Abstract
Although most Salmonella serovars are able to infect a range of animal hosts, some have acquired the ability to cause systemic infections of specific hosts. For example, Salmonella enterica serovar Choleraesuis is primarily associated with systemic infection in swine. Adherence to host epithelial cells is considered a prerequisite for initial infection, and fimbrial appendages on the outer membrane of the bacteria are implicated in this process. Although type 1 fimbriae encoded by the fim gene cluster are commonly found in Salmonella serovars, it is not known whether S. Choleraesuis produces this fimbrial type and if and how fimbriae are involved in pathogenesis. In the present study, we demonstrated that only four out of 120 S. Choleraesuis isolates from pigs with salmonellosis produced type 1 fimbriae as assayed by the yeast agglutination test and electron microscopy. One of the 116 non-type 1 fimbria-producing isolates was transformed with plasmids carrying different fim genes from S. Typhimurium LB5010, a type 1 fimbria-producing strain. Our results indicate that non-type 1 fimbria-producing S. Choleraesuis required only an intact fimH to regain the ability to produce fimbrial appendages. Sequence comparison revealed six amino acid variations between the FimH of the non-type 1 fimbria-producing S. Choleraesuis isolates and those of the type 1 fimbria-producing S. Choleraesuis isolates. S. Choleraesuis that produced type 1 fimbriae contained FimH with an amino acid sequence identical to that of S. Typhimurium LB5010. Site-directed mutagenesis leading to the replacement of the non-conserved residues revealed that a change from glycine to valine at position of 63 (G63V) resulted in a non-type 1 fimbria-producing S. Choleraesuis being able to express type 1 fimbriae on its outer membrane. It is possible that this particular amino acid change prevents this polypeptide from proper interaction with other Fim subunits required for assembly of an intact type 1 fimbrial shaft in S. Choleraesuis; however, it remains to be determined if and how the absence of type 1 fimbriae production is related to the systemic infection of the swine host by S. Choleraesuis.
Highlights
The Salmonella genus is composed of Salmonella enterica and Salmonella bongori species, which comprise six subspecies (I, II, IIa, IIb, IV, and V) subdivided into about 2800 serovars [1]
The phenotypic expression of type 1 fimbriae is primarily a result of cooperation among several Fim proteins and arginine tRNA encoded by fimU within the fim gene cluster
Choleraesuis is limited, the present study investigated the distribution of the expression of fimbrial appendages among S
Summary
The Salmonella genus is composed of Salmonella enterica and Salmonella bongori species, which comprise six subspecies (I, II, IIa, IIb, IV, and V) subdivided into about 2800 serovars [1]. Type 1 fimbriae adhere to a variety of cells that possess mannose residues, such as erythrocytes, leukocytes, yeast, and respiratory cells [8] This binding capacity is conferred by the FimH adhesin [9]. The precise contribution of type 1 fimbriae to virulence is still unclear because several factors, such as the Salmonella strain used, the inoculation route, and the laboratory animal chosen, affect the results [16, 17]. This type of fimbria may play an important role at some stage of the infectious cycle of Salmonella [18]
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