Effect of type 1 piliation on in vitro killing of Escherichia coli by mouse peritoneal macrophages

Abstract

Escherichia coli K-12 mutants possessing defined lesions affecting type 1 pilus production, receptor binding, or length were examined for their ability to resist killing by mouse peritoneal macrophages in vitro. Mutants were mixed pairwise at known ratios in wells containing macrophages, and after incubation, the ratio of the survivors was assayed. The difference in phagocytic killing between type 1 piliated cells and isogenic nonpiliated cells was significant, the piliated cells being approximately threefold more resistant. Pilus length had little effect upon survival, as the long-piliated mutants were no more resistant to killing than the normal-length parents. Interestingly, the receptor-binding function of type 1 pili was mostimportant-in effecting resistance, as mutants lacking the ability to bind receptor were killed as effectively as nonpiliated mutants. These data are consistent with the notion that pili actually-impede killing by macrophages rather than serve as passive physical barriers to uptake.

Non-lethal exposure to H2O2 boosts bacterial survival and evolvability against oxidative stress

“…Following the inversion of the phase switch to 'on state' of fimbriae production by environmental signals, this element can remain phase-locked in the 'on orientation' due to integration of insertion sequence elements at various positions the fimE gene [38]. Interestingly, fim operon expression allows E. coli to attach to abiotic surfaces, host tissues and to survive better inside macrophages protecting against the presence of extracellular antibacterials [39,40]. Reactive oxygen species (ROS) are critical components of the antimicrobial repertoire of macrophages to kill bacteria [41].…”

Purification and Characterization of Type 1 Fimbriae of Salmonella typhi

“…Their presence is usually detected by electron microscopy and by assaying the ability of bacteria to cause a mannose-inhibitable (MI) agglu tination of some species of erythrocytes or of yeast cells (17,25). The binding properties of type 1 fimbriae contribute to bacterial colonization of some host mucosal surfaces and are important for enterobacterial communicability (2,6,20,(24)(25)(26), and some evidence has also been produced pointing to a role of type 1 fimbriae as determinants of microbial pathogenicity (1,9,12,26,30,32).…”

F1651fimbriae of the P fimbrial family inhibit the oxidative response of porcine neutrophils

“…Similarly, non‐fimbrial adhesins (NFA) of uropathogenic E. coli induce adherence to hPMNLs resulting in an oxidative response and phagocytic killing of bacteria [11]. Nevertheless, interaction of F1‐positive bacteria with phagocytes may result in bacterial resistance to macrophage bactericidal activity, although the mechanism for this resistance is not well defined [7].…”

“…Wild‐type E. coli strain 5131 was isolated from the intestinal contents of a diarrheic and septicemic piglet at the Faculté de Médecine Vétérinaire, Université de Montréal, Saint‐Hyacinthe, Que., Canada. This strain is serum‐resistant, induces septicemia in experimentally inoculated piglets, and is resistant to phagocytic killing by pPMNLs [2–16]. Strain HB101 (pCJ7) is a transformant from plasmid pACYC184 in which was inserted a 10‐kb fragment of DNA (from an F165 1 ‐positive wild‐type septicemia‐inducing E. coli strain 4787) into the Bam HI site [15].…”

“…However, lectinophagocytosis induced by mannose‐sensitive (MS) F1 fimbriae may not always lead to killing of bacteria. Some reports [7] indicate that these fimbriae may induce resistance of bacteria to phagocytosis whereas others indicate the contrary [8,9]. Furthermore, it has been reported that F1 fimbriae may stimulate the human polymorphonuclear leukocyte (hPMNL) oxidative response both in the absence and presence of opsonins [10].…”