JCT  Vol.4 No.2 , April 2013
TLR4 May Accelerate Hypoxia Reaction to Promote the Occurrence and Progress of Cervical Lesions by Infected Pathogenic Microorganisms Other than HPV
ABSTRACT

Objective: To explore what role the inflammatory immune response is playing in the occurrence and development of HPV related cervical disease. Methods: To detect the expression of TLR4, HIF-1α and HPV16 E7 in the specimens of HPV related cervical lesions, for example normal cervix, cervicitis, cervical intraepithelial neoplasia and cervical cancer by RT PCR methods. Results: The expression of TLR4 and HIF-1α ascent from normal cervix to cervicitis, then to CIN tissue, and then to cervical cancer (P < 0.05). The expression of HPV16 E7 was higher in cervicitis than that in normal cervix (P < 0.05) while there was no significant ascendance from cervicitis to CIN tissue, either from CIN tissue to cervical cancer although it seemed ascending (P > 0.05). Conclusion: TLR4 may promote the occurrence and progress of cervical lesions by accelerating the hypoxia reaction. And the natural immune reaction mediated by TLR4 may be correlated to other pathogenic microorganisms infecting the cervical tissue, rather than HPV.


Cite this paper
Y. Cheng, G. Chen, X. Wang, Y. Huang, J. Ding, J. Huang and L. Hong, "TLR4 May Accelerate Hypoxia Reaction to Promote the Occurrence and Progress of Cervical Lesions by Infected Pathogenic Microorganisms Other than HPV," Journal of Cancer Therapy, Vol. 4 No. 2, 2013, pp. 549-553. doi: 10.4236/jct.2013.42069.
References
[1]   M. F. Abdul-Careem, M. Firoz Mian, A. E. Gillgrass, et al., “FimH, a TLR4 Ligand, Induces Innate Antiviral Responses in the Lung Leading to Protection against Lethal Influenza Infection in Mice,” Antiviral Research, Vol. 92, No. 2, 2011, pp. 346-355. doi:10.1016/j.antiviral.2011.09.004

[2]   G. Raicevic, M. Najar, K. Pieters, et al., “Inflammation and TLR Ligation Differentially Affect the Osteogenic Potential of Human Mesenchymal Stromal Cells (MSC) Depending on Their Tissue Origin,” Tissue Engineering Part A, Vol. 25, 2012.

[3]   S. Challa, M. Woelfel, M. Guildford, et al., “Viral Cell Death Inhibitor MC159 Enhances Innate Immunity against Vaccinia Virus Infection,” Journal of Virology, Vol. 84, No. 20, 2010, pp. 10467-10476. doi:10.1128/JVI.00983-10

[4]   M. Ramanathan, W. Luo, B. Csóka, et al., “Differential Regulation of HIF-1Alpha Isoforms in Murine Macrophages by TLR4 and Adenosine A2A Receptor Agonists,” Journal of Leukocyte Biology, Vol. 86, No. 3, 2009, pp. 681-689. doi:10.1189/jlb.0109021

[5]   J. Hu, D. Lou, B. Carow, et al., “LPS Regulates SOCS2 Transcription in a Type I Interferon Dependent AutocrineParacrine Loop,” PLoS One, Vol. 7, No. 1, 2012, Article ID: e30166. doi:10.1371/journal .pone.0030166

[6]   C. B. Lu, M. J. Yang, L. Luo, et al., “Detection and Typing of Human Papillomavirus by a GeXP Based Multiplex PCR Assay,” Chinese Journal of Experimental and Clinical Virology, Vol. 25, No. 1, 2011, pp. 69-72.

[7]   E. F. Dunne, M. Sternberg, L. E. Markowitz, et al., “Human Papillomavirus (HPV) 6, 11, 16, and 18 Prevalence among Females in the United States—National Health and Nutrition Examination Survey, 2003-2006: Opportunity to Measure HPV Vaccine Impact?” The Journal of Infectious Diseases, Vol. 204, No. 4, 2011, pp. 562-565.

[8]   B. S. Bowser, S. Alam and C. Meyers, “Treatment of a Human Papillomavirus Type 31b-Positive Cell Line with Benzo[a]Pyrene Increases Viral Titer through Activation of the Erk1/2 Signaling Pathway,” Journal of Virology, Vol. 85, No. 10, 2011, pp. 4982-4992. doi:10.1128/JVI.00133-11

[9]   X. W. Lu, C. Y. Xiao and H. Ye, “The Research Progress on the Correlationship of Cyto Factor and Human Pappiloma Virus to Cervical Cancer,” The Clinical Physician Magazine: Electronic Edition, Vol. 5, No. 14, 2011, pp. 4163-4166.

[10]   A. M. Chaussé, O. Grépinet, E. Bottreau, et al., “Expression of Toll-Like Receptor 4 and Downstream Effectors in Selected Cecal Cell Subpopulations of Chicks Resistant or Susceptible to Salmonella Carrier State,” Infection and Immunity, Vol. 79, No. 8, 2011, pp. 3445-3454. doi:10.1128/IAI.00025-11

[11]   M. Bosmann, V. R. Patel, N. F. Russkamp, et al., “MyD88-Dependent Production of IL-17F Is Modulated by the Anaphylatoxin C5a via the Akt Signaling Pathway,” The FASEB Journal, Vol. 25, No. 12, 2011, pp. 4222-4232. doi:10.1096/fj.11-191205

[12]   M. G. De Boer, H. Jolink, C. J. Halkes, et al., “Influence of Polymorphisms in Innate Immunity Genes on Susceptibility to Invasive Aspergillosis after Stem Cell Transplantation,” PLoS One, Vol. 6, No. 4, 2011, Article ID: e18403.

[13]   M. Nakamura, J. M. Bodily, M. Beglin, et al., “HypoxiaSpecific Stabilization of HIF-1Alpha by Human Papillomaviruses,” Virology, Vol. 387, No. 2, 2009, pp. 442-448. doi:10.1016/j.virol.2009.02.036

[14]   G. Kleveta, K. Borz?cka, M. Zdioruk, et al., “LPS Induces Phosphorylation of Actin-Regulatory Proteins Leading to Actin Reassembly and Macrophage Motility,” Journal of Cellular Biochemistry, Vol. 113, No. 1, 2012, pp. 80-92. doi:10.1002/jcb.23330

 
 
Top