scholarly journals The effect of vaginal probiotic therapy on the outcome of papillomavirus infection

2022 ◽  
Vol 20 (4) ◽  
pp. 11-17
Author(s):  
V. V. Oleynik ◽  
E. A. Kremleva ◽  
A. V. Sgibnev
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Hpv Infection ◽  
Vaginal Flora ◽  
Papillomavirus Infection ◽  
Vaginal Epithelial Cells ◽  
Vaginal Lactobacilli ◽  
Before And After ◽  
Infected Cells ◽  
Cell Death Pattern

Aim. To study the effect of vaginal probiotic therapy on the outcome of human papillomavirus (HPV) infection.Materials and methods. The study included HPV-infected patients: 29 patients with normal vaginal flora and 146 patients with a deficiency of vaginal lactobacilli, of which 117 patients received vaginal probiotic therapy. In samples obtained before and after the therapy, the effect of the probiotic on the change in the ratio of living, apoptotic, and necrotic vaginal epithelial cells after preliminary exposure to oxidative stress was studied.Results. It was found that probiotics reduce the number of infected epithelial cells that survived the oxidative damage and shift the balance of cell death forms towards apoptosis. Vaginal probiotic therapy in patients with a deficiency of lactobacilli increased the frequency of HPV elimination by 2.5 times and reduced the likelihood of treatment failure from 1.5 to 4 times, depending on the viral load. The probiotic therapy made the structure of HPV outcomes in Lactobacillus-deficient patients similar to that in patients with normal vaginal flora.Conclusion. Vaginal probiotic therapy improves outcomes of HPV infection in patients with a deficiency of lactobacilli by reducing the number of survived infected cells and shifting the cell death pattern towards apoptosis. 

Influence of normal vaginal microbiota on papillomavirua infection

2020 ◽  
Vol 19 (4) ◽  
pp. 63-69
Author(s):  
V.V. Oleynik ◽  
◽  
Е.А. Kremleva ◽  
А.V. Sgibnev ◽  
◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Elimination Rate ◽  
Hpv Infection ◽  
Key Words Apoptosis ◽  
Vaginal Microbiota ◽  
Sexually Transmitted ◽  
Vaginal Epithelial Cells ◽  
And Shifts ◽  
Hpv Viral Load

Objective. To study the influence of normal vaginal microbiota on papillomavirus (HPV) infection. Patients and methods. We examined 160 women with HPV infection. We assessed the state of normal flora, the presence of sexually transmitted infections (STIs), and the HPV elimination rate. The correlation of living, apoptotic and necrotic epithelial cells depending on the levels of lactobacilli in native and stress-influenced specimens was studied in 140 HPV-positive and 20 HPV-negative patients. Results. We have found a stronger relation between HPV viral load and deficiency of lactobacilli (r = 0.498; р = 0.021) than between the former and the presence of STIs (r = 0.121; р = 0.072). High baseline levels of vaginal lactobacilli increase the likelihood of HPV elimination. Normal levels of lactobacilli enhance the survival of noninfected epithelial cells and reduce the levels of infected ones, which ensures a predominantly apoptotic form of cell death. HPV enhances the survival of infected cells and shifts the cell death structure toward necrosis. Conclusion. Lactobacilli counteract the influence of HPV on the vital conditions of vaginal epithelial cells. This accounts for better outcomes of HPV infection in patients with normal levels of flora. Key words: apoptosis, human papillomavirus, vagina, lactobacilli, cervix, epithelial cells

Bafilomycin A1inhibits rhinovirus infection in human airway epithelium: effects on endosome and ICAM-1

2001 ◽  
Vol 280 (6) ◽  
pp. L1115-L1127 ◽  
Author(s):  
Tomoko Suzuki ◽  
Mutsuo Yamaya ◽  
Kiyohisa Sekizawa ◽  
Masayoshi Hosoda ◽  
Norihiro Yamada ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelium ◽  
Primary Cultures ◽  
Nuclear Factor Κb ◽  
Intercellular Adhesion Molecule ◽  
Nuclear Factor ◽  
Tracheal Epithelial Cells ◽  
Before And After ◽  
Infected Cells ◽  
Viral Titers

