Everything You Always Wanted to Know About Salmonella Type 1 Fimbriae, but Were Afraid to Ask

Abstract

Initial attachment to host intestinal mucosa after oral infection is one of the most important stages during bacterial pathogenesis. Adhesive structures, widely present on the bacterial surface, are mainly responsible for the first contact with host cells and of host-pathogen interactions. Among dozens of different bacterial adhesins, type 1 fimbriae (T1F) are one of the most common adhesive organelles in the members of the Enterobacteriaceae family, including Salmonella spp., and are important virulence factors. Those long, thin structures, composed mainly of FimA proteins, are responsible for recognizing and binding high-mannose oligosaccharides, which are carried by various glycoproteins and expressed at the host cell surface, via FimH adhesin, which is presented at the top of T1F. In this review, we discuss investigations into the functions of T1F, from the earliest work published in 1958 to operon organization, organelle structure, T1F biogenesis, and the various functions of T1F in Salmonella -host interactions. We give special attention to regulation of T1F expression and their role in binding of Salmonella to cells, cell lines, organ explants, and other surfaces with emphasis on biofilm formation and discuss T1F role as virulence factors based on work using animal models. We also discuss the importance of allelic variation in fimH to Salmonella pathogenesis, as well as role of FimH in Salmonella host specificity.

Identification of Natural Mutations Responsible for Altered Infection Phenotypes of Salmonella enterica Clinical Isolates by Using Cell Line Infection Screens

“…Salmonella has evolved various strategies for adhesion and invasion, and different serovars have developed specific combinations of various adhesins or variants of the same adhesin for host cell attachment (11,12). Adhesive structures of Salmonella enterica can be divided into three groups: fimbrial adhesins, non-fimbrial adhesins, and atypical adhesive structures (13).…”

“…Despite an overwhelming amount of research and a seemingly clear picture of the adhesion and invasion process, largely based on work with the serovar S. Typhimurium, our understanding of these phenomena is still not complete. For example, it is now evident that adhesion and invasion can be affected by expression of different adhesin variants, mutations in genes encoding T3SS effectors, environmental factors, stress, metabolism, and various regulatory proteins (12,17). Additionally, around 35-40% of bacterial genes have no experimentally validated function and their contribution to the bacterial virulence, including adhesion and invasion, remains unknown (18).…”

“…In an effort to explain the differences in infectivity among isolates, we focused our efforts to Noteworthy is the fact that bacteria for adhesion assays with T1F are usually grown under different conditions from those used in our screens (12,51).…”

Enrofloxacin shifts intestinal microbiota and metabolic profiling and hinders recovery from Salmonella enterica subsp. enterica serovar Typhimurium infection in neonatal chickens

“…Salmonella can use type I flagellates to bind to mannose residues distributed on the surface of the mucin layer to attach to the mucin surface and colonize the intestine (34). In this study, IL-18 expression was inhibited in the enrofloxacin group.…”

Factors required for adhesion of Salmonella enterica serovar Typhimurium to lettuce (Lactuca sativa)

“…All operons encoding C/U fimbriae consists at least of a fimbrial main subunit, a specific periplasmic chaperone, and an usher located in the outer membrane (12). Best characterized C/U fimbriae so far are the mannose-sensitive type 1 fimbriae encoded by fimAICDHF (13), and pef fimbriae encoded by genes on pSLT2. Pef fimbriae are involved in the binding to Le x blood group antigen and in the formation of biofilm on chicken intestinal epithelium (14, 15).…”