Immunohistochemical Localization of Aspergillus and p53 in Human Lung Tissues

Abstract

Aspergilli are filamentous fungi which can cause opportunistic infections in Acquired Immunodeficiency Syndrome (AIDS) patients. Aspergilli can be found in human tissues either in the form of spores or hyphae. p53 is a tumor suppressor gene located in the short arm of chromosome 17. It is a potent transcriptional regulator of genes which are involved in many cellular activities including cell cycle arrest, apoptosis and angiogenesis. A loss of tumor suppressor function of p53 is the most common event leading to the development of human cancers. The rate by which p53 has a homology between different species has been reported from human to other vertebrates, it has been reported that it is available within Drosophila melanogaster and C. elegans [1] [2]. The aim of this study is to check if p53 is localized within Aspergilli or not using immunohistochemical techniques and study the relationship between Aspergilli infection and p53 in human lung tissues. 45 different samples of lung tissues, diagnosed as being none tumor, were taken randomly during the year of 2003-2004 from the autopsy cases submitted to the forensic medicine center in Irbid, Jordan. The sample group consisted of 12 females and 33 males. Labeled Streptavidin Biotin (LSAB) method and Mach-4 method were used to determine the Aspergilli infection and p53. The results show that the Aspergillus is presented in all used samples (100% of the infection) in the form of spores or hyphae and all infected samples have mutant p53 molecules (p53 was located in Aspergillus spores and hyphae). According to this study, it is safe to posit that the mutant p53 molecules may be used by Aspergillus for its multiplication. Seemingly it is a biological behavior of Aspergillus to produce p53. The fate of the p53 is questioned, is it going to interact with the human cells initiating cancer? Further experimental investigations are required to determine such pathway. In conclusion, this study shows that Aspergillus is a producing agent for p53 and Aspergillus pathogenicity is caused by production of p53.

Share and Cite:

G. Al-Saghir, M. , A. Alkhatatbeh, M. and J. Alkhatib, A. (2015) Immunohistochemical Localization of Aspergillus and p53 in Human Lung Tissues. American Journal of Molecular Biology, 5, 117-123. doi: 10.4236/ajmb.2015.54010.

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1] Schumacher, B., Hofmann, K., Boulton, S. and Gartner A. (2001) The C. elegans Homolog of the p53 Tumor Suppressor Is Required for DNA Damage-Induced Apoptosis. Current Biology, 11, 1722-1727.
http://www.ncbi.nlm.nih.gov/pubmed/11696333
http://dx.doi.org/10.1016/S0960-9822(01)00534-6
[2] Michael, O., Young, L., DiComo, C., Karim, F., Belvin, M., Robertson, S., Whittaker, K., Demsky, M., Fisher, W., Buchman, A., Duyk, G., Friedman, L., CPrives, C. and Kopczynski, C. (2000) Drosophila p53 Is a Structural and Functional Homolog of the Tumor Suppressor p53. Cell, 101, 91-101.
http://www.sciencedirect.com/science/article/pii/S0092867400806261
http://dx.doi.org/10.1016/S0092-8674(00)80626-1
[3] Young, R.C., Bennett, J.E., Vogel, C.L., Carbone, P.P. and DeVita, V.T. (1970) Aspergillosis: The Spectrum of Disease in 98 Patients. Medicine, 49, 147-73.
http://www.ncbi.nlm.nih.gov/pubmed/4913991
http://dx.doi.org/10.1097/00005792-197003000-00002
[4] Van Burik, J.A. and Magee, P.T. (2001) Aspects of Fungal Pathogenesis in Humans. Annual Review of Microbiology, 55, 743-772.
http://www.ncbi.nlm.nih.gov/pubmed/11544373
http://dx.doi.org/10.1146/annurev.micro.55.1.743
[5] Marterre, W.F., Mong, A.T. and Pulito, A.R. (1992) Locally Invasive Aspergillosis of the Bowel. Journal of Pediatric Surgery, 27, 1611-1613.
http://www.ncbi.nlm.nih.gov/pubmed/1469594
http://dx.doi.org/10.1016/0022-3468(92)90527-e
[6] Mori, T., Matsumara, M., Ymada, K., Irie, S., Oshimi, K., Suda, K., Oguri, T. and Ichinoe, M. (1998) Systemic Aspergillosis Caused by an Aflatoxin-Producing Strain of Aspergillus flavus. Medical Mycology, 36, 107-112.
http://informahealthcare.com/doi/abs/10.1080/02681219880000171
http://dx.doi.org/10.1080/02681219880000171
[7] Smela, M.E., Currier, S.S., Bailey, E.A. and Essigmann, J.M. (2001) The Chemistry and Biology of Aflatoxin B(1): from Mutational Spectrometry to Carcinogenesis. Carcinogenesis, 22, 535-545.
http://www.ncbi.nlm.nih.gov/pubmed/11285186
http://dx.doi.org/10.1093/carcin/22.4.535
[8] Livingstone, L.R., White, A., Sprouse, J., et al. (1992) Altered Cell Cycle Arrest and Gene Amplification Potential Accompany Loss of Wild-Type p53. Cell, 70, 923-935.
http://www.ncbi.nlm.nih.gov/pubmed/1356076
http://dx.doi.org/10.1016/0092-8674(92)90243-6
[9] Hussain, S.P. and Harris, C.C. (2000) Molecular Epidemiology and Carcinogenesis: Endogenous and Exogenous Carcinogens. Mutation Research, 462, 311-322.
http://www.ncbi.nlm.nih.gov/pubmed/10767641
http://dx.doi.org/10.1016/s1383-5742(00)00015-6
[10] Huncharek, M., Kupelnick, B., Geschwind, J.F., et al. (2000) Prognostic Significance of p53 Mutations in Non-Small Cell Lung Cancer: A Meta-Analysis of 829 Cases from Eight Published Studies. Cancer Letter, 153, 219-226.
http://www.ncbi.nlm.nih.gov/pubmed/10779652
http://dx.doi.org/10.1016/S0304-3835(00)00381-5

Copyright © 2023 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.