To examine the effects of bafilomycin A1, a blocker of vacuolar H+-ATPase, on rhinovirus (RV) infection in the airway epithelium, primary cultures of human tracheal epithelial cells were infected with RV14. Viral infection was confirmed by showing that viral RNA in the infected cells and the viral titers in the supernatants of infected cells increased with time. RV14 infection upregulated the production of cytokines and mRNA of intercellular adhesion molecule (ICAM)-1 in epithelial cells. Bafilomycin A1reduced the viral titers of RV14 and inhibited the production of cytokines and ICAM-1 before and after RV14 infection. Bafilomycin A1reduced susceptibility of epithelial cells to RV14 infection. RV14 increased activated nuclear factor-κB in the cells, and bafilomycin A1reduced the activated nuclear factor-κB. Bafilomycin A1decreased the number of acidic endosomes in the epithelial cells. These results suggest that bafilomycin A1may inhibit infection by RV14 by not only blocking RV RNA entry into the endosomes but also reducing ICAM-1 expression in the epithelial cells. Bafilomycin A1may therefore modulate airway inflammation after RV infection.

scholarly journals Pet secretion, internalization and induction of cell death during infection of epithelial cells by enteroaggregative Escherichia coli

Microbiology ◽  
2009 ◽  
Vol 155 (9) ◽  
pp. 2895-2906 ◽  
Author(s):  
Miguel Betancourt-Sanchez ◽  
Fernando Navarro-Garcia
Keyword(s):  
Escherichia Coli ◽  
Cell Death ◽  
Epithelial Cells ◽  
Morphological Changes ◽  
Eukaryotic Cell ◽  
Transcriptional Level ◽  
Cell Detachment ◽  
Wild Type ◽  
Infected Cells

In an in vitro model using HEp-2 cells treated with purified plasmid-encoded toxin (Pet), we have identified morphological changes characterized by cell rounding and detachment after toxin internalization; these changes progress to cell death. However, these effects have not yet been shown to occur during the infection of epithelial cells by enteroaggregative Escherichia coli (EAEC). Here, we show that the secretion of Pet by EAEC is regulated at the transcriptional level, since secretion was inhibited in eukaryotic cell culture medium, although Pet was efficiently secreted in the same medium supplemented with tryptone. Inefficient secretion of Pet by EAEC in DMEM prevented cell detachment, whereas efficient Pet secretion in DMEM/tryptone increased cell detachment in a HEp-2 cell adherence assay. Interestingly, Pet toxin was efficiently delivered to epithelial cells, since it was internalized into epithelial cells infected with EAEC at similar concentrations to those obtained by using 37 μg ml−1 purified Pet protein. Additionally, Pet was not internalized when the epithelial cells were infected with a pet clone, HB101(pCEFN1), unlike the wild-type strain, which has a high adherence capability. There is a correlation between Pet secretion by EAEC, the internalization of Pet into epithelial cells, cell detachment and cell death in EAEC-infected cells. The ratio between live and dead cells decreased in cells treated with wild-type EAEC in comparison with cells treated with an isogenic mutant in the pet gene, whereas the effects were restored by complementing the mutant with the pet gene. All these data indicate that Pet is an important virulence factor in the pathogenesis of EAEC infection.

Intralesional Beta-Interferon Treatment of Cervical Intraepithelial Neoplasia Associated with Human Papillomavirus Infection

1994 ◽  
Vol 80 (2) ◽  
pp. 146-150 ◽  
Author(s):  
Carlo Penna ◽  
Maria Grazia Fallani ◽  
Rodolfo Gordigiani ◽  
Lorella Sonni ◽  
Gian Luigi Taddei ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Side Effects ◽  
Cervical Intraepithelial Neoplasia ◽  
Treatment Options ◽  
Intraepithelial Neoplasia ◽  
Hpv Infection ◽  
Cure Rate ◽  
Papillomavirus Infection ◽  
Before And After ◽  
Ifn Therapy

