Bu çalışmada herhangi bir insan ve/veya hayvan deneği ya da onlardan alınan örnekler kullanılmamıştır. Bu nedenle söz konusu çalışma için herhangi bir etik onaya ihtiyaç yoktur.
Fimbriae is an important virulence factor which plays a key role in cell attachment and colonization of the intestinal mucosa during an infection of Salmonella, a pathogen that causes gastroenteritis and systemic infection in humans. In S. Typhimurium, type 1 fimbriae production strengthens the oxidative stress response. This study aimed to determine the effectiveness of the fimF gene and its N-terminal domain on biofilm formation in S. Typhimurium and their contribution to the oxidative stress response. Before the experiments to prove whether the N-terminal domain of the FimF protein is the region that determines the mechanism and function of the fimF gene; only the N-terminal domain of the fimF gene was cloned behind the pBAD promoter. As a result of biofilm experiments on polystyrene surfaces, it was determined that the biofilm production capacity was reduced significantly in mutant strains in terms of fimF and dam genes (p < 0.05). In the oxidative stress response experiment conducted in the presence of hydrogen peroxide (H2O2), it was determined that the mutant strains were more resistant to hydrogen peroxide than the wild-type strain, therefore Salmonella cells perceived the absence of Dam methylase enzyme and FimF protein as a critical internal stress condition and produced strong responses to these stress conditions. As a result of comparative analysis of the N-terminal domain cloned mutant strain with the wild-type, it was proven that the N-terminal domain of the protein in question acts as an adapter protein, due to its close similarities with the wild-type.
Biofilm formation fimF gene N-terminal domain Oxidative stress Salmonella Typhimurium Type 1 fimbriae
Birincil Dil | İngilizce |
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Konular | Veteriner Bakteriyoloji, Veteriner Mikrobiyolojisi |
Bölüm | Araştırma Makalesi |
Yazarlar | |
Erken Görünüm Tarihi | 28 Haziran 2024 |
Yayımlanma Tarihi | |
Gönderilme Tarihi | 13 Kasım 2023 |
Kabul Tarihi | 20 Mart 2024 |
Yayımlandığı Sayı | Yıl 2024Accepted Papers |