Fimbria-mediated interaction with the host elicits both innate and adaptive immune responses, and thus their expression may not always be beneficial in vivo. Furthermore, the metabolic drain of producing fimbriae is significant. It is not surprising, therefore, to find that fimbrial production in Escherichia coli and Salmonella enterica is under extensive environmental regulation. In many instances, fimbrial expression is regulated by phase variation, in which individual cells are capable of switching between fimbriate and afimbriate states to produce a mixed population. Mechanisms of phase variation vary considerably between different fimbriae and involve both genetic and epigenetic processes. Notwithstanding this, fimbrial expression is also sometimes controlled at the posttranscriptional level. In this chapter, we review key features of the regulation of fimbrial gene expression in E. coli and Salmonella. The occurrence and distribution of fimbrial operons vary significantly among E. coli pathovars and even among the many Salmonella serovars. Therefore, general principles are presented on the basis of detailed discussion of paradigms that have been extensively studied, including Pap, type 1 fimbriae, and curli. The roles of operon specific regulators like FimB or CsgD and of global regulatory proteins like Lrp, CpxR, and the histone-like proteins H-NS and IHF are reviewed as are the roles of sRNAs and of signalling nucleotide cyclic-di-GMP. Individual examples are discussed in detail to illustrate how the regulatory factors cooperate to allow tight control of expression of single operons. Molecular networks that allow coordinated expression between multiple fimbrial operons and with flagella in a single isolate are also presented. This chapter illustrates how adhesin expression is controlled, and the model systems also illustrate general regulatory principles germane to our overall understanding of bacterial gene regulation.