![]() Fimbriae are grouped into three classes according to their mode of assembly. Fimbriae have also been shown to contribute to interactions with macrophages, intestinal persistence, biofilm formation and bacterial aggregation in other Salmonella serovars ( Edwards et al., 2000 Zhang et al., 2000 Boddicker et al., 2002 Tsui et al., 2003 Weening et al., 2005 Ledeboer et al., 2006). Typhi.įimbriae are proteinaceous extracellular structures mainly involved in adhesion, a crucial initial step for colonization and entry into host cells. Due to this lack of direct information, crucial questions still remain concerning host-specificity and pathogenicity mechanisms of S. Typhi pathogenesis and virulence factors is based on the systemic infection of mice with S. It also evades the host innate immune response by the production of an extracellular capsule, the Vi antigen, encoded on SPI-7 ( Wilson et al., 2008 Winter et al., 2008 Wangdi et al., 2014). Typhi invades the human host by a variety of virulence factors such as two type III secretion systems (T3SS) encoded by Salmonella pathogenicity islands (SPI)−1 and−2, the presence of 10 SPIs in the genome, the human-restricted typhoid toxin and the flagella ( Galan and Zhou, 2000 Galán, 2001 Waterman and Holden, 2003 Chang et al., 2016 Horstmann et al., 2017). Salmonella species enter their host by the intestinal tract and cross the intestinal barrier ( Clark et al., 1994). Typhi pathogenesis is required to better control and treat typhoid ( Obaro et al., 2017). Typhi strains can complicate treatment and can lead to a higher death rate ( Rowe et al., 1997 Thong et al., 2000 Pokharel et al., 2006 WHO, 2012). However, the increased emergence of multidrug resistant S. ![]() Over the years, the number of cases has increased, but the use of antibiotics has controlled the eventual burden. It causes ~22 million infections and 200,000 deaths annually worldwide ( WHO, 2012 Qamar et al., 2015). Salmonella enterica serovar Typhi is a human-specific pathogen responsible for a systemic disease called typhoid fever. Overall, chaperone-usher fimbriae seem to be an important part of the balance between the different steps (motility, adhesion, host invasion and persistence) of S. However, only Fim fimbriae had a deleterious effect on motility when overexpressed. ![]() ![]() Several fimbriae modified bacterial interactions with human cells (THP-1 and INT-407) and biofilm formation. Typhi afimbrial strain were tested for interactions with host cells, biofilm formation and motility. The impact of fimbrial deletion in a wild-type strain or addition of each individual fimbrial system to an S. Six of these (Fim, Saf, Sta, Stb, Std, and Tcf) also show extracellular structure by electron microscopy. Each system was overexpressed and only the fimbrial gene clusters without pseudogenes demonstrated a putative major subunits of about 17 kDa on SDS-PAGE. Typhi fimbriae were better expressed in minimal broth. Typhi chaperone-usher fimbriae and their potential roles in pathogenesis such as interaction with host cells, motility, or biofilm formation were assessed. These fimbriae are weakly expressed in laboratory conditions and only a few are actually characterized. Typhi possesses 14 fimbrial gene clusters including 12 chaperone-usher fimbriae ( stg, sth, bcf, fim, saf, sef, sta, stb, stc, std, ste, and tcf). Several aspects of its pathogenesis are still poorly understood. The human-specific pathogen Salmonella enterica serovar Typhi causes typhoid, a major public health issue in developing countries.
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