• Title/Summary/Keyword: Mucosal infection

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Treatment Protocol for Secondary Burning Mouth Syndrome in Candida albicans- or Non-albicans-Positive Patients

  • Ju, Hye-Min;Jeong, Sung-Hee;Ahn, Yong-Woo;Jeon, Hye-Mi;Ok, Soo-Min
    • Journal of Oral Medicine and Pain
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    • v.47 no.3
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    • pp.126-134
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    • 2022
  • Purpose: This study aimed to propose an efficient treatment approach for infection with different candida species. Methods: Fifty-three patients who presented with a chief complaint of oral mucosal pain and exhibited positive candida culture findings were divided into two groups (Candida albicans and non-albicans). Pain, mucosal manifestations, salivary flow rates, durations of disease and treatment, and responses to treatment (nystatin and clonazepam) were investigated in both groups. Results: Patients in the C. albicans group exhibited more prominent clinical characteristics (erythematous lesions, tongue coatings, and hyperalgesia) than those in the non-albicans group. In total, 70% of patients in the non-albicans group showed no abnormalities in the oral mucosa. Patients in the C. albicans group showed increased resistance to nystatin treatment compared to those in the non-albicans group, especially with longer disease durations. The patients resistant to nystatin treatment showed positive responses to clonazepam. Conclusions: Patients with oral mucosal pain should be tested for the presence of Candida, even in the absence of mucosal abnormalities, especially those infected with non-albicans species. If no response to antifungal therapy is observed, treatment with clonazepam should be initiated, especially in patients infected with C. albicans.

Flagellin Administration Protects Respiratory Tract from Burkholderia cepacia Infection

  • Zgair, Ayaid Khadem
    • Journal of Microbiology and Biotechnology
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    • v.22 no.7
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    • pp.907-916
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    • 2012
  • Burkholderia cepacia is an important pathogen that often causes pneumonia in immunocompromised individuals. Here, it was demonstrated that the TLR5 agonist flagellin could locally activate innate immunity. This was characterized by rapid expressions of IL-$1{\beta}$, TNF-${\alpha}$, and iNOS mRNA and a delay in the expression of IL-10 mRNA. A significant elevation in the IL-$1{\beta}$, TNF-${\alpha}$, and nitric oxide levels was also noted. In the respiratory tract, flagellin induced neutrophil infiltration into the airways, which was observed by histopathological examination and confirmed by the neutrophil count and level of myeloperoxidase activity. This was concomitant with a high activity of alveolar macrophages that engulfed and killed B. cepacia in vitro. The flagellin mucosal treatment improved the B. cepacia clearance in the mouse lung. Thus, the present findings illustrate the profound stimulatory effect of flagellin on the lung mucosal innate immunity, a response that needs to be exploited therapeutically to prevent the development of respiratory tract infection by B. cepacia.

Non-atrophic gastric mucosa is an independently associated factor for superficial non-ampullary duodenal epithelial tumors: a multicenter, matched, case-control study

  • Azusa Kawasaki;Kunihiro Tsuji;Noriya Uedo;Takashi Kanesaka;Hideaki Miyamoto;Ryosuke Gushima;Yosuke Minoda;Eikichi Ihara;Ryosuke Amano;Kenshi Yao;Yoshihide Naito;Hiroyuki Aoyagi;Takehiro Iwasaki;Kunihisa Uchita;Hisatomi Arima;Hisashi Doyama
    • Clinical Endoscopy
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    • v.56 no.1
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    • pp.75-82
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    • 2023
  • Background/Aims: The etiology of superficial non-ampullary duodenal epithelial tumors (SNADETs) remains unclear. Recent studies have reported conflicting associations between duodenal tumor development and Helicobacter pylori infection or endoscopic gastric mucosal atrophy. As such, the present study aimed to clarify the relationship between SNADETs and H. pylori infection and/or endoscopic gastric mucosal atrophy. Methods: This retrospective case-control study reviewed data from 177 consecutive patients with SNADETs who underwent endoscopic or surgical resection at seven institutions in Japan over a three-year period. The prevalence of endoscopic gastric mucosal atrophy and the status of H. pylori infection were compared in 531 sex- and age-matched controls selected from screening endoscopies at two of the seven participating institutions. Results: For H. pylori infection, 85 of 177 (48.0%) patients exhibited SNADETs and 112 of 531 (21.1%) control patients were non-infected (p<0.001). Non-atrophic mucosa (C0 to C1) was observed in 96 of 177 (54.2%) patients with SNADETs and 112 of 531 (21.1%) control patients (p<0.001). Conditional logistic regression analysis revealed that non-atrophic gastric mucosa was an independent risk factor for SNADETs (odds ratio, 5.10; 95% confidence interval, 2.44-8.40; p<0.001). Conclusions: Non-atrophic gastric mucosa, regardless of H. pylori infection status, was a factor independently associated with SNADETs.

