Publications by authors named "Xiaofa Qin"

75 Publications

High Fecal Proteolytic Activity That Precedes Ulcerative Colitis Likely Results From Impaired Inactivation of Pancreatic Proteases Rather Than Bacteria.

Authors:
Xiaofa Qin

Inflamm Bowel Dis 2021 Jun 14. Epub 2021 Jun 14.

GI Biopharma Inc., Westfield, New Jersey, USA.

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http://dx.doi.org/10.1093/ibd/izab142DOI Listing
June 2021

More Epidemiological Studies Warranted to Determine the Cause of Inflammatory Bowel Disease.

Authors:
Xiaofa Qin

Inflamm Bowel Dis 2021 Mar;27(4):e43-e44

GI Biopharma Inc, Westfield, New Jersey, USA.

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http://dx.doi.org/10.1093/ibd/izaa329DOI Listing
March 2021

Sucralose Promotes Colitis-Associated Colorectal Cancer Risk in a Murine Model Along With Changes in Microbiota.

Front Oncol 2020 3;10:710. Epub 2020 Jun 3.

Department of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.

Sucralose is a calorie-free high-intensity artificial sweetener that is widely used in thousands of foods and beverages all over the world. Although it was initially regarded as a safe, inert food additive, its adverse effect on gut microbiota and health has drawn more and more attention as evidence accumulates. Studies by us and others revealed that sucralose exacerbated gut damage and inflammation in animal models for inflammatory bowel disease (IBD), including those for both ulcerative colitis, and Crohn's disease. Our study demonstrated that sucralose greatly aggravated dextran sulfate sodium (DSS)-induced colitis along with causing changes in gut microbiota, the gut barrier and impaired inactivation of digestive proteases mediated by deconjugated bilirubin. It is well-documented that IBD greatly increases the risk of colorectal cancer (CRC), the globally third-most-common cancer, which, like IBD, has a high rate in the developed countries. Azoxymethane (AOM)/DSS has been the most commonly used animal model for CRC. In this study, we further explored the effect of sucralose on tumorigenesis and the possible mechanism involved using the AOM/DSS mouse model. First, 1.5 mg/ml sucralose was included in the drinking water for 6 weeks to reach a relatively stable phase of impact on gut microbiota. Then, 10 mg/kg AOM was administered through intraperitoneal injection. Seven days later, 2.5% DSS was put in the drinking water for 5 days, followed by 2 weeks without DSS. The 5 days of DSS was then repeated, and the mice were sacrificed 6 weeks after AOM injection. The results showed that sucralose caused significant increases in the number and size of AOM/DSS-induced colorectal tumors along with changes in other parameters such as body and spleen weight, pathological scores, mortality, fecal β-glucuronidase and digestive proteases, gut barrier molecules, gut microbiota, inflammatory cytokines and pathways (TNFα, IL-1β, IL-6, IL-10, and TLR4/Myd88/NF-κB signaling), and STAT3/VEGF tumor-associated signaling pathway molecules. These results suggest that sucralose may increase tumorigenesis along with dysbiosis of gut microbiota, impaired inactivation of digestive protease, damage to the gut barrier, and exacerbated inflammation.
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http://dx.doi.org/10.3389/fonc.2020.00710DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7286428PMC
June 2020

The Functional Role of Fecal Microbiota Transplantation on Dextran Sulfate Sodium-Induced Colitis in Mice.

Front Cell Infect Microbiol 2019 15;9:393. Epub 2019 Nov 15.

Department of Biochemistry and Molecular Biology, Heilongjiang Provincial Science and Technology Innovation Team in Higher Education Institutes for Infection and Immunity, Harbin Medical University, Harbin, China.

