; 6: 727–730, DOI: 10.1038/nrrheum.2010.139.
3.
Albrecht K, Zink A. Poor prognostic factors guiding treatment decisions in rheumatoid arthritis patients: a review of data from randomized clinical trials and cohort studies. Arthritis Res Ther 2017; 19: 68, DOI: 10.1186/s13075-017-1266-4.
4.
Rooney CM, Mankia K, Emery P. The role of the microbiome in driving RA-related autoimmunity. Front Cell Dev Biol 2020; 8: 538130, DOI: 10.3389/fcell.2020.538130.
5.
Müller N, Schwarz JM. The role of immune system in schizophrenia. Curr Immunol Rev 2010; 6: 213–220, DOI: 10.2174/ 157339510791823673.
6.
Demjaha A, MacCabe JH, Murray RM. How genes and environmental factors determine the different neurodevelopmental trajectories of schizophrenia and bipolar disorder. Schizophr Bull 2012; 38: 209–214, DOI: 10.1093/schbul/sbr100.
7.
Van Os J, Rutten BP, Myin-Germeys I, et al. European Network of National Networks studying Gene-Environment Interactions in Schizophrenia. Identifying gene–environment interactions in schizophrenia: contemporary challenges for integrated, large-scale investigations. Schizophr Bull 2014; 40: 729–736, DOI: 10.1093/schbul/sbu069.
8.
International Schizophrenia Consortium; Purcell SM, Wray NR, Stone JL, et al. Common polygenic variation contributes to risk of schizophrenia and bipolar disorder. Nature 2009; 460: 748–752, DOI: 10.1038/nature08185.
9.
Jones AL, Mowry BJ, Pender MP, Greer JM. Immune dysregulation and self-reactivity in schizophrenia: do some cases of schizophrenia have an autoimmune basis? Immunol Cell Biol 2005; 83: 9–17, DOI: 10.1111/j.1440-1711.2005.01305.x.
10.
Boulanger LM. Immune proteins in brain development and synaptic plasticity. Neuron 2009; 64: 93–109, DOI: 10.1016/j.neuron.2009.09.001.
11.
Abegunde AT, Muhammad BH, Bhatti O, Ali T. Environmental risk factors for inflammatory bowel diseases: evidence based literature review. World J Gastroenterol 2016; 22: 6296–6317, DOI: 10.3748/wjg.v22.i27.6296.
12.
Fond G, Godin O, Boyer L, et al. Chronic low-grade peripheral inflammation is associated with ultra resistant schizophrenia. Results from the FACE-SZ cohort. Eur Arch Psychiatry Clin Neurosci 2018; 269: 985–992, DOI: 10.1007/s00406-018-0908-0.
13.
Paul BJ, Kandy HI, Krishnan V. Pre-rheumatoid arthritis and its prevention. Eur J Rheumatol 2017; 4: 161–165, DOI: 10.5152/eurjrheum.2017.16006.
14.
Maeda Y, Takeda K. Role of gut microbiota in rheumatoid arthritis. J Clin Med 2017; 6: 60, DOI: 10.3390/jcm6060060.
15.
Ramírez-Jirano LJ, Velasco-Ramírez SF, Pérez-Carranza GA, et al. Cytokines and nervous system: relationship with schizophrenia. Rev Med Inst Mex Seguro Soc 2019; 57: 107-112.
16.
Çakici N, Sutterland AL, Penninx BWJH, et al. Altered peripheral blood compounds in drug-naïve first-episode patients with either schizophrenia or major depressive disorder: a meta-analysis. Brain Behav Immun 2020; 88: 547–558, DOI: 10.1016/j.bbi.2020.04.039.
17.
McAllister AK. Major histocompatibility complex in brain development and schizophrenia. Biol Psychiatry 2014; 75: 262–268, DOI: 10.1016/j.biopsych.2013.10.003.
18.
Hornig M. The role of microbes and autoimmunity in the pathogenesis of neuropsychiatric illness. Curr Opin Rheumatol 2013; 25: 488–795, DOI: 10.1097/BOR.0b013e32836208de.
19.
Cukrowska B, Sowinska A, Bierla JB, et al. Intestinal epithelium, intraepithelial lymphocytes and the gut microbiota – key players in the pathogenesis of celiac disease. World J Gastroenterol 2017; 23: 7505–7518, DOI: 10.3748/wjg.v23.i42.7505.
20.
Gomes RG, Brito CAA, Martinelli VF, et al. HLA-G is expressed in intestinal samples of ulcerative colitis and Crohn’s disease patients and HLA-G5 expression is differentially correlated with TNF and IL-10 cytokine expression. Hum Immunol 2018; 79: 477–484, DOI: 10.1016/j.humimm.2018.03.006.
21.
Wekerle H. Brain autoimmunity and intestinal microbiota: 100 trillion game changers. Trends Immunol 2017; 38: 483–497, DOI: 10.1016/j.it.2017.03.008.