Aims and backround Interferons (IFN) have offered considerable advances in the therapy of genital warts even those associated with cervical intraepithelial neoplasia (CIN); intralesional therapy either alone or in combination with other modalities such as cryosurgery and laser surgery provides improved clearing and cure of these often recalcitrant lesions. The purpose of this study was to evaluate the effectiveness of intralesional IFN therapy in patients with CIN associated with human papillomavirus (HPV) infection. Methods Beta-IFN was injected intra-perilesionally into the cervix in 41 patients with CIN associated with HPV infection. Results The regimen of 3 million international units (IU) injected intralesionally daily in the 1st week and 3 times a week in the 2nd and 3rd weeks for a total of 11 injections and a total dosage of 33 million IU yielded an 80 percent cure rate and may be more advantageous than other treatment options in certain instances. Cytocolposcopic and histologic examination was carried out before and after treatment and 24 lesions were also analyzed for type-specific papillomaviruses using in situ DNA hybridization. CIN disappeared in 33 patients 6 months after the end of therapy. Side effects of intralesional IFN therapy are dose related and for the most part readily tolerated. Conclusions Intralesional IFN proved to be effective treatment for CIN associated with HPV infection (cure rate: 80%) and well accepted because hospitalization is not required and no important side effects occur.

scholarly journals Nanotechnology-Based Weapons to Combat Human Papillomavirus Infection Associated Diseases

2021 ◽  
Vol 9 ◽  
Author(s):  
Luyao Pan ◽  
Bingxin Li ◽  
Jiahua Chen ◽  
Haofeng Zhang ◽  
Xi Wang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Gene Therapy ◽  
Human Papillomavirus ◽  
Mammalian Cells ◽  
Hpv Infection ◽  
Associated Diseases ◽  
Human Papillomavirus Infection ◽  
Papillomavirus Infection ◽  
Infected Cells ◽  
Clinical Problems

Persistent human papillomavirus (HPV) infection will eventually lead to clinical problems, varying from verrucous lesions to malignancies like cervical cancer, oral cancer, anus cancer, and so on. To address the aforementioned problems, nanotechnology-based strategies have been applied to detect the virus, prevent the interaction between virus and mammalian cells, and treat the virus-infected cells, due mainly to the unique physicochemical properties of nanoparticles. In this regard, many nanotechnology-based chemotherapies, gene therapy, vaccination, or combination therapy have been developed. In this Minireview, we outline the pathogenesis of HPV infection and the recent advances in nanotechnology-based weapons that can be applied in combating HPV-associated diseases.

scholarly journals The NADase-Negative Variant of the Streptococcus pyogenes Toxin NAD + Glycohydrolase Induces JNK1-Mediated Programmed Cellular Necrosis

mBio ◽  
2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Sukantha Chandrasekaran ◽  
Michael G. Caparon
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Host Cell ◽  
Streptococcus Pyogenes ◽  
Host Cells ◽  
Programmed Necrosis ◽  
Nad Glycohydrolase ◽  
Streptolysin O ◽  
Different Types ◽  
Infected Cells