Increasingly studies revealed that dysbiosis of gut microbiota plays a pivotal role in the pathogenesis of ulcerative colitis (UC). Fecal microbiota transplantation (FMT) has drawn more and more attention and become an important therapeutic approach. This study aims to examine the facts about the effective components and look into potential mechanisms of FMT. Colitis was induced by 3% (w/v) dextran sulfate sodium (DSS) in drinking water for 7 days. Colitis mice were administered by oral gavage with fecal suspension, fecal supernatant, fecal bacteria, or boiling-killed fecal bacteria from healthy controls and the disease activity index was monitored daily. On the seventh day, mice were euthanized. The length, histological score, parameters related to inflammation, gut barrier functions of the colon, activities of digestive protease and β-glucuronidase in feces were measured. All of the four fecal components showed certain degree of efficacy in DSS-induced colitis, while transplantation of fecal suspension showed the most potent effect as demonstrated by less body weight loss, lower disease activity scores, more expression of tight junction proteins and TRAF6 and IκBα, less expression of TNF-α, IL-1β, IL-10, TLR-4, and MyD88 in gut tissue, as well as restoration of fecal β-glucuronidase and decreases in fecal digestive proteases. These results provide a novel insight into the possible mechanism of FMT and may help to improve and optimize clinical use of FMT.
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http://dx.doi.org/10.3389/fcimb.2019.00393DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6873233PMC
August 2020

Bacterial β-glucuronidase alleviates dextran sulfate sodium-induced colitis in mice: A possible crucial new diagnostic and therapeutic target for inflammatory bowel disease.

Biochem Biophys Res Commun 2019 05 6;513(2):426-433. Epub 2019 Apr 6.

Department of Biochemistry and Molecular Biology, Heilongjiang Provincial Science and Technology Innovation Team in Higher Education Institutes for Infection and Immunity, Harbin Medical University, Harbin, China. Electronic address:

Objective: Inflammatory bowel diseases (IBD) including ulcerative colitis and Crohn's disease are devastating diseases of the gut. At present, all the treatments are mainly targeting symptoms like inflammation. The disease remains regarded as incurable, largely due to lacking of knowledge on its etiology. Our previous studies suggested that impaired inactivation of digestive proteases by deconjugated bilirubin in experimental colitis, thus bacterial β-glucuronidase for catalyzing the reaction, may have played critical role in the pathogenesis of IBD.

Methods: We first analyzed β-glucuronidase activity in gut tissue and feces of mice by a colitis model. Then the effect of β-glucuronidase on experimental colitis was investigated in detail by administration of β-glucuronidase (from E. coli) and fecal material transplantation to mice with 3% DSS in drinking water for 7 days.

Results: Mice with colitis showed unchanged activity of β-glucuronidase in colon tissue but decreased activity in feces. Treatment with bacterial β-glucuronidase at 100 U or above alleviated DSS-induced colitis as demonstrated by the less body weight loss, less disease activity score, increased expression of tight junction proteins and decreased gut permeability, decreases in MPO, TNF-α, IL-1β, TLR-4 and MyD88, and increase in IL-10 and IκBα in gut, restored fecal β-glucuronidase and gut microbiota along with decreases in fecal digestive proteases. Transplantation of fecal material from control to colitis mice showed similar effects as treatment with β-glucuronidase.

Conclusions: Bacterial β-glucuronidase showed strong inhibition on colitis along with the reduction in fecal digestive proteases, which may be a crucial diagnostic and therapeutic target for IBD.
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http://dx.doi.org/10.1016/j.bbrc.2019.03.196DOI Listing
May 2019

Sucralose Increased Susceptibility to Colitis in Rats.

Inflamm Bowel Dis 2019 01;25(2):e3-e4

GI Biopharma Inc., Westfield, New Jersey.

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http://dx.doi.org/10.1093/ibd/izy196DOI Listing
January 2019

Unconjugated bilirubin ameliorates the inflammation and digestive protease increase in TNBS-induced colitis.

Mol Med Rep 2017 Aug 21;16(2):1779-1784. Epub 2017 Jun 21.

Department of Biochemistry and Molecular Biology, Heilongjiang Provincial Science and Technology Innovation Team in Higher Education Institutes for Infection and Immunity, Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.

