Elhosseiny, N. M., T. M. Samir, A. A. Ali, A. A. El-Kholy, and A. S. Attia, "Development of an Immunochromatographic Strip Using Conjugated Gold Nanoparticles for the Rapid Detection of Klebsiella pneumoniae Causing Neonatal Sepsis", Pharmaceutics, vol. 13, pp. 1141, 2021. pharmaceutics-13-01141.pdf
Elhosseiny, N. M., and A. S. Attia, "Acinetobacter: an emerging pathogen with a versatile secretome", Emerging Microbes and Infections, vol. 7, issue 33, 2018. acinetobacter_an_emerging_pathogen_with_a_versatile_secretome.pdf
Sanchez-Larrayoz, A. F., N. M. Elhosseiny, M. G. Chevrette, Y. Fu, P. Giunta, R. G. Spallanzani, K. Ravi, G. B. Pier, S. Lory, and T. Maira-Litrán, "Complexity of Complement Resistance Factors Expressed by Acinetobacter baumannii Needed for Survival in Human Serum", The Journal of Immunology, vol. 199, issue 8, pp. 2803-2814, 2017.
Samir, R., S. H. Hussein, N. M. Elhosseiny, M. S. Khattab, A. E. Shawky, and A. S. Attia, "Adaptation to Potassium-Limitation Is Essential for Acinetobacter baumannii Pneumonia Pathogenesis", Journal of Infectious Diseases, vol. 214, issue 12, pp. 2006-2013, 2016. j_infect_dis.-2016-samir-2006-13.pdf
Elhosseiny, N. M., O. M. El-Tayeb, A. S. Yassin, S. Lory, and A. S. Attia, "The secretome of Acinetobacter baumannii ATCC 17978 type II secretion system reveals a novel plasmid encoded phospholipase that could be implicated in lung colonization", International Journal of Medical Microbiology, vol. 306, issue 8, pp. 633-641, 2016. t2ss_paper_final.pdf
Elhosseiny, N. M., M. A. Amin, A. S. Yassin, and A. S. Attia, "Acinetobacter baumannii universal stress protein A plays a pivotal role in stress response and is essential for pneumonia and sepsis pathogenesis", Int J Med Microbiol, vol. 305, no. 1, pp. 114-23, Jan, 2015. Abstractelhosseiny_et_al._2014_ijmm_main.pdfWebsite

Acinetobacter baumannii is one of the most significant threats to global public health. This threat is compounded by the fact that A. baumannii is rapidly becoming resistant to all relevant antimicrobials. Identifying key microbial factors through which A. baumannii resists hostile host environment is paramount to the development of novel antimicrobials targeting infections caused by this emerging pathogen. An attractive target could be a molecule that plays a role in the pathogenesis and stress response of A. baumannii. Accordingly, the universal stress protein A (UspA) was chosen to be fully investigated in this study. A platform of A. baumannii constructs, expressing various levels of the uspA gene ranging from zero to thirteen folds of wild-type level, and a recombinant E. coli strain, were employed to investigate the role of UspA in vitro stress and in vivo pathogenesis. The UspA protein plays a significant role in protecting A. baumannii from H2O2, low pH, and the respiratory toxin 2,4-DNP. A. baumannii UspA protein plays an essential role in two of the deadliest types of infection caused by A. baumannii; pneumonia and sepsis. This distinguishes A. baumannii UspA from its closely related homolog, the Staphylococcus aureus Usp2, as well as from the less similar Burkholderia glumae Usps. Heterologous and overexpression experiments suggest that UspA mediates its role via an indirect mechanism. Our study highlights the role of UspA as an important contributor to the A. baumannii stress and virulence machineries, and polishes it as a plausible target for new therapeutics.

el-Hennawy, M. G., H. Sultan, N. M. Elhosseiny, N. A. Sabry, and A. S. Attia, "The effect of alpha 1 antitrypsin deficiency and bacterial loads on the efficacy of chronic obstructive pulmonary disease pharmacotherapy in Egyptian patients", 2014 ACCP Virtual Poster Symposium: PHARMACOTHERAPY 34 (6), pp. e99-e100, 2014. Abstract

OBJECTIVES: Chronic obstructive pulmonary disease (COPD) is caused by the combination of smoking, genetic susceptibilityand exacerbated by bacterial infection. The genetic cause of COPD is a1-antitrypsin (AAT) deficiency. The goal of the study is to screen for AAT deficiency in the Egyptian population both phenotypically and genotypically to assess the contribution of (PI*S, PI*Z, PIMmalton and Q0Cairo) in the development of COPD in Egypt. The role of the bacterial burden in the COPD patients and its possible link to the AAT- deficiency genotype will be determined. Finally, any correlations between the identified mutations and/or the bacterial loads and the patients’ response to the medication will be determined.

METHODS: Three medical centers in Egypt participated in the study. Eligible patients (> GOLD II, < GOLD IV, FEV1/FVC ratio < 0.7, with post-bronchodilator FEV1 < 80% predicted) were offered testing for AATD, 6 minutes walk test and arterial blood gas (ABG).

RESULTS: A total of 21 patients were tested, of whom 20 were eligible. 25% were carriers (MZ). 65% showed single microbial species, 25% showed 2 microbial species and 10% had no microorganisms. Distribution of the isolated microorganisms based on Gram-reactions showed that 52.2% are Gram Positive while 47.8% are Gram Negative bacteria. Upon receiving treatment (LABA and Corticosteroid inhaler) for 6 months; 6 minutes walk test results increased by average 14.14%, FEV1/FVC ratio increased by average 20.75% and Oxygen Saturation increased by average 0.51%. Still the correlation between the gene variation and response to treatment is under investigation.

CONCLUSION: The prevalence of AATD among patients undergoing pulmonary function test was 25% MZ variant carriers. Pulmonary Function testing was effectively conducted
throughout the study.

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