Cytopathic Effect

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Alain Blanchard - One of the best experts on this subject based on the ideXlab platform.

  • role of mycoplasma infection in the Cytopathic Effect induced by human immunodeficiency virus type 1 in infected cell lines
    Infection and Immunity, 1992
    Co-Authors: M Lemaitre, Luc Montagnier, Y Henin, F Destouesse, C Ferrieux, Alain Blanchard
    Abstract:

    In addition to previously reported tetracycline analogs, other antibiotics known for antimycoplasmal activities inhibited the Cytopathic Effect in CEM cl13 cells infected with human immunodeficiency virus type 1 (HIV-1) or HIV-2 but were unable to block virus replication. A contaminating mycoplasma was isolated from our CEM cl13 cells and identified as a strain of Mycoplasma fermentans. Following infection of lymphoblastoid (CEM) or promonocytic (U937 and THP1) cell lines with HIV-1, Cytopathic Effect was observed only in association with mycoplasmal contamination. Moreover, HIV-1 infection of U937 cells after experimental inoculation with a human isolate of M. fermentans led to pronounced cell killing. We have verified that this Effect is not merely an artifact caused by arginine and/or glucose depletion in the cell culture medium. These results confirm that mollicutes, in particular M. fermentans, are able to act synergistically with HIV-1 to kill infected cells in some in vitro systems.

Noorjahan Panjwani - One of the best experts on this subject based on the ideXlab platform.

  • milk components inhibit acanthamoeba induced Cytopathic Effect
    Investigative Ophthalmology & Visual Science, 2008
    Co-Authors: Chandrassegar Saravanan, Zhiyi Cao, J Kumar, Jiazhou Qiu, Andrew G Plaut, David S Newburg, Noorjahan Panjwani
    Abstract:

    PURPOSE. Acanthamoebae provoke a vision-threatening corneal infection known as Acanthamoeba keratitis (AK). It is thought that Acanthamoeba-specific IgA antibodies present in mucosal secretions such as human tears, milk, and saliva provide protection against infection by inhibiting the adhesion of parasites to host cells. The goal of the present study was to determine whether human mucosal secretions have the potential to provide protection against the Acanthamoeba-induced Cytopathic Effect (CPE) by an additional mechanism that is independent of IgA. METHODS. Breast milk was used as a model of human mucosal secretions. In vitro CPE assays were used to examine the CPE inhibitory Effect of IgA-depleted milk and various milk fractions obtained by gel filtration. The activity of amebic proteinases was examined by zymography. RESULTS. IgA-depleted milk inhibited the Acanthamoeba-induced CPE in a concentration-dependent manner. Milk proteins were separated into four major fractions (F1-F4) by gel filtration. Of these four fractions, CPE inhibitory activity was detected largely in fraction F3. In contrast, fractions F1, F2, and F4 lacked CPE inhibitory activity. Moreover, fraction F3, but not F1, F2, or F4, inhibited amebic proteinases. CONCLUSIONS. These data, in conjunction with published findings showing that amebic proteinases are responsible for the induction of Acanthamoeba CPE, led us to propose that human mucosal secretions have the potential to provide protection against Acanthamoeba-induced CPE by an additional mechanism that is independent of IgA and that involves the inhibition of cytotoxic proteinases of amebae.

  • Effect of human tears on acanthamoeba induced Cytopathic Effect
    Archives of Ophthalmology, 2008
    Co-Authors: Zhiyi Cao, Chandrassegar Saravanan, Michael H Goldstein, Gunisha Pasricha, Savitri Sharma, Noorjahan Panjwani
    Abstract:

    Objective To determine whether tears of healthy individuals provide protection againstAcanthamoeba-induced Cytopathic Effect (CPE) in vitro. Methods Acanthamoebae were added to confluent cultures of corneal epithelium in 24-well plates, and co-cultures were incubated overnight in a serum-free medium containing varying amounts of tears or immunoglobulin A (IgA)–depleted tears. At the end of the incubation period, the cells were stained with Giemsa, and the extent of target cell damage (ie, CPE) was quantified. Results Acanthamoebae produced extensive CPE. The presence of even a low concentration of tears (10 μL of undiluted tears per milliliter of media) almost completely inhibitedAcanthamoeba-induced CPE. The CPE was inhibited by pretreatment of the parasites with tears. In contrast, the pretreatment of host cells with tears was not protective. This finding suggests that the target of the inhibitory factor is the parasite. IgA-depleted tears also inhibitedAcanthamoeba-induced CPE, albeit with a lower potency than total tears. Conclusion In addition to known IgA-dependent protective factors, human tears contain factors that inhibitAcanthamoeba-induced CPE independently of IgA. Clinical Relevance Identification and characterization of factors that protect againstAcanthamoeba-induced CPE should help in the development of novel, rationally designed strategies to manage and protect against keratitis.