The authors previously demonstrated that unconjugated bilirubin (UCB) may inhibit the activities of various digestive proteases, including trypsin and chymotrypsin. The digestive proteases in the lower gut are important in the pathogenesis of inflammatory bowel diseases. The effects of UCB on the inflammation and levels of digestive proteases in feces of rats with colitis have not yet been revealed. The present study investigated the effect of UCB on the inflammatory status and levels of trypsin and chymotrypsin in the feces of rats with trinitrobenzenesulfonic acid (TNBS)‑induced colitis. The data indicated that treatment with TNBS resulted in a marked reduction in weight gain, which was significantly alleviated in UCB‑treated rats. Furthermore, UCB treatment alleviated the inflammation induced by TNBS, detected via macroscopic damage and microscopic inflammation scores, and pro‑inflammatory markers including myeloperoxidase (MPO), tumor necrosis factor (TNF)‑α and interleukin (IL)‑1β. Furthermore, rats with colitis demonstrated significant increases in fecal trypsin and chymotrypsin levels, whereas UCB treatment significantly alleviated these increases. A significant positive correlation was additionally revealed among the pro‑inflammatory markers (MPO, TNF‑α and IL‑1β) and fecal digestive proteases (trypsin and chymotrypsin) in colitis. The results of the present study demonstrated that UCB ameliorated the inflammation and digestive protease increase in TNBS-induced colitis.
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http://dx.doi.org/10.3892/mmr.2017.6825DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5562003PMC
August 2017

Impaired inactivation of digestive proteases: The possible key factor for the high susceptibility of germ-free and antibiotic-treated animals to gut epithelial injury.

Authors:
Xiaofa Qin

World J Gastrointest Pathophysiol 2017 Feb;8(1):1-2

Xiaofa Qin, GI Biopharma Inc, Westfield, NJ 07090, United States.

Recent study shows that germ-free and antibiotic-treated animals are highly susceptible to gut epithelial injury. This paper addresses that impaired inactivation of digestive proteases may be the key factor for the increased susceptibility.
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http://dx.doi.org/10.4291/wjgp.v8.i1.1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5311466PMC
February 2017

Increased Digestive Proteases and Decreased β-Glucuronidase in Feces of Rats Treated with Sucralose and Saccharin-Another Critical Evidence That These Dietary Chemicals May Be Important Causative Factors for Inflammatory Bowel Disease.

Inflamm Bowel Dis 2016 08;22(8):E29-30

*Department of Biochemistry and Molecular Biology, Heilongjiang Provincial Science and Technology Innovation Team in Higher Education Institutes for Infection and Immunity, Harbin Medical University, Harbin, China†Department of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China‡GI Biopharma Inc., Westfield, NJ.

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http://dx.doi.org/10.1097/MIB.0000000000000859DOI Listing
August 2016

How Sugar and Soft Drinks Are Related to Inflammatory Bowel Disease?

Authors:
Xiaofa Qin

Inflamm Bowel Dis 2016 06;22(6):E18-9

GI Biopharam Inc., Westfield, New Jersey.

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http://dx.doi.org/10.1097/MIB.0000000000000774DOI Listing
June 2016

Is Colonic Crohn's Disease More Closely Related to Ulcerative Colitis or Crohn's Disease by Nature?

Authors:
Xiaofa Qin

Inflamm Bowel Dis 2016 May;22(5):E15

GI Biopharam Inc., Westfield, New Jersey.

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http://dx.doi.org/10.1097/MIB.0000000000000777DOI Listing
May 2016

Food Additives Should Not Be Ruled Out as the Possible Causative Factors of Inflammatory Bowel Disease in Korea.

Authors:
Xiaofa Qin

Inflamm Bowel Dis 2016 Jan;22(1):E1

GI Biopharam Inc, Westfield, New Jersey.

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http://dx.doi.org/10.1097/MIB.0000000000000668DOI Listing
January 2016

How to Explain the Dramatic Increase Around 2000 but Recent Leveling Off of Inflammatory Bowel Disease in Korea?

Authors:
Xiaofa Qin

Inflamm Bowel Dis 2015 Aug;21(8):E16-7

GI Biopharam Inc., Westfield, New Jersey.

