Association between intestinal flora and feces inflammatory factors in recurrent oral ulcer#br#

XIAOYAN -Chen; HONGWEI -zhu; RUILI -Hou; ZHIHUI -Li; JUN -Lu; MULAN -Jin

doi:10.16098/j.issn.0529-1356.2020.04.021

PDF(12240 KB)

Acta Anatomica Sinica ›› 2020, Vol. 51 ›› Issue (4) : 595-604. DOI: 10.16098/j.issn.0529-1356.2020.04.021

Histology,Embryology and Developmental Biology

Association between intestinal flora and feces inflammatory factors in recurrent oral ulcer#br#

CHEN Xiao-yan^1,2,3 ZHU Hong-wei⁴ HOU Rui-li⁵ LI Zhi-hui⁴ LU Jun^1* JIN Mu-lan^1*

Author information +

History +

Abstract

Objective To identify whether gut microbial changes were associated with recurrent oral ulcer (ROU) and to determine possible factors associated with the pathogenesis of ROU. Methods We performed metagenomic sequencing and detected inflammatory cytokines ［interleukin (IL)-10, IL-22］ using ELISA in faeces. Eight students who frequently suffered from oral ulcers were selected as the experimental group (HR); accordingly, 14 healthy volunteers served as the control group (HN). Results There were some differences in intestinal microbial community structures and core flora between the HR and the HN. At the phylum level, the abundance of Firmicutes in the HR was higher than that in the HN (P<0.05). At the genus level, the abundance of Escherichia/Shigella and Bifidobacterium in the HN were higher than that in the HR (P<0.05). The abundance of enterococcus in the HR was higher than that in the HN (P<0.05). IL-10 levels in feces were similar in HN and HR, and there was no statistical difference between the two groups (P>0.05). IL-22 level in HR was higher than that in HN, and there was statistical significance between the two groups (P<0.05). Univariate Logistic regression analysis showed that IL-22 was a risk factor for ROU. Multivariate Logistic regression analysis showed that Bifidobacterium abundance may be a protective factor for ROU, IL-22 in faeces may be a risk factor. Conclusion Our results suggest that there is an interaction between IL-22 and the distribution of intestinal flora in the patients with ROU, the occurrence of ROU may be related to the decrease of the abundance of Bifidobacteriumand the increase of IL-22 in the faeces, and IL-22 has a stronger proinflammatory effect than the antiinflammatory effect generated by IL-10 and itself in the occurrence of ROU, but further research will be needed.

Key words

Recurrent oral ulcer

/ Intestinal flora / Interleukin-10 / Interleukin-22 / High-throughput sequencing / Enzyme linked immunosorbent a ssay / Adult

Cite this article

EndNote

Ris (Procite)

Bibtex

Download Citations

CHEN Xiao-yan ZHU Hong-wei HOU Rui-li LI Zhi-hui LU Jun JIN Mu-lan. Association between intestinal flora and feces inflammatory factors in recurrent oral ulcer#br#[J]. Acta Anatomica Sinica. 2020, 51(4): 595-604 https://doi.org/10.16098/j.issn.0529-1356.2020.04.021

References

［1］ Slebioda Z, Szponar E, Kowalska A.Recurrent aphthous stomatitis: genetic aspects of etiology［J］. Postepy Dermatol Alergol, 2013，30（2）： 96-102.

［2］ Liu NN，Guan S， Wang HY， et al. The antimicrobial peptide Nal-P-13 exerts a reparative effect by promoting cell proliferation, migration, and cell cycle progression［J］. Biomed Res Int， 2018，2018：7349351.

［3］ Vaillant L， Samimi M. Aphthous ulcers and oral ulcerations［J］. Presse Med，2016，45(2)：215-226.

［4］ Liu T, Yang Z, Zhang X, et al. 16S rDNA analysis of the effect of fecal microbiota transplantation on pulmonary and intestinal flora［J］. 3 Biotech, 2017，7（6）：370-379.

［5］ Walters WA, Xu Z, Knight R. Meta-analyses of human gut microbes associated with obesity and IBD［J］. FEBS Lett， 2014，588（22）：4223-4233.

［6］ Abrahamsson TR， Jakobsson HE，Andersson AF，et al. Low gut microbiota diversity in early infancy precedes asthma at school age［J］. ClinExp Allergy， 2014，44（6）：842-850.

［7］ Qin J, Li Y, Cai Z, et al. A metagenome-wide association study of gut microbiota in type 2 diabetes［J］. Nature， 2012，490（7418）：55-60.

［8］ Jie Z，Xia H，Zhong SL,et al. The gut microbiome in atherosclerotic cardiovascular disease［J］. Nat Commun， 2017，8（1）：845.

［9］ Maeda Y， Takeda K . Role of gut microbiota in rheumatoid arthritis［J］. J Clin Med， 2017，6（6）：60-66.

［10］ Scher JU， Ubeda C， Artacho A. Decreased bacterial diversity characterizes the altered gut microbiota in patients with psoriatic arthritis,resemblingdysbiosis in inflammatory bowel disease［J］. Arthritis Rheumatol， 2015，67（1）：128-139.

［11］ Geng H， Shu S， Dong JJ， et al. Association study of gut flora in Wilson’s disease through high-throughput sequencing［J］. Medicine， 2018，97（31）： 1-7.

［12］ Sunil T， Jacques I， Emily W， et al . The host microbiome regulates and maintains human health: a primer and perspective for non-microbiologists［J］. Cancer Res ，2017，77（8）：1783-1812.

