• Title/Summary/Keyword: cell infection

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P53 and PCNA is Positively Correlated with HPV Infection in Laryngeal Epitheliopapillomatous Lesions in Patiets with Different Ethnic Backgrounds in Xinjiang

  • Sun, Jie;Xiong, Ju;Zhen, Yan;Chen, Zhao-Lun;Zhang, Hua
    • Asian Pacific Journal of Cancer Prevention
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    • v.13 no.11
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    • pp.5439-5444
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    • 2012
  • Objective: To explore the correlation of human papillomavious (HPV) infection with expression of p53 and proliferating cell nuclear antigen (PCNA) in patients with different ethnicity in Xinjiang, China. Methods: 166 biopsy specimens from 83 laryngeal squamous cell carcinomas (LSCC), 63 laryngeal papillomas (LP), and 20 laryngeal inflammatory polyps (LIP) were included in this study. HPV infection was determined by polymerase chain reaction (PCR) using specific types of HPV primers. Expression of p53 and PCNA was assessed using immunohistostaining. Results: The frequency of HPV 6/11 was higher in LP (33.3%) than in LSCC (9.6%) (P<0.0005), whereas the frequency of HPV 16/18 was higher in LSCC (37.3 %) than in LP (6.3%) (P<0.0005). Patients of the Han ethnic group with LSCC had a higher infection rate with HPV 6/11 or HPV 6/11 and HPV 16/18 coinfection than those of Uygur and Kazak ethnicity (P<0.05). Overexpression of p53 and PCNA were higher in LSCC (62.7%, 57.8%) than in LP (38%, 33.3%) (P<0.005, and P<0.005, respectively). That of p53 was not associated with lymph-node metastases and clinical stages, but overexpression of PCNA closely correlated with clinical stage. Conclusions: These results strongly implicate HPV6/11 infection in the carcinogenesis of LSCC and LP, respectively. There was a higher coincidence of increased malignancy of laryngeal tumors with overexpression of p53 and PCNA. Overexpression of p53 may serve as an early risk marker for malignant transformation in HPV infected cells while the overexpression of PCNA may serve as a late marker for progression of LSCC.

Chemically-induced delayed cutaneous hypersensitivity in dogs infected with Demodex canis (Demodex canis 감염이 화학적으로 유발된 지연형 피부과민증에 미치는 영향)

  • Lee, Chai-yong;Ham, Hyeon-woo;Lee, Chung-gil;Seo, Kye-won
    • Korean Journal of Veterinary Research
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    • v.35 no.4
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    • pp.843-851
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    • 1995
  • To observe the effect of Demodex canis infection on the cellular immune response and hematological profile, 8 Doberman pinschers experimentally infected with D cains and 4 uninfected control dogs were sensitized with 2, 4-dinitro-chlorobenzene(DNCB) on the skin and were challenged with DNCB 14 days after the initial sensitization to elicit allergic contact dermatitis. Histological and hematological changes of these dogs were then observed. Macroscopic changes of skin challenged with DNCB in D canis-infected dogs included significantly reduced area of allergic reaction(p<0.05) than in uninfected control group. Infiltration of inflammatory cells in the D canis-infected group was also significantly reduced(p<0.05) than in the uninfected control group. These changes indicated that the cell-mediated immune response of the animals was suppressed by the infection with D canis. Total white blood cell count in dogs infected with D canis was increased when dogs were sensitized with DNCB (p<0.01). The result appeared to be caused by stress due to D canis infection, secondary bacterial infection and decreased efficacy of general body defense system. Blood eosionophils were increased in D canis-infected dogs which appreared to be caused by the allergic contact dermatitis. Blood chemistry analysis revealed that total protein and globulin were increased(p<0.05), while albumin level was decreased. This result appeared to be caused by secondary bacterial infection.