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http://dx.doi.org/10.1097/MIB.0000000000000491DOI Listing
August 2015

Can inflammatory bowel disease really be solved by the multiple -omics and meta-omics analyses?

Authors:
Xiaofa Qin

Immunol Lett 2015 Jun 28;165(2):107-8. Epub 2015 Mar 28.

GI Biopharma Inc, 918 Willow Grove Road, Westfield, NJ 07090, USA. Electronic address:

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http://dx.doi.org/10.1016/j.imlet.2015.03.007DOI Listing
June 2015

Role of bilirubin in digestive proteases inactivation in the lower intestine.

Dig Liver Dis 2015 May 7;47(5):438-9. Epub 2015 Feb 7.

Department of Biochemistry and Molecular Biology, Heilongjiang Provincial Science and Technology Innovation Team in Higher Education Institutes for Infection and Immunity, Harbin Medical University, Harbin, China. Electronic address:

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http://dx.doi.org/10.1016/j.dld.2015.01.158DOI Listing
May 2015

Dissolution of lipids from mucus: a possible mechanism for prompt disruption of gut barrier function by alcohol.

Toxicol Lett 2015 Jan 25;232(2):356-62. Epub 2014 Nov 25.

Department of Surgery, Rutgers-New Jersey Medical School, Newark, NJ 07103, USA.

Acute and/or chronic alcohol ingestion has been shown to exacerbate the morbidity and mortality rate associated with acute mechanical and/or thermal trauma. While alcohol ingestion can affect many organs and systems, clinical and preclinical studies indicate that alcohol ingestion can cause a 'leaky gut' syndrome which in turn contributes to infection and systemic organ dysfunction. This study investigated the acute effect of alcohol on gut barrier function. Using an in vivo isolated gut sac model of naïve male rats, each individual gut sac was injected with different concentrations (0, 5, 10, 20, and 40%, v/v) of alcohol. After different times of alcohol exposure, each isolated gut segment was harvested and intestinal permeability and mucosal surface hydrophobicity (a physiologic marker of mucus barrier function) were measured as well as luminal DNA, mucus, protein and free fatty acids. The results showed that alcohol caused dose-dependent and time-dependent increases in gut permeability and decreases in mucosal surface hydrophobicity, with significant changes to be observed 5 min after treatment with 10% alcohol. In addition, it is further found that these changes in permeability and hydrophobicity are more closely associated with increased intestinal luminal free fatty acids levels but not protein or DNA levels. These results suggest that alcohol may cause loss of gut barrier function by extracting and dissolving lipids from the mucus with a resultant decrease in mucosal surface hydrophobicity, which is a critical component of gut barrier function.
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http://dx.doi.org/10.1016/j.toxlet.2014.11.027DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4291284PMC
January 2015

May bacterial or pancreatic proteases play a critical role in inflammatory bowel disease?

Authors:
Xiaofa Qin

World J Gastroenterol 2014 Sep;20(35):12709-10

Xiaofa Qin, GI Biopharma Inc,Westfield, NJ 07090, United States.

In a recent review paper, Carroll and Maharshak discussed a critical role of enteric bacterial proteases in the pathogenesis of inflammatory bowel disease (IBD). I take a great interest in this paper as I also suspected proteases, not from the bacteria, but those originated from the pancreas that failed to be inactivated in the lower gut due to a reduction in gut bacteria, may have played a critical role in the pathogenesis of IBD, which was first published more than a decade ago and discussed again in more detail in a recent paper published in this journal. Antibiotics may result in a big reduction in gut bacteria and bacterial proteases, but multiple studies demonstrated dramatic increased of pancreatic proteases like trypsin and chymotrypsin in the feces of animals or patients treated with antibiotics. Multiple large-scale studies also demonstrated use of antibiotics caused an increase but not decrease in the risk of developing IBD, suggesting impaired inactivation and degradation of pancreatic proteases may have played a more critical role in the pathogenesis of IBD.
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http://dx.doi.org/10.3748/wjg.v20.i35.12709DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4168115PMC
September 2014
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