ABSTRACT Virulence factors are often multifunctional and contribute to pathogenesis through synergistic mechanisms. For the human pathogen Streptococcus pyogenes , two factors that act synergistically are the S. pyogenes NAD + glycohydrolase (SPN) and streptolysin O (SLO). Through distinct mechanisms, SLO forms pores in host cell membranes and translocates SPN into the host cell cytosol. Two natural variants of SPN exist, one that exhibits NADase activity and one that lacks this function, and both versions are translocated and act in concert with SLO to cause an accelerated death response in epithelial cells. While NADase + SPN is known to trigger a metabolic form of necrosis through the depletion of NAD + , the mechanism by which NADase − SPN induces cell death was unknown. In the studies described here, we examined the pathway of NADase − cell death through analysis of activation patterns of mitogen-activated protein kinases (MAPKs). S. pyogenes infection resulted in activation of members of three MAPK subfamilies (p38, ERK, and JNK). However, only JNK was activated in an SLO-specific manner. NADase − SPN induced necrosis in HeLa epithelial cells associated with depolarization of mitochondrial membranes, activation of NF-κB, and the generation of reactive oxygen species. Remarkably, RNA interference (RNAi) silencing of JNK protected cells from NADase − -SPN-mediated necrosis, suggesting that NADase − SPN triggers a form of programmed necrosis dependent on JNK signaling. Taken together, these data demonstrate that SPN acts with SLO to elicit necrosis through two different mechanisms depending on its NADase activity, i.e., metabolic (NADase + ) or programmed (NADase − ), leading to distinct inflammatory profiles. IMPORTANCE Many bacterial pathogens produce toxins that alter how infected host cells interact with the immune system. For Streptococcus pyogenes , two toxins, a NAD + glycohydrolase (SPN) and streptolysin O (SLO), act in combination to cause infected cells to die. However, there are two natural forms of SPN, and these variants cause dying cells to produce different types of signaling molecules. The NADase + form of SPN kills cells by depleting reserves of NAD + and cellular energy. The other form of SPN lacks this activity (NADase − ); thus, the mechanism by which this variant induces toxicity was unknown. Here, we show that infected cells recognize NADase − SPN through a specific signaling molecule called JNK, which causes these cells to undergo a form of cellular suicide known as programmed necrosis. This helps us to understand how different forms of toxins alter host cell signaling to help S. pyogenes cause different types of diseases.

scholarly journals Tritrichomonas foetus Induces Apoptotic Cell Death in Bovine Vaginal Epithelial Cells

2004 ◽  
Vol 72 (7) ◽  
pp. 4151-4158 ◽  
Author(s):  
B. N. Singh ◽  
J. J. Lucas ◽  
G. R. Hayes ◽  
Ish Kumar ◽  
D. H. Beach ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Molecular Mass ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Peptide Sequence ◽  
Mass Spectrometry Analysis ◽  
Tritrichomonas Foetus ◽  
Vaginal Epithelial Cells

ABSTRACT Tritrichomonas foetus is a serious veterinary pathogen, causing bovine trichomoniasis, a sexually transmitted disease leading to infertility and abortion. T. foetus infects the mucosal surfaces of the reproductive tract. Infection with T. foetus leads to apoptotic cell death of bovine vaginal epithelial cells (BVECs) in culture. An affinity-purified cysteine protease (CP) fraction yielding on sodium dodecyl sulfate-polyacrylamide gel electrophoresis a single band with an apparent molecular mass of 30 kDa (CP30) also induces BVEC apoptosis. Treatment of CP30 with the protease inhibitors TLCK (Nα-p-tosyl-l-lysine chloromethyl ketone) and E-64 [l-trans-epoxysuccinyl-leucylamide-(4-guanido)-butane] greatly reduces induction of BVEC apoptosis. Matrix-assisted laser desorption ionization-time-of-flight MALDI-TOF mass spectrometry analysis of CP30 reveals a single peak with a molecular mass of 23.7 kDa. Mass spectral peptide sequence analysis of proteolytically digested CP30 reveals homologies to a previously reported cDNA clone, CP8 (D. J. Mallinson, J. Livingstone, K. M. Appleton, S. J. Lees, G. H. Coombs, and M. J. North, Microbiology 141:3077-3085, 1995). Induction of apoptosis is highly species specific, since the related human parasite Trichomonas vaginalis and associated purified CPs did not induce BVEC death. Fluorescence microscopy along with the Cell Death Detection ELISAPLUS assay and flow cytometry analyses were used to detect apoptotic nuclear condensation, DNA fragmentation, and changes in plasma membrane asymmetry in host cells undergoing apoptosis in response to T. foetus infection or incubation with CP30. Additionally, the activation of caspase-3 and inhibition of cell death by caspase inhibitors indicates that caspases are involved in BVEC apoptosis. These results imply that apoptosis is involved in the pathogenesis of T. foetus infection in vivo, which may have important implications for therapeutic interference with host cell death that could alter the course of the pathology in vivo.

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