22.
Sekar A, Bialas AR, de Rivera H, et al. Schizophrenia risk from complex variation of complement component 4. Nature 2016; 530: 177–183, DOI:10.1038/nature16549.
23.
Prasad KM, Chowdari KV, D’Aiuto LA, et al. Neuropil contraction in relation to complement c4 gene copy numbers in independent cohorts of adolescent-onset and young adult-onset schizophrenia patients – a pilot study. Transl Psychiatry 2018; 8: 134, DOI: 10.1038/s41398-018-0181-z.
24.
Bernstein CN, Hitchon CA, Walld R, et al. Increased burden of psychiatric disorders in inflammatory bowel disease. Inflamm Bowel Dis 2018; 25: 360–368, DOI: 10.1093/ibd/izy235.
25.
Kharlamova N, Jiang X, Sherina N, et al. Antibodies to Porphyromonas gingivalis indicate interaction between oral infection, smoking, and risk genes in rheumatoid arthritis etiology. Arthritis Rheumatol 2016; 68: 604–613, DOI: 10.1002/art.39491.
26.
Maeda Y, Takeda K. Host-microbiota interactions in rheumatoid arthritis. Exp Mol Med 2019; 51: 1–6, DOI: 10.1038/s12276-019-0283-6.
27.
Zhang X, Zhang D, Jia H, et al. The oral and gut microbiomes are perturbed in rheumatoid arthritis and partly normalized after treatment. Nat Med 2015; 21: 895–905, DOI: 10.1038/nm.3914.
28.
Shen Y, Xu J, Li Z, et al. Analysis of gut microbiota diversity and auxiliary diagnosis as a biomarker in patients with schizophrenia: a cross-sectional study. Schizophr Res 2018; 197: 470–477, DOI: 10.1016/j.schres.2018.01.002.
29.
Kannan G, Gressitt KL, Yang S, et al. Pathogen-mediated NMDA receptor autoimmunity and cellular barrier dysfunction in schizophrenia. Transl Psychiatry 2017; 7: e1186, DOI: 10.1038/tp.2017.162.
30.
Balu DT. The NMDA receptor and schizophrenia: from pathophysiology to treatment. Adv Pharmacol 2016; 76: 351–382, DOI: 10.1016/bs.apha.2016.01.006.
31.
Severance EG, Yolken RH. Deciphering microbiome and neuroactive immune gene interactions in schizophrenia. Neurobiol Dis 2020; 135: 104331, DOI: 10.1016/j.nbd.2018.11.016.
32.
Erny D, Hrabé de Angelis AL, Jaitin D, et al. Host microbiota constantly control maturation and function of microglia in the CNS. Nat Neurosci 2015; 18: 965–977, DOI: 10.1038/nn.4030.
33.
Luczynski P, Whelan SO, O’Sullivan C, et al. Adult microbiota- deficient mice have distinct dendritic morphological changes: differential effects in the amygdala and hippocampus. Eur J Neurosci 2016; 44: 2654–2666, DOI: 10.1111/ejn.13291.
34.
Sampson TR, Mazmanian SK. Control of brain development, function, and behavior by the microbiome. Cell Host Microbe 2015; 17: 565–576, DOI: 10.1016/j.chom.2015.04.011.
35.
Zheng P, Zeng B, Liu M, et al. The gut microbiome from patients with schizophrenia modulates the glutamate-glutamine-GABA cycle and schizophrenia-relevant behaviors in mice. Sci Adv 2019; 5: eaau8317, DOI: 10.1126/sciadv.aau8317.
36.
Chen SF, Wang LY, Chiang J, et al. Assessing whether the association between rheumatoid arthritis and schizophrenia is bidirectional: a nationwide population-based cohort study. Sci Rep 2019; 9: 4493, DOI: 10.1038/s41598-018-38149-3.
37.
Sellgren C, Frisell T, Lichtenstein P, et al. The association between schizophrenia and rheumatoid arthritis: a nationwide population-based Swedish study on intraindividual and familial risks. Schizophr Bull 2014; 40: 1552–1559, DOI: 10.1093/schbul/sbu054.
38.
Broce I, Karch CM, Wen N, et al. Immune-related genetic enrichment in frontotemporal dementia: An analysis of genome-wide association studies. PLoS Med 2018; 15: e1002487, DOI: 10.1371/journal.pmed.1002487.
39.
Süß P, Rothe T, Hoffmann A, et al. The joint-brain axis: insights from rheumatoid arthritis on the crosstalk between chronic peripheral inflammation and the brain. Front Immunol 2020; 11: 612104, DOI: 10.3389/fimmu.2020.612104.
40.
El Aidy S, Dinan TG, Cryan JF. Immune modulation of the brain–gut–microbe axis. Front Microbiol 2014; 5: 146, DOI: 10.3389/fmicb.2014.00146.
41.