［13］ Dinan TG， Stanton C，Cryan JF. Psychobiotics: a novel class of psychotropic［J］. Biol Psychiatry， 2013，74（10）：720-726.

［14］ Sara S， Sara CT， Chiara V， et al. Effect of a multistrain probiotic(Lactoflorene? Plus) on inflammatory parameters and microbiota composition in subjects with stress-related symptoms［J］. Neurobiol Stress， 2019，10：100138.

［15］ Yu ZQ， Wang WF， Dai YC， et al. Interleukin-22 receptor 1 is expressed in multinucleated giant cells: a study on intestinal tuberculosis and Crohn’s disease［J］. World J Gastroenterol， 2019，25（20）：2473-2488.

［16］ Dudakov JA， Hanash AM， van den Brink MR. Interleukin-22: immunobiology and pathology［J］. Annu Rev Immunol， 2015，33：747-785.

［17］ Wang W， Chen L， Zhou R. Increased proportions of Bifidobacterium and the Lactobacillus group and loss of butyrate producing bacteria in inflammatory bowel disease［J］. J ClinMicrobiol， 2014，52（2）：398-406.

［18］ Faubion WA Jr， Fletcher JG，O’Byrne S. Emerging biomARKers in inflammatory bowel disease(EMBARK) study identifies fecal calprotectin, serum MMP9, and serum IL-22 as a novel combination of biomarkers for Crohn’s disease activity:role of cross-sectional imaging［J］. Am J Gastroenterol，2013，108（5）：1891-1900.

［19］Monteleone I， Franchi L， Biancone L，et al. Enhanced expression of the Fas pathway inhibitor, Flip, in the mucosa of patients with Crohn’s disease［J］. Eur Rev Med PharmacolSci， 2004，8：192.

［20］ Zhang J， Chen SL， Li LB. Correlation between intestinal flora and serum inflammatory factors in patients with Crohn’s disease［J］. Eur Rev Med Pharmacol Sci ， 2017，21（21）：4913-4917.

［21］ Marchini L， Campos MS， Silva AM， et al. Bacterial diversity in aphthous ulcers［J］. Oral Microbiol Immunol， 2007， 22（4）：225-231.

［22］ Brij B， Yadav AP， Singh SB ，et al. Diversity and functional analysis of salivary microflora of Indian Antarctic expeditionaries［J］. J Oral Microbiol， 2019，11（1）：1581513.

［23］ Kim YJ， Choi YS，Baek KJ，et al. Mucosal and salivary microbiota associated with recurrent aphthous stomatitis［J］. BMC Microbiol， 2016，16(Suppl 1)：57.

［24］ Chakradhar S. A curious connection: teasing apart the link between gut microbes and lung disease［J］. Nat Med， 2017， 23（4）：402-404.

［25］ Shen LJ. Oral Histopathology［M］. Wuhan: Huazhong Science and Technology University， 2013:224-242.

［26］ Org E， Parks BW， Joo JW， et al. Genetic and environmental control of host-gut microbiota interactions［J］. Genome Res， 2015，25（10）：1558-1569.

［27］ Fang ZZ，Jiang R， Zhang LR，et al. In situ fabrication of radiopaque microcapsules for oral delivery and real-time gastrointestinal tracking of Bifidobacterium［J］. Int J Nanomedicine， 2018，13： 4093-4105.

［28］ Huda MN, Lewis Z, Kalanetra KM， et al. Stool microbiota and vaccine responses of infants［J］. Pediatrics， 2014，134（2）：e362-372.

［29］ Holscher HD，Czerkies LA，Cekola P，et al. Bifidobacterium lactis Bb12 enhances intestinal antibody response in formula-fed infants: a randomized, double-blind, controlled trial［J］. JPEN J Parenter Enteral Nutr，2012，36（Suppl 1）：106S-117S.

［30］ Chichlowski M, De Lartigue G, German JB，et al. Bifidobacteria isolated from infants and cultured on human milk oligosaccharides affect intestinal epithelial function［J］. J Pediatr Gastroenterol Nutr， 2012，55（3）： 321-327.

［31］ Taft DH，Liu JX，Maldonado-Gomez MX， et al. Bifidobacterial dominance of the Gut in early life and acquisition of antimicrobial resistance［J］. mSphere，2018，3（5）. pii: e00441-18. doi: 10.1128/mSphere.00441-18.

［32］ Michalek RD， Gerriets VA，Jacobs SR， et al. Cutting edge: distinct glycolytic and lipid oxidative metabolic programs are essential for effector and regulatory CD4+ T cell subsets［J］. J Immunol， 2011，186（6）：3299-3303.

［33］ Zeng H， Chi H. Metabolic control of regulatory T cell development and function［J］. Trends Immunol， 2015，36（1）：3-12.

［34］ Galgani M， De Rosa V， La Cava A，et al. Role of metabolism in the immunobiology of regulatory T cells［J］. J Immunol， 2016，197（7）：2567-2575.

［35］ Wang F，Yin Q，Chen L，et al. Bifidobacterium can mitigate intestinal immunopathology in the context of CTLA-4 blockade ［J］. PNAS，2018，115（1）：157-161.

［36］ Round JL， Mazmanian SK. The gut microbiota shapes intestinal immune responses during health and disease［J］. Nat Rev Immunol， 2009，9（5）：313-323.