Robert W Finberg - One of the best experts on this subject based on the ideXlab platform.

R S Chauhan - One of the best experts on this subject based on the ideXlab platform.

  • newcastle disease virus induced Cytopathic Effect in infected cells is caused by apoptosis
    Virus Research, 2009
    Co-Authors: P V Ravindra, Ashok K Tiwari, Barkha Ratta, Uttara Chaturvedi, S K Palia, R S Chauhan
    Abstract:

    The velogenic Newcastle disease virus (NDV) causes highly infectious and economically significant Newcastle disease (ND) in birds of various species. In cell culture NDV induces Cytopathic Effect (CPE) characterized by rounding, vacuolation, syncytia formation and cell death. Aside from cell to cell fusion caused by the F and HN glycoprotein of the virus molecular events leading to cell death are not known. In the current study, NDV-infected Vero cells, at 48 h p.i., showed nuclear condensation, cytoplasm blebbing, DNA fragmentation, and phosphatidylserine translocation to the cell surface. In addition, virus-infected cells demonstrated decreased DNA content and an increased Bax to Bcl-2 ratio, p53 level and caspase 3, 8, 9 expression compared to mock-infected cells. Based on these results, it was concluded that CPE in NDV-infected cells was caused by to the induction of apoptosis with the involvement of p53 and the Bax, dependent apoptotic pathways.

Kenji Yagita - One of the best experts on this subject based on the ideXlab platform.

  • Cytopathic Effect of Acanthamoeba on human corneal fibroblasts
    2016
    Co-Authors: Noriko Takaoka-sugihara, Satoru Yamagami, Seiichi Yokoo, Masao Matsubara, Kenji Yagita
    Abstract:

    Purpose: Acanthamoeba keratitis is associated with keratocyte depletion in humans. We investigated how Acanthamoebae isolated from corneas affected by Acanthamoeba keratitis interacted with human corneal stromal cells in vitro. Methods: Acanthamoebae were isolated from 6 patients with Acanthamoeba keratitis and genotyping was done. Whether the isolated Acanthamoebae could invade the corneal stroma was assessed with denuded corneal stroma ex vivo. The Cytopathic Effect of Acanthamoeba on cultured corneal fibroblasts from donor corneas was quantitatively evaluated by the MTT assay after culture under various conditions. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) and Annexin V staining were employed to detect apoptotic cells among the corneal fibroblasts co-cultured with Acanthamoebae. Results: All 6 Acanthamoebae isolated from the patients with Acanthamoeba keratitis were shown to have the T4 genotype by 18S rDNA sequence analysis. Acanthamoebae invaded the denuded corneal stroma in the ex vivo experiments and had a Cytopathic Effect on human corneal fibroblasts after direct adhesion, but not via chemical mediators. A Cytopathic Effect was detected with all 6 Acanthamoebae and corneal fibroblasts mainly died by apoptosis, as evidenced by Annexin V staining. Conclusions: Acanthamoebae isolated from patients with Acanthamoeba keratitis had a Cytopathic Effect on huma

  • Cytopathic Effect of Acanthamoeba on human corneal fibroblasts.
    Molecular vision, 2012
    Co-Authors: Noriko Takaoka-sugihara, Satoru Yamagami, Seiichi Yokoo, Masao Matsubara, Kenji Yagita
    Abstract:

    Purpose: Acanthamoeba keratitis is associated with keratocyte depletion in humans. We investigated how Acanthamoebae isolated from corneas affected by Acanthamoeba keratitis interacted with human corneal stromal cells in vitro. Methods: Acanthamoebae were isolated from 6 patients with Acanthamoeba keratitis and genotyping was done. Whether the isolated Acanthamoebae could invade the corneal stroma was assessed with denuded corneal stroma ex vivo. The Cytopathic Effect of Acanthamoeba on cultured corneal fibroblasts from donor corneas was quantitatively evaluated by the MTT assay after culture under various conditions. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) and Annexin V staining were employed to detect apoptotic cells among the corneal fibroblasts cocultured with Acanthamoebae. Results: All 6 Acanthamoebae isolated from the patients with Acanthamoeba keratitis were shown to have the T4 genotype by 18S rDNA sequence analysis. Acanthamoebae invaded the denuded corneal stroma in the ex vivo experiments and had a Cytopathic Effect on human corneal fibroblasts after direct adhesion, but not via chemical mediators. A Cytopathic Effect was detected with all 6 Acanthamoebae and corneal fibroblasts mainly died by apoptosis, as evidenced by Annexin V staining. Conclusions: Acanthamoebae isolated from patients with Acanthamoeba keratitis had a Cytopathic Effect on human corneal fibroblasts, mainly via induction of apoptosis after direct adhesion. Our findings may provide some clues to the pathophysiology of corneal keratocyte depletion in patients with Acanthamoeba keratitis.