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Mucosal Immune Responses of Mice Experimentally Infected with Pygidiopsis summa (Trematoda: Heterophyidae)

  • Chai, Jong-Yil;Park, Young-Jin;Park, Jae-Hwan;Jung, Bong-Kwang;Shin, Eun-Hee
    • Parasites, Hosts and Diseases
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    • v.52 no.1
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    • pp.27-33
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    • 2014
  • Mucosal immune responses against Pygidiopsis summa (Trematoda: Heterophyidae) infection were studied in ICR mice. Experimental groups consisted of group 1 (uninfected controls), group 2 (infection with 200 metacercariae), and group 3 (immunosuppression with Depo-Medrol and infection with 200 metacercariae). Worms were recovered in the small intestine at days 1, 3, 5, and 7 post-infection (PI). Intestinal intraepithelial lymphocytes (IEL), mast cells, and goblet cells were counted in intestinal tissue sections stained with Giemsa, astra-blue, and periodic acid-Schiff, respectively. Mucosal IgA levels were measured by ELISA. Expulsion of P. summa from the mouse intestine began to occur from days 3-5 PI which sustained until day 7 PI. The worm expulsion was positively correlated with proliferation of IEL, mast cells, goblet cells, and increase of IgA, although in the case of mast cells significant increase was seen only at day 7 PI. Immunosuppression suppressed all these immune effectors and inhibited worm reduction in the intestine until day 7 PI. The results suggested that various immune effectors which include IEL, goblet cells, mast cells, and IgA play roles in regulating the intestinal mucosal immunity of ICR mice against P. summa infection.

Anti-Toxoplasmosis Effect of Citrus Unshiu Markovich against Toxoplasma Gondii (한약제 진피의 항 톡소포자충 효과 확인)

  • Kim, Hye-Kung;Jiang, Jing-Hua;Lee, Dong-Hwan;Kim, Hye-Sook;Park, Hyun
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.22 no.1
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    • pp.96-99
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    • 2008
  • Toxoplasma gondiiis a widespread apicomplexan parasite which is able to infect virtually all warm-blooded vertebrates. Twenty-two percent of the U.S. population is infected, but severe disease in adults is mainly limited to immunosuppressed patients. In patients with acquired immunodeficiency syndrome(AIDS), T. gondii causes a life-threatening opportunistic infection, with Toxoplasma encephalitis as its most severe manifestations. T. gondii is also known to cause congenital infection and is among the pathogens with the highest incidence of complications in pregnancies. Despite its clinical importance, only very few therapeutic drugs against T. gondii are available, all of which target the rapidly dividing tachyzoites, leaving the dormant encysted bradyzoite stage unaffected. We searched 15 traditional medicines that have anti-inflammatory effect from dongyibogam and Traditional Chinese medicine. In vitro studies were performed with HeLa cell cultures, with quantification of Toxoplasma growth by a cell proliferation assay. The result of experiment shows the selectivity of Citrus unshiu Markovich is 6.0. This is higher than sulfadiazine (selectivity was 1.63). For in vivo studies, mice were acutely infected intraperitoneally with $10^5$ tachyzoites of the virulent RH strain and then treated per orally for 4 days from 6 hours postinfection. Efficacy was assessed by sequential determination of parasite burdens in peritoneal cavity. In vivo, Citrus unshiu Markoviche inhibited Toxoplasma growth at a concentration of 10㎎/㎏ of body weight per day, the inhibition ratio was estimated to be 64.01%.

Protease-Activated Receptor 2 Is Involved in Th2 Responses against Trichinella spiralis Infection

  • Park, Mi-Kyung;Cho, Min-Kyoung;Kang, Shin-Ae;Park, Hye-Kyung;Kim, Yun-Seong;Kim, Ki-Uk;Ahn, Soon-Cheol;Kim, Dong-Hee;Yu, Hak-Sun
    • Parasites, Hosts and Diseases
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    • v.49 no.3
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    • pp.235-243
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    • 2011
  • In order to get a better understanding of the role of protease-activated receptor 2 (PAR2) in type 2 helper T (Th2) cell responses against Trichinella spiralis infection, we analyzed Th2 responses in T. spiralis-infected PAR2 knockout (KO) mice. The levels of the Th2 cell-secreted cytokines, IL-4, IL-5, and IL-13 were markedly reduced in the PAR2 KO mice as compared to the wild type mice following infection with T. spiralis. The serum levels of parasite-specific IgE increased significantly in the wild type mice as the result of T. spiralis infection, but this level was not significantly increased in PAR2 KO mice. The expression level of thymic stromal lymphopoietin, IL-25, and eotaxin gene (the genes were recently known as Th2 response initiators) of mouse intestinal epithelial cells were increased as the result of treatment with T. spiralis excretory-secretory proteins. However, the expression of these chemokine genes was inhibited by protease inhibitor treatments. In conclusion, PAR2 might involve in Th2 responses against T. spiralis infection.