Invasion of Metagonimus yokogawai into the submucosal layer of the small intestine of immunosuppressed mice (면역억제 마우스에 있어서 요코가와흡충의 소장 점막하 조직 침입)

  • CHAI, Jong-Yil;KIM, Jin;LEE, Soon-Hyung
    • Parasites, Hosts and Diseases
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    • v.33 no.4
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    • pp.313-322
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    • 1995
  • Metosonimus yokosawai was found deeply invaded into the submucosa of the small intestine of mice (ICR) when they were immunosuppressed by prednisolone injection. Experimental groups consisted of control, fluke infection (1,800 metacercariae per mouse) and fluke infection plus immunosuppression. In fluke infection group, many worms were found sectioned in the intervillous space of the jejunum and ileum at 6 hrs, 12 hrs, and 1 day after infection, and pathological changes characterized by villous atrophy and crypt hyperplasia were observed. After 3 days, only a few worms were found in intestinal sections, and after 7 days, the pathological changes became minimal. No worm was found penetrated beyond the mucosal layer. On the other hand, in immunosuppressed mice, numerous worms were found sectioned in the duodenum and jejunum, irrespective of the infection period up to 14 days. Pathological changes of the mucosa were minimal until 3 days after infection, but at 5 days marked destruction of the mucosal layer was observed. At this time many flukes were found invaded deeply into the submucosa facing the muscular layer. Despite continuous immunosuppression, the mucosal damage was gradually recovered at 7-21 days post-infection. The results showed that immunosuppression of ICR mice can induce, for a short perid of time, severe mucosal damage, and allow deep invasion of M. yokogcuwai into the submucosa of the small intestine.

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Bovine Lactoferricin Induces Intestinal Epithelial Cell Activation through Phosphorylation of FAK and Paxillin and Prevents Rotavirus Infection

  • Jeong, Ye Young;Lee, Ga Young;Yoo, Yung Choon
    • Journal of Microbiology and Biotechnology
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    • v.31 no.8
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    • pp.1175-1182
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    • 2021
  • We investigated the effect of bovine lactoferricin (Lfcin-B), a peptide derived from bovine lactoferrin, on activation of intestinal epithelial cells in IEC-6 intestinal cell, and protection against in vivo rotavirus (RV) infection. Treatment with Lfcin-B significantly enhanced the growth of IEC-6 cells and increased their capacity for attachment and spreading in culture plates. Also, Lfcin-B synergistically augmented the binding of IEC-6 cells to laminin, a component of the extracellular matrix (ECM). In the analysis of the intracellular mechanism related to Lfcin-B-induced activation of IEC-6 cells, this peptide upregulated tyrosine-dependent phosphorylation of focal adhesion kinase (FAK) and paxillin, which are intracellular proteins associated with cell adhesion, spreading, and signal transduction during cell activation. An experiment using synthetic peptides with various sequences of amino acids revealed that a sequence of 9 amino acids (FKCRRWQWR) corresponding to 17-25 of the N-terminus of Lfcin-B is responsible for the epithelial cell activation. In an in vivo experiment, treatment with Lfcin-B one day before RV infection effectively prevented RV-induced diarrhea and significantly reduced RV titers in the bowels of infected mice. These results suggest that Lfcin-B plays meaningful roles in the maintenance and repair of intestinal mucosal tissues, as well as in protecting against intestinal infection by RV. Collectively, Lfcin-B is a promising candidate with potential applications in drugs or functional foods beneficial for intestinal health and mucosal immunity.

