Expression of hemolysin specific for S. aureus in different bacterial species isolated from variant clinical sources

Main Article Content

Zeena Hashim Abd Al- Wahid
Munaff Jawdat Abd Al- Abbas

Keywords

Hemolysins, Bacterial, Gene

Abstract

Staphylococcus aureus is the main source of the virulence factors, particularly hemolysins causing serious and fatal infections. The hemolysins were overexpressed in several bacterial species from various clinical sources indicating the actual problem of gene transfer. The highest expression level was detected in the hld gene comparison to hla, hlb and hlg. Furthermore, they all showed variable expression levels depending on the bacterial species and isolation sources. Finally, the presence of the hemolysin substrate such as blood in the bacterial culture media increased the expression level.

Abstract 127 | PDF Downloads 178

References

1. Abd Al-Wahid, Z. H., & Abd Al-Abbas, M. J. (2023). Distribution of hla, hlb, hlgC, hld & cylA
hemolysin genes and their alleles in different bacterial species isolated from the variant clinical sources in Basrah. Journal of Population Therapeutics and Clinical Pharmacology, 30(3), 180-198.
2. Adame-Gómez, R., Castro-Alarcón, N., Vences-Velázquez, A., Toribio-Jiménez, J., Pérez-Valdespino, A., Leyva-Vázquez, M. A., & Ramírez-Peralta, A. (2020). Genetic diversity and virulence factors of S. aureus isolated from food, humans, and animals. International journal of microbiology, 2020.
3. Bartlett, J. G. (2008). Methicillin-resistant Staphylococcus aureus infections. Top HIV Med, 16(5), 151-155.
4. Blake, K. J., Baral, P., Voisin, T., Lubkin, A., Pinho-Ribeiro, F. A., Adams, K. L., ... & Chiu, I. M. (2018). Staphylococcus aureus produces pain through pore-forming toxins and neuronal TRPV1 that is silenced by QX-314. Nature communications, 9(1), 1-15.
5. Cafiso, V., Bertuccio, T., Spina, D., Purrello, S., Campanile, F., Di Pietro, C., ... & Stefani, S. (2012). Modulating activity of vancomycin and daptomycin on the expression of autolysis cell-wall turnover and membrane charge genes in hVISA and VISA strains. PLoS One, 7(1), e29573.
6. Dekker, D., Wolters, M., Mertens, E., Boahen, K. G., Krumkamp, R., Eibach, D., ... & May, J. (2016). Antibiotic resistance and clonal diversity of invasive Staphylococcus aureus in the rural Ashanti Region, Ghana. BMC Infectious Diseases, 16(1), 1-6.
7. Dings, M. M., Orwin, P. M., & Schlievert, P. M. (2000). Exotoxins of Staphylococcus aureus. Clin. Microbiol. Rev, 13, 16-34.
8. Gordon, R. J., & Lowy, F. D. (2008). Pathogenesis of methicillin-resistant Staphylococcus aureus infection. Clinical infectious diseases, 46(Supplement_5), S350-S359.
9. Huseby, M. J., Kruse, A. C., Digre, J., Kohler, P. L., Vocke, J. A., Mann, E. E., ... & Earhart, C. A. (2010). Beta toxin catalyzes formation of nucleoprotein matrix in staphylococcal biofilms. Proceedings of the National Academy of Sciences, 107(32), 14407-14412
10. Kong, C., Neoh, H. M., & Nathan, S. (2016). Targeting Staphylococcus aureus toxins: a potential form of anti-virulence therapy. Toxins, 8(3), 72.
11. Livak, K.J. and Schmittgen, T.D., 2001. Analysis of relative gene expression data using real-time quantitative PCR and the 2− ΔΔCT method. methods, 25(4), pp.402-408. 12. Mahdi, M. A., Abd Al-Abbas, M. J., & Alsamak, A. M. (2021). Distribution of OatA alleles detected by a new designed primer in bacteria isolated from eye infections in Basrah governorate/Iraq. Annals of the Romanian Society for Cell Biology, 8258-8277.
13. Monecke, S., Müller, E., Büchler, J., Stieber, B., & Ehricht, R. (2014). Staphylococcus aureus in vitro secretion of alpha toxin (hla) correlates with the affiliation to clonal complexes. PloS one, 9(6), e100427.
14. Nakamura, Y., Oscherwitz, J., Cease, K. B., Chan, S. M., Muñoz-Planillo, R., Hasegawa, M., ... & Núñez, G. (2013). Staphylococcus δ-toxin induces allergic skin disease by activating mast cells. Nature, 503(7476), 397-401.
15. Otto, M. (2014). Phenol-soluble modulins. International Journal of Medical Microbiology, 304(2), 164-169.
16. Pivard, M., Caldelari, I., Brun, V., Croisier, D., Jaquinod, M., Anzala, N., & Vandenesch, F. (2022). Complex regulation of gamma-hemolysin expression impacts S. aureus virulence. bioRxiv, 2022-10.
17. Recsei, P., Kreiswirth, B., O'reilly, M., Schlievert, P. M., Gruss, A., & Novick, R. P. (1986). Regulation of exoprotein gene expression in Staphylococcus aureus by agr. Molecular and General Genetics MGG, 202(1), 58-61.
18. Tarenzi, T., Lattanzi, G., & Potestio, R. (2022). Membrane binding of pore-forming γ-hemolysin components studied at different lipid compositions. Biochimica et Biophysica Acta (BBA)-Biomembranes, 183970.
19. Tavares, A., Nielsen, J. B., Boye, K., Rohde, S., Paulo, A. C., Westh, H., ... & Miragaia, M. (2014). Insights into alpha-hemolysin (Hla) evolution and expression among Staphylococcus aureus clones with hospital and community origin. PLoS One, 9(7), e98634.
20. Zhang, H., Zheng, Y., Gao, H., Xu, P., Wang, M., Li, A., ... & Du, H. (2016). Identification and characterization of Staphylococcus aureus strains with an incomplete hemolytic phenotype. Frontiers in cellular and infection microbiology, 6, 146.
21. Zhou, X., Zheng, Y., Lv, Q., Kong, D., Ji, B., Han, X., ... & Jiang, Y. (2021). Staphylococcus aureus N-terminus formylated δ-toxin tends to form amyloid fibrils, while the deformylated δ-toxin tends to form functional oligomer complexes. Virulence, 12(1), 1418-1437.