Evaluation of host and bacterial gene modulation during Lawsonia intracellularis infection in immunocompetent C57BL/6 mouse model

  • Kirthika, Perumalraja;Park, Sungwoo;Jawalagatti, Vijayakumar;Lee, John Hwa
    • Journal of Veterinary Science
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    • v.23 no.3
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    • pp.41.1-41.15
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    • 2022
  • Background: Proliferative enteritis caused by Lawsonia intracellularis undermines the economic stability of the swine industry worldwide. The development of cost-effective animal models to study the pathophysiology of the disease will help develop strategies to counter this bacterium. Objectives: This study focused on establishing a model of gastrointestinal (GI) infection of L. intracellularis in C57BL/6 mice to evaluate the disease progression and lesions of proliferative enteropathy (PE) in murine GI tissue. Methods: We assessed the murine mucosal and cell-mediated immune responses generated in response to inoculation with L. intracellularis. Results: The mice developed characteristic lesions of the disease and shed L. intracellularis in the feces following oral inoculation with 5 × 107 bacteria. An increase in L. intracellularis 16s rRNA and groEL copies in the intestine of infected mice indicated intestinal dissemination of the bacteria. The C57BL/6 mice appeared capable of modulating humoral and cell-mediated immune responses to L. intracellularis infection. Notably, the expression of genes for the vitamin B12 receptor and for secreted and membrane-bound mucins were downregulated in L. intracellularis -infected mice. Furthermore, L. intracellularis colonization of the mouse intestine was confirmed by the immunohistochemistry and western blot analyses. Conclusions: This is the first study demonstrating the contributions of bacterial chaperonin and host nutrient genes to PE using an immunocompetent mouse model. This mouse infection model may serve as a platform from which to study L. intracellularis infection and develop potential vaccination and therapeutic strategies to treat PE.

Radiologic Abnormalities in Prolonged SARS-CoV-2 Infection: A Systematic Review

  • Kyongmin Sarah Beck;Jeong-Hwa Yoon;Soon Ho Yoon
    • Korean Journal of Radiology
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    • v.25 no.5
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    • pp.473-480
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    • 2024
  • We systematically reviewed radiological abnormalities in patients with prolonged SARS-CoV-2 infection, defined as persistently positive polymerase chain reaction (PCR) results for SARS-CoV-2 for > 21 days, with either persistent or relapsed symptoms. We extracted data from 24 patients (median age, 54.5 [interquartile range, 44-64 years]) reported in the literature and analyzed their representative CT images based on the timing of the CT scan relative to the initial PCR positivity. Our analysis focused on the patterns and distribution of CT findings, severity scores of lung involvement on a scale of 0-4, and the presence of migration. All patients were immunocompromised, including 62.5% (15/24) with underlying lymphoma and 83.3% (20/24) who had received anti-CD20 therapy within one year. Median duration of infection was 90 days. Most patients exhibited typical CT appearance of coronavirus disease 19 (COVID-19), including ground-glass opacities with or without consolidation, throughout the follow-up period. Notably, CT severity scores were significantly lower during ≤ 21 days than during > 21 days (P < 0.001). Migration was observed on CT in 22.7% (5/22) of patients at ≤ 21 days and in 68.2% (15/22) to 87.5% (14/16) of patients at > 21 days, with rare instances of parenchymal bands in previously affected areas. Prolonged SARS-CoV-2 infection usually presents as migrating typical COVID-19 pneumonia in immunocompromised patients, especially those with impaired B-cell immunity.

