Research progress on the relationship between Fusobacterium nucleatum,Staphylococcus aureus and inflammatory bowel disease
LIU Si-yao1 GAO Lian-chao1 HUAI Bing-cheng1 WANG Hui2▲
1. College of Medical Technology, Qiqihar Medical University, Heilongjiang Province, Qiqihar 161006, China;
2. Department of Immunology, College of Medical Technology, Qiqihar Medical University, Qiqihar 161006, China
Abstract：Inflammatory bowel disease (IBD) is a chronic non-specific inflammatory bowel disease. The incidence of IBD in China is on the rise, and the main risk factor for IBD may be intestinal bacterial infection, among which, Fusobacterium nucleatum (Fn) and Staphylococcus aureus (SA) infection, which solve IBD, have become the focus. This paper focuses on the relationship between the occurrence and development of Fn and SA and the pathogenesis of IBD.In addition, some new ideas about Fn and SA are also discussed. This paper aims to help researchers to continuously understand IBD, and to provide theoretical basis for finding new methods of diagnosis and treatment of IBD, hoping to make a modest contribution to the field of IBD.
刘思尧；高连超；怀炳成；王慧. 具核梭杆菌、金黄色葡萄球菌与炎症性肠病相关性的研究进展[J]. 中国当代医药, 2021, 28(12): 38-041.
LIU Si-yao；GAO Lian-chao；HUAI Bing-cheng；WANG Hui. Research progress on the relationship between Fusobacterium nucleatum,Staphylococcus aureus and inflammatory bowel disease. 中国当代医药, 2021, 28(12): 38-041.
Hillman ET，Lu H，Yao T，et al.Microbial ecology along the gastrointestinal tract[J].Microbes Environ，2017，32（4）：300-313.
[3]
Liang J，Sha SM，Wu KC.Role of the intestinal microbiota and fecal transplantation in inflammatory bowel diseases[J].J Dig Dis，2014，15（12）：641-646.
[4]
Strauss J，White A，Ambrose C，et al.Phenotypic and genotypic analyses of clinical Fusobacterium nucleatum andFusobacterium periodonticumisolates from the human gut[J].Anaerobe，2008，14（6）：301-309.
[5]
Ghosh SK，Gupta S，Jiang B，et al.Fusobacterium nucleatum and human β-defensins modulate the release of antimicrobial chemokine CCL20/macrophage inflammatory protein 3α[J].Infect Immun，2011，79（11）：4578-4587.
[6]
王倩婷，吴武超，吴亚菲.具核梭杆菌Fad A 黏附素的研究进展[J].中华口腔医学杂志，2014，49（12）：770-773.
Han YW，Shen T，Chung P，et al.Uncultivated bacteria as etiologic agents of intra-amniotic inflammation leading to preterm birth[J].J Clin Microbi，2009，47（1）：38-47.
[9]
Sparks Stein P，Steffen MJ，Smith C，et al.Serum antibodies to periodontal pathogens are a risk factor for Alzheimer′s disease[J].Alzheimers Dement，2012，8（3）：196-203.
[10]
Han YW，Ikegami A，Rajanna C，et al.Identification and Characterization of a Novel Adhesin Unique to Oral Fusobacteria[J].J Bacteriol，2005，187（15）：5330-5340.
Habashneh RA，Khader YS，Alhumouz MK，et al.The association between inflammatory bowel disease and periodontitis among Jordanians：a case-control study[J].J Periodontal Res，2012，47（3）：293-298.
[13]
Strauss J，Kaplan GG，Beck PL，et al.Invasive potential of gut mucosa-derivedFusobacterium nucleatumpositively correlates with IBD status of the host[J].Inflamm Bowel Dis，2011，17（9）：1971-1978.
[14]
Cao P，Chen Y，Chen Y，et al.Fusobacterium nucleatumActivates Endoplasmic Reticulum Stress to Promote Crohn′s Disease Development via the Upregulation of CARD3 Expression[J].Front Pharmacol，2020，11：106.
Cheung AL，Zhang G.Global regulation of virulence determi-nants inStaphylococcus aureusby the SarA protein family[J].Front Biosci，2002，（7）：1825-1842.
[17]
Liu X，Chauhan VS，Marriott I.NOD2 contributes to the in-flammatory responses of primary murine microglia and astro-cytes toStaphylococcus aureus[J].Neurosci Lett，2010，474（2）：93-98.
[18]
Volz T，Nega M，Buschmann J，et al.NaturalStaphylococcus aureus-derived peptid oglycan fragments activate NOD2 and act as potent costimulators of the innate immune system ex-clusively in the presence of TLR signals[J].FASEB J，2010，24（10）：4089-4102.
[19]
Berg RD，Garlington AW.Translocation of certain indigenous bacteria from the gastrointestinal tract to the mesenteric lymph nodes and other organs in a gnotobiotic mouse model[J].Infect Immun，1979，23（2）：403-411.
[20]
Tsianos EV，Katsanos K.Do we really understand what the immunological disturbances in inflammatory bowel disease mean?[J].World J Gastroenterol，2009，15（5）：521-525.
[21]
Kohler JE，Zaborina O，Wu L，et al.Components of intestinal epithelial hypoxia activate the virulence circuitry of Pseudo-monas[J].Am J Physiol Gastrointest Liver Physiol，2005，288（5）：G1048-G1054.
京公网安备 11010502046607号