Oral Mucosal Lesions (구강점막질환)

  • Ryu, Mi Heon
    • The Journal of the Korean dental association
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    • v.55 no.7
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    • pp.468-480
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    • 2017
  • A wide variety of benign and malignant lesions and other diseases can develop on oral mucosa. Oral mucosal lesions can also be associated with an underlying systemic disease, so their correct diagnosis, which may even share similar clinical and demographic features, is always a challenge for a dentist. Common oral mucosal lesions include candidiasis, herpes viral infection, leukoplakia, recurrent aphthous stomatitis, pemphigus, lichen planus and benign migratory glossitis. The differential diagnosis of these lesions are based on a thorough review of the patient's past medical and dental history and a complete oral examination. The knowledge of clinical features such as size, location, morphology, color, and pain is helpful in establishing a diagnosis. In addition, diagnostic tests, including microbiologic and laboratory tests and biopsies are usually required for establishing a proper diagnosis.

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Effect of Hwang-Ryeon-Hae-Dok-Tang on the Release of IL-8 in Human Nasal Mucosal Fibroblast (黃連解毒湯의 사람 비점막 섬유아세포 IL-8 분비에 대한 효과)

  • Lee, In-su;Kim, Hee-taek;Lee, Eun-yong;Kim, E-hwa;Ryu, Ju-hyun
    • The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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    • v.16 no.3
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    • pp.68-81
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    • 2003
  • It is proposed that Hwang-Ryeon-Hae-Dok-Tang may modulate the immune response on allergy or asthma. Human nasal mucosal fibroblasts are a rich source cytokines, inflammatory mediators, and chemokines. Chemokines are important for the recruitment of leukocytes to sites of infection, which is essential in host defense. Objectives : The objective of this study was to investigate the effect of Hwang-Ryeon-Hae-Dok-Tang(HH) on the release of the IL-8 chemokine in human nasal mucosal fibroblasts after stimulation with cytokines like interleukin-4(IL-4), tumor necrosis factor- (TNF- ), interferon- (lFN- ), and interle ukin-l (IL-I ). Methods : To detect the release of IL-8, enzyme-linked immunosorbent assay(ELISA) kit was performed. The cytotoxicity was measured by MTT assay. Results : HH significantly inhibited the secretion of IL-8 with a dose-dependant manner. The effective dosage did not have the cytotoxicity on human nasal mucosal fibroblasts Conclusions : Results of our study show that HH would play an important role in modulation of IL-8 in human nasal mucosal fibroblasts.

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Mucosal mast cell responses in the small intestine of rats infected with Echinostoma hortense

  • Kim, In-sik;Im, Jae-Aee;Lee, Kyu-Je;Ryang, Yong-Suk
    • Parasites, Hosts and Diseases
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    • v.38 no.3
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    • pp.139-143
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    • 2000
  • Mucosal mast cell (MMC) responses and worm recovery rates in rats infected with Echinostona hortense were investigated from day 3 to day 56 post-infection (p.i.). Experimental infected group showed apparently higher number of MMC in each part of the small intestine than that of the control group. The number of MMC in the duodenum increased gradually after the infection and reached a peak on day 35 p.i. Thereafter, the number of MMC continued to decrease at a slow pace. The kinetics of MMC responses in the upper and lower jejunum were similar to that of the duodenum, but the number of MMC in the jejunum was lower. The worm recovery rate decreased with respect to time of which it was markedly reduced on day 49 and 56 p.i. The duration in which a high number of MMC appeared was similar to that in which a low rate in worm recovery was recorded . These results indicate dlat intestinal mastocytosis may play an important role in the expulsion of 5. hortense.

