Genetic polymorphisms in interleukin-1beta were associated with typhoid fever in Babylon City in Iraq

Zaineb Fareed Hassan Mussa; Shaimaa Jassim Al Sultany

doi:10.53730/ijhs.v6nS2.5239

Authors

Zaineb Fareed Hassan Mussa
zunab.hassien@student.uobabylon.edu.iq
Department of biology, College of Science, Babylon University, Iraq
Shaimaa Jassim Al Sultany Department of biology, College of Science, Babylon University, Iraq

Keywords:

Babylon, infection, interleukin-1beta, typhoid fever

Abstract

A total of 50 clinical samples were taken from the blood of typhoid fever patients who visited Al-Hillah Surgical Teaching Hospital and private laboratories in the AL-Hillah/Babylon region between February and August 2021. This research included 50 people who looked to be healthy and disease-free. Individuals with genotype GA were significantly represented among the patients with typhoid fever: 33 (66%), P-value = 0.0030, as compared with healthy control subjects, 18 (36%), and had an increased risk of developing typhoid fever infection. The IL-1beta (G) allele was less frequent among patients (51%, n =51) than control, and the (A) allele was more frequent among patients than control (49%, n =49). The results showed that there was a significant association between GA genotype and typhoid fever under most inheritance models. The A allele represents a risk factor for patients with typhoid fever and the inheritance of codominant, dominant, and overdominant models as risk factors. The GA genotype has an odd ratio of 4.07 (1.54–10.79) in the model of inheritance. Codominant and dominant models have a related odd ratio of 3.04 (1.21–7.60) and the overdominant model has a related odd ratio of 3.45 (1.52–7.85).

Downloads

Download data is not yet available.

References

Antillón, M.; Warren, J.; Crawford, F.; Weinberger, D. Kürüm, E.; Pak, G.; Marks, F. and Pitzer, V. (2017). The burden of typhoid fever in low and middle income countries: A meta-regression approach. PLoS neglected tropical diseases. 11(2), e0005376.

Pouzol, S.; Tanmoy, A.; Ahmed, D.; Khanam, F.; Brooks, W.; Bhuyan, G.; Fabre, L.; Bryant, J.; Gustin, M.; Vanhems, P.; Carman, B.; Weill, F.; Qadri, F.; Saha, S. and Endtz, H. (2019). Clinical evaluation of a multiplex PCR for the detection of Salmonella enterica serovars typhi and paratyphi A from blood specimens in a high endemic setting. Am. J. Trop. Med. Hyg. 101(3): 513-520.

Phetsavanh, C.; Mayfong, M.; Phouthapanya, X.; Tamalee, R.; Sayaphet, R.; Manivanh, V.; Paul, N. and John, A. (2020). Estimation of incidence of typhoid and paratyphoid fever in Vientiane, Lao People’s Democratic Republic. Am. J. Trop. Med. Hyg. 102(4), pp. 744-748.

Dinarello, C. (2006). Interleukin-1 and interleukin-18 as mediators of inflammation and the aging process. Am. J. Clin. Nutr. 83:447-455.

Ulaganathan, V. K.; Sperl, B.; Rapp, U. R. and Ullrich, A. (2015). Germline variant FGFR4 p. G388R exposes a membrane-proximal STAT3 binding site. Nature. 528(7583), 570-574.

Ishigame, H.; Kakuta, S.; Nagai, T.; Kadoki, M.; Nambu, A.; Komiyama, Y. and Sudo, K. (2009). Differential roles of interleukin-17A and-17F in host defense against mucoepithelial bacterial infection and allergic responses. Immunity. 30(1), 108-119.

Halle, A., Hornung; V., Petzold, G. C.; Stewart, C. R.; Monks, B. G.; Reinheckel, T.; Fitzgerald, K. A.; Latz, E.; Moore, K. J. and Golenbock, D. T. (2008). The NALP3 inflammasome is involved in the innate immune response to amyloid-beta. Nature immunology. 9(8), 857-865.

Estfanous, S., Ali, S. A., Seif, S. M., Soror, S., & Abdelaziz, D. (2019). Inflammasome genes' polymorphisms in egyptian chronic hepatitis C patients: Influence on vulnerability to infection and response to treatment. Mediators of inflammation. 3273645.

Pontillo, A.; Reis, E. C.; Liphaus, B. L.; Silva, C. A., and Carneiro-Sampaio, M. (2015). Inflammasome polymorphisms in juvenile systemic lupus erythematosus. Autoimmunity. 48(7), 434.437.

Ali, S.; Vollaard, A. M.; Kremer, D.; de Visser, A. W.; Martina, C. A.; Widjaja, S.; Surjadi, C.; Slagboom, E.; van de Vosse, E. and van Dissel, J. T. (2007). Polymorphisms in proinflammatory genes and susceptibility to typhoid fever and paratyphoid fever. Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research. 27(4), 271-279.

Park, J. W.; Choi, J. S.; Han, K. J.; Lee, S. H.; Kim, E. J. and Cho, J. H. (2018). Association of a genetic polymorphism of IL1RN with risk of acute pancreatitis in a Korean ethnic group. The Korean journal of internal medicine. 33(6), 1103-1110.

Ogimoto, A.; Suzuki, J. Inoue, K.; Nishimura,K.; Nagai, T. Shigematsu, Y.; H.; Okayama, and J. Higaki. (2018). Interaction between polymorphisms in inflammation-related genes and atrial fibrillation in patients with dilated cardiomyopathy. Circulation. 2011;124:A16747.

Reis, C., Barbosa, M., Machado, B., Baratto, S., de Lima, D. C., Paza, A. O., Filho, F. B., Brancher, J. A., Küchler, E. C., & de Oliveira, D. (2021). Genetic polymorphisms in interleukin-6 and interleukin-1-beta were associated with dental caries and gingivitis. Acta. Odontologica. Scandinavica. 79(2), 96-102.

Ersig, A. L.; Schutte, D. L.; Standley, J.; Leslie, E.; Zimmerman, B.; Kleiber, C.; Hanrahan, K.; Murray, J. C. and McCarthy, A. M. (2017). Relationship of genetic variants with procedural pain, anxiety, and distress in children. Biological research for nursing. 19(3), 339-349.