Approach to the Children with Recurrent Infections (재발성 감염 질환의 접근 방법)

  • Lee, Jae Ho
    • Clinical and Experimental Pediatrics
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    • v.48 no.5
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    • pp.461-468
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    • 2005
  • The major function of immune system is to protect infections. The immune systems are composed of innate and adaptive immunity. In adaptive immunity, the cellular and humoral components interact each other. Neonates and infants are infected frequently, because immune systems are naive and easy to expose to infectious agents. The complete history and physical examination is essential to evaluate the child with recurrent infections. The environmental risk factors of recurrent infections are day care center, cigarette smoke, and air pollution. The underlying diseases such as immunodeficiency, autoimmune diseases, allergy, and disorders of anatomy or physiology increase the susceptibility to infections. In immunodeficiency, infections are characterized by severe, chronic, recurrent, and unusual microbial agents infection. The defects of antibody production are susceptible to sinopulmonary bacterial infections. T cells defects are vulerable to numerous organisms such as virus, fungi, bacteria and etc. The screening tests for immune functions are the quantitative and qualitative measurements of each immune components. A complete blood count with white blood cell, differential, and platelet provide quantitative informations of immune components. Total complement and immunoglobulin levels represent the humoral component. Antibody levels of previously injected vaccines also provide informations of the antigen specific antibody immune responses. T cell and subsets count is quantitative measurement of cell mediated immunity. Delayed hypersensitivity skin test is a crude measurement of T cell function. The long term outcome of children with recurrent infections is completely dependent on the underlying diseases, the initial time of diagnosis and therapy, continued management, and genetic counscelling.

Ultrastructural Study on Induced Resistance of Cucumber Plants against Sphaerotheca fuliginea by Oligochitosan

  • Ma, Qing;Zhao, Xiao-Ming;Sun, Hui;Shang, Hong-Sheng
    • The Plant Pathology Journal
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    • v.27 no.1
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    • pp.8-13
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    • 2011
  • The induced resistance of cucumber leaves treated with oligochitosan to the infection of the cucumber powdery mildew, Sphaerotheca fuliginea, was investigated using transmission electron microscopy. The results showed that when the plants were treated with oligochitosan and challenged with inoculum, a significant decrease of the disease occurred. The mycelial development in the treated leaves was markedly inhibited. The cytoplasm of the powdery mildew mycelium was aggregated, with its organelles disintegrated and the cytoplasm collapsed. The protoplasm in haustoria became electron-dense. Haustoria became malformed, their organelles disintegrated, the hausterial wall thickened and eventually the whole complex necrotized. The host cells produced defence structures and materials associated with infection and a hypersensitive response. The host cell wall was thickened and deeply stained; several layers of papilla structure were produced under the cell wall; dark materials were deposited between the cell wall and plasmalemma; extrahaustorial plasmalemma was deeply stained and extrahaustorial matrix appositions had large deposits of electron-dense material; the cytoplasm was disordered, host organelles disintegrated and eventually the whole host cell disintegrated and necrotized.

Host Innate Immunity against Hepatitis E Virus and Viral Evasion Mechanisms

  • Kang, Sangmin;Myoung, Jinjong
    • Journal of Microbiology and Biotechnology
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    • v.27 no.10
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    • pp.1727-1735
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    • 2017
  • Hepatitis E virus (HEV) infections cause epidemic or sporadic acute hepatitis, which are mostly self-limiting. However, viral infection in immunocompromised patients and pregnant women may result in serious consequences, such as chronic hepatitis and liver damage, mortality of the latter of which reaches up to 20-30%. Type I interferon (IFN)-induced antiviral immunity is known to be the first-line defense against virus infection. Upon HEV infection in the cell, the virus genome is recognized by pathogen recognition receptors, leading to rapid activation of intracellular signaling cascades. Expression of type I IFN triggers induction of a barrage of IFN-stimulated genes, helping the cells cope with viral infection. Interestingly, some of the HEV-encoded genes seem to be involved in disrupting signaling cascades for antiviral immune responses, and thus crippling cytokine/chemokine production. Antagonistic mechanisms of type I IFN responses by HEV have only recently begun to emerge, and in this review, we summarize known HEV evasion strategies and compare them with those of other hepatitis viruses.