Chavan SS, Pavlov VA, Tracey KJ. Mechanisms and therapeutic relevance of neuro-immune communication. Immunity 2017; 46: 927–942, DOI: 10.1016/j.immuni.2017.06.008.
42.
Kwiatkowska B, Maślińska M. The place of omega-3 and omega-6 acids in supplementary treatment of inflammatory joint diseases. Reumatologia 2020; 58: 34–41, DOI: 10.5114/reum.2020.93511.
43.
Picchianti Diamanti A, Panebianco C, Salerno G, et al. Impact of Mediterranean diet on disease activity and gut microbiota composition of rheumatoid arthritis patients. Microorganisms 2020; 8: 1989, DOI: 10.3390/microorganisms8121989.
44.
Stavropoulos-Kalinoglou A, Metsios GS, Koutedakis Y, Kitas GD. Obesity in rheumatoid arthritis. Rheumatology (Oxford) 2011; 50: 450–462, DOI: 10.1093/rheumatology/keq266.
45.
Yang F, Zheng J. Understand spiciness: mechanism of TRPV1 channel activation by capsaicin. Protein Cell 2017; 8: 169–177, DOI: 10.1007/s13238-016-0353-7.
46.
Basnet P, Skalko-Basnet N. Curcumin: an anti-inflammatory molecule from a curry spice on the path to cancer treatment. Molecules 2011; 16: 4567–4598, DOI: 10.3390/molecules16064567.
47.
Yang CY, Leung PS, Adamopoulos IE, Gershwin ME. The implication of vitamin D and autoimmunity: a comprehensive review. Clin Rev Allergy Immunol 2013; 45: 217–226, DOI: 10.1007/s12016-013-8361-3.
48.
Kostoglou-Athanassiou I, Athanassiou P, Lyraki A, et al. Vitamin D and rheumatoid arthritis. Ther Adv Endocrinol Metab 2012; 3: 181–187, DOI: 10.1177/2042018812471070.
49.
Vadell AKE, Bärebring L, Hulander E, et al. Anti-inflammatory Diet In Rheumatoid Arthritis (ADIRA) – a randomized, controlled crossover trial indicating effects on disease activity. Am J Clin Nutr 2020; 111: 1203–1213, DOI: 10.1093/ajcn/nqaa019.
50.
Häger J, Bang H, Hagen M, et al. The role of dietary fiber in rheumatoid arthritis patients: a feasibility study. Nutrients 2019; 11: 2392, DOI: 10.3390/nu11102392.
51.
Milajerdi A, Mousavi SM, Sadeghi A, et al. The effect of probiotics on inflammatory biomarkers: a meta-analysis of randomized clinical trials. Eur J Nutr 2020; 59: 633–649, DOI: 10.1007/s00394-019-01931-8.
52.
Pełka-Wysiecka J, Kaczmarczyk M, Bąba-Kubiś A, et al. Analysis of gut microbiota and their metabolic potential in patients with schizophrenia treated with olanzapine: results from a six-week observational prospective cohort study. J Clin Med 2019; 8: pii: E1605, DOI: 10.3390/jcm8101605.
53.
Ng QX, Soh AYS, Venkatanarayanan N, et al. A systematic review of the effect of probiotic supplementation on schizophrenia symptoms. Neuropsychobiology 2019; 78: 1–6, DOI: 10.1159/000498862.
54.
Doğan Bulut S, Bulut S, Görkem Atalan D, et al. The relationship between symptom severity and low vitamin D levels in patients with schizophrenia. PLoS One 2016; 11: e0165284, DOI: 10.1371/journal.pone.0165284.
Copyright: © Narodowy Instytut Geriatrii, Reumatologii i Rehabilitacji w Warszawie. This is an Open Access journal, all articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License (https://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
Udostępnij
ARTYKUŁ POWIĄZANY
| eISSN: | 2084-9834 |
| ISSN: | 0034-6233 |
Przetwarzamy dane osobowe zbierane podczas odwiedzania serwisu. Realizacja funkcji pozyskiwania informacji o użytkownikach i ich zachowaniu odbywa się poprzez dobrowolnie wprowadzone w formularzach informacje oraz zapisywanie w urządzeniach końcowych plików cookies (tzw. ciasteczka). Dane, w tym pliki cookies, wykorzystywane są w celu realizacji usług, zapewnienia wygodnego korzystania ze strony oraz w celu monitorowania ruchu zgodnie z Polityką prywatności. Dane są także zbierane i przetwarzane przez narzędzie Google Analytics (więcej).
Możesz zmienić ustawienia cookies w swojej przeglądarce. Ograniczenie stosowania plików cookies w konfiguracji przeglądarki może wpłynąć na niektóre funkcjonalności dostępne na stronie.
Możesz zmienić ustawienia cookies w swojej przeglądarce. Ograniczenie stosowania plików cookies w konfiguracji przeglądarki może wpłynąć na niektóre funkcjonalności dostępne na stronie.
