Erratum to: Orally-Administered Bifidobacterium animalis subsp. lactis Strain BB12 on Dextran Sodium Sulfate-Induced Colitis in Mice.

This erratum is being published to correct the author's contribution of above manuscript by Chae et al. that was published in Journal of Microbiology and Biotechnology (2018, 28:11, 1800-1805). The ninth author (Jin Hyup Lee) should be marked as corresponding author (*) with latest author (Young Jun Kim). The correspondence should appear as: *Corresponding authors Young Jun Kim Phone: +82-44-860-1435; Fax: +82-44-860-1586; E-mail: yk46@korea.ac.kr Jin Hyup Lee Phone: +82-44-860-1437 Fax: +82-44-860-1586; E-mail: jinhyuplee@korea.ac.kr.

LB-9, Novel Probiotic Lactic Acid Bacteria, Ameliorates Dextran Sodium Sulfate-Induced Colitis in Mice by Inhibiting TNF-α-Mediated Apoptosis of Intestinal Epithelial Cells.

Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease, is a group of chronic and relapsing inflammatory conditions within the gastrointestinal tract. An increase in intestinal epithelial cell (IEC) apoptosis is a major characteristic of UC. Tumor necrosis factor-α (TNF-α) plays an essential role in the regulation of apoptosis. Aberrant activation of the immune response to resident microflora contributes to overproduction of TNF-α in the mucosal tissue of the gastrointestinal tract; a hallmark of UC. There are no curative medications for IBD. Thus, establishment of novel strategies for the treatment of this disease is imperative. Lactic acid bacteria (LAB) have been characterized as probiotics that can alleviate imbalances in indigenous microflora in UC, exhibiting beneficial effects for the treatment and prevention of IBD. In this study, we elucidate the potential of LB-9, a novel probiotic LAB, to protect against colitis development using a dextran sodium sulfate (DSS)-induced mouse model of UC. Treatment using LB-9 reduced clinical symptoms of colitis. In addition, both colitis-induced and NF-κB-mediated IEC apoptosis was markedly reduced in mice treated with LB-9. Moreover, these results were closely associated with reduced TNF-α levels. Our study demonstrates that the LB-9 probiotic exhibits therapeutic potential for UC through suppression of TNF-α-mediated IEC apoptosis in a murine DSS-induced colitis model, with important biological implications for treatment of IBD in humans.

Effects of Orally-Administered Bifidobacterium animalis subsp. lactis Strain BB12 on Dextran Sodium Sulfate-Induced Colitis in Mice.

Inflammatory bowel disease, including Crohn's disease and ulcerative colitis (UC), is a chronically relapsing inflammatory disorder of the gastrointestinal tract. Intestinal epithelial cells (IECs) constitute barrier surfaces and play a critical role in maintaining gut health. Dysregulated immune responses and destruction of IECs disrupt intestinal balance. Dextran sodium sulfate (DSS) is the most widely used chemical for inducing colitis in animals, and its treatment induces colonic inflammation, acute diarrhea, and shortening of the intestine, with clinical and histological similarity to human UC. Current treatments for this inflammatory disorder have poor tolerability and insufficient therapeutic efficacy, and thus, alternative therapeutic approaches are required. Recently, dietary supplements with probiotics have emerged as promising interventions by alleviating disturbances in the indigenous microflora in UC. Thus, we hypothesized that the probiotic Bifidobacterium animalis subsp. lactis strain BB12 could protect against the development of colitis in a DSS-induced mouse model of UC. In the present study, oral administration of BB12 markedly ameliorated DSS-induced colitis, accompanied by reduced tumor necrosis factor-α-mediated IEC apoptosis. These findings indicate that the probiotic strain BB12 can alleviate DSS-induced colitis and suggest a novel mechanism of communication between probiotic microorganisms and intestinal epithelia, which increases intestinal cell survival by modulating pro-apoptotic cytokine expression.

[A Case of Primary Gastric Amyloidosis with Fulminant Heart Failure].

A 53-year-old woman was admitted with epigastric discomfort and weakness. Laboratory examination at admission showed mild anemia and proteinuria. Esophagogastroduodenoscopy revealed marked mucosal atrophy, diffuse nodularity and granular appearance with mucosal friability. Biopsy was performed on the antrum and body of the stomach. On the next day, the patient began to complain of severe dyspnea, and hypoxia was present on pulse oximetry. Therefore, emergency echocardiography was conducted and it showed restrictive cardiomyopathy along with thrombus in the left atrium. With time, heart failure was aggravated despite intensive management. The result of gastric biopsy revealed amyloid deposits which stained positively with Congo red. On immunohistochemistry study, kappa and lambda chain were present. In addition, kappa chain was significantly elevated in urine and serum on electrophoresis. Although the patient was finally diagnosed as having primary gastric amyloidosis with restrictive cardiomyopathy, her general condition rapidly deteriorated and died at 12th hospital day. When obscure gastric lesion is encountered, performing gastric biopsy is strongly recommended since it be primary gastric amyloidosis. Herein, we present an unusual case of primary gastric amyloidosis.

A case of endoscopic full-thickness resection in a patient with gastric high-grade dysplasia unsuitable for endoscopic submucosal dissection.

Gastric high-grade dysplasia is an important premalignant lesion in gastric epithelial cells and has a high possibility of transforming to adenocarcinoma. Therefore, biopsy-proven high-grade dysplasia should be treated with en bloc resection methods such as endoscopic mucosal resection or endoscopic submucosal dissection (ESD). We report the case of a 63-year-old male patient, diagnosed with gastric high-grade dysplasia at the angle and lesser curvature side of the lower body. The patient was initially treated with ESD, although histopathology subsequently showed horizontal margin involvement. Since the lesion was diffusely edematous and margins were uncertain because of the previous ESD treatment, we chose to treat the patient with laparoscopy-assisted endoscopic full-thickness resection (EFTR). EFTR is a recently developed procedure, which uses both endoscopic and laparoscopic techniques to resect the full-thickness of the tissue. The final pathologic report revealed high-grade dysplasia and a focal intramucosal carcinoma of 0.8×0.7 cm. We conclude that EFTR can be an effective alternative treatment in gastric high-grade dysplasia unsuitable for ESD.