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Establishment of ethanol-pretreating animal model to study Helicobacter pylori infection (Helicobacter pylori의 in vivo 연구를 위한 ethanol-pretreating animal model의 개발)

  • Lee, Jin-Uk;Kim, Seung-Hee;Park, Tan-Woo;Kim, Okjin
    • Korean Journal of Veterinary Research
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    • v.46 no.4
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    • pp.327-335
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    • 2006
  • A stable and reliable Helicobacter pylori (H. pylori) infection animal model would be necessary for evaluating vaccine efficacy and helpful for understanding the pathological mechanism of the organism. The aim of the present study is to investigate the effect of ethanol treatment prior to H. pylori inoculation on associated gastric mucosal injury and to establish ethanol-pretreating animal model to study H. pylori infection. Male Mongolian gerbils were used for the study. H. pylori was orally inoculated after 12 h fasting. 3 h prior to H. pylori inoculation, a group of gerbils was orally treated with absolute ethanol, 60% and 40% ethanol respectively. Another group of animals was treated either with H. pylori culture media alone or with different concentrations of ethanol plus culture media. Gerbils were killed 4 or 8 weeks after H. pylori inoculation. The colonization of H. pylori was confirmed by both histological examination and rapid urease test. Mucosal damage was evaluated grossly and histologically according to the criteria. The colonization of H. pylori and pathological changes in gastric mucosa of the animals were also observed. Although no significant change to the gastric mucose was observed in the animals treated either with H. pylori culture media alone or with different concentrations of ethanol plus culture media, persistent H. pylori infection was seen in the mucosa and mucosal leucocyte infiltration and severe epithelial damage was observed in the Helicobacter and ethanol + Helicobacter groups after 4 weeks. The gross and histological scores were higher in the ethanol + Helicobacter than in the Helicobacter alone group. As the results, ethanol-pretreatment with 60% concentration induced severe pathogenic changes by H. pylori infection in 5 weeks-old Mongolian gerbils. These results suggested that ethanol-pretreatment before H. pylori inoculation could increase the severity of gastric mucosal inflammation and enhance the colonization of H. pylori. The established ethanol-pretreating animal model would contribute to screen new drugs against H. pylori and be used as an useful tool for various animal experiments with H. pylori strains.

Protective Immunity Induced by Systemic and Mucosal Delivery of DNA Vaccine Expressing Glycoprotein B of Pseudorabies Virus

  • Yoon, Hyun-A;Han, Young-Woo;Aleyas, Abi George;George, June Abi;Kim, Seon-Ju;Kim, Hye-Kyung;Song, Hee-Jong;Cho, Jeong-Gon;Eo, Seong-Kug
    • Journal of Microbiology and Biotechnology
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    • v.18 no.3
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    • pp.591-599
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    • 2008
  • A murine model immunized by systemic and mucosal delivery of plasmid DNA vaccine expressing glycoprotein B (pCIgB) of pseudorabies virus (PrV) was used to evaluate both the nature of the induced immunity and protection against a virulent virus. With regard to systemic delivery, the intramuscular (i.m.) immunization with pCIgB induced strong PrV-specific IgG responses in serum but was inefficient in generating a mucosal IgA response. Mucosal delivery through intranasal (i.n.) immunization of pCIgB induced both systemic and mucosal immunity at the distal mucosal site. However, the levels of systemic immunity induced by i.n. immunization were less than those induced by i.m. immunization. Moreover, i.n. genetic transfer of pCIgB appeared to induce Th2-biased immunity compared with systemic delivery, as judged by the ratio of PrV-specific IgG isotypes and Th1- and Th2-type cytokines produced by stimulated T cells. Moreover, the immunity induced by i.n. immunization did not provide effective protection against i.n. challenge of a virulent PrV strain, whereas i.m. immunization produced resistance to viral infection. Therefore, although i.n. immunization was a useful route for inducing mucosal immunity at the virus entry site, i.n. immunization did not provide effective protection against the lethal infection of PrV.