scholarly journals Multiple phase-variable mechanisms, including capsular polysaccharides, modify bacteriophage susceptibility in Bacteroides thetaiotaomicron

2019 ◽  
Author(s):  
Nathan T. Porter ◽  
Andrew J. Hryckowian ◽  
Bryan D. Merrill ◽  
Jaime J. Fuentes ◽  
Jackson O. Gardner ◽  
...  

AbstractA variety of cell surface structures, including capsular polysaccharides (CPS), dictate interactions between bacteria and their environment including their viruses (bacteriophages). Members of the prominent human gut Bacteroidetes characteristically produce several phase-variable CPS, but their contributions to bacteriophage interactions are unknown. We used engineered strains of the human symbiont Bacteroides thetaiotaomicron, which differ only in the CPS they express, to isolate bacteriophages from two locations in the United States. Testing each of 71 bacteriophages against a panel of strains that express wild-type phase-variable CPS, one of eight different single CPS, or no CPS at all, revealed that each phage infects only a subset of otherwise isogenic strains. Deletion of infection-permissive CPS from B. thetaiotaomicron was sufficient to abolish infection for several individual bacteriophages, while infection of wild-type B. thetaiotaomicron with either of two different bacteriophages rapidly selected for expression of non-permissive CPS. Surprisingly, acapsular B. thetaiotaomicron also escapes complete killing by these bacteriophages, but surviving bacteria exhibit increased expression of 8 distinct phase-variable lipoproteins. When constitutively expressed, one of these lipoproteins promotes resistance to multiple bacteriophages. Finally, both wild-type and acapsular B. thetaiotaomicron were able to separately co-exist with one bacteriophage for over two months in the mouse gut, suggesting that phase-variation promotes resistance but also generates sufficient numbers of susceptible revertants to allow bacteriophage persistence. Our results reveal important roles for Bacteroides CPS and other cell surface structures that allow these bacteria to persist despite bacteriophage predation and hold important implications for using bacteriophages therapeutically to target gut symbionts.


2012 ◽  
Vol 78 (16) ◽  
pp. 5882-5889 ◽  
Author(s):  
Suengwook Seo ◽  
Karl R. Matthews

ABSTRACTConsumption of fresh and fresh-cut fruits and vegetables contaminated withEscherichia coliO157:H7 has resulted in hundreds of cases of illness and, in some instances, death. In this study, the influence of cell surface structures ofE. coliO157:H7, such as flagella, curli fimbriae, lipopolysaccharides, or exopolysaccharides, on plant defense responses and on survival or colonization on the plant was investigated. The population of theE. coliO157:H7 ATCC 43895 wild-type strain was significantly lower on wild-typeArabidopsisplants than that of the 43895 flagellum-deficient mutant. The population of theE. coliO157:H7 43895 flagellum mutant was greater on both wild-type andnpr1-1mutant (nonexpressor of pathogenesis-related [PR] genes) plants and resulted in less PR gene induction, estimated based on a weak β-glucuronidase (GUS) signal, than did the 43895 wild-type strain. These results suggest that the flagella, among the other pathogen-associated molecular patterns (PAMPs), made a substantial contribution to the induction of plant defense response and contributed to the decreased numbers of theE. coliO157:H7 ATCC 43895 wild-type strain on the wild-typeArabidopsisplant. A curli-deficientE. coliO157:H7 86-24 strain survived better on wild-typeArabidopsisplants than the curli-producing wild-type 86-24 strain did. The curli-deficientE. coliO157:H7 86-24 strain exhibited a GUS signal at a level substantially lower than that of the curli-producing wild-type strain. Curli were recognized by plant defense systems, consequently affecting bacterial survival. The cell surface structures ofE. coliO157:H7 have a significant impact on the induction of differential plant defense responses, thereby impacting persistence or survival of the pathogen on plants.



1993 ◽  
Vol 8 (3) ◽  
pp. 151-154 ◽  
Author(s):  
A. Anichini ◽  
R. Mortarini ◽  
G. Parmiani

A number of different cytokines, including IL-1α. and ß, IL-2, IL-3, IL-4, IL-6, IL-7, IL-8, IFN-α, -ß and γ, TNF-α -ß, and TGF-ß1, can modulate the expression of distinct cell surface antigens of normal and neoplastic cells. Both induction/increase of expression and reduction of expression can be achieved depending on the antigen and on the cytokine. Antigens subjected to the modulating activity of cytokines include distinct families of cell surface structures such as the molecules coded by the major histocompatibility complex (MHC), the superfamily of adhesion receptors that regulate cell-cell and cell-matrix interaction, receptors for cytokines and growth factors and tumor-associated antigens. The modulating activity of cytokines is a consequence of their influence on gene expression, protein synthesis, membrane expression and shedding of antigens from the cell surface. The changes of phenotype due to the action of cytokines can influence the signalling pathways dependent on the expression and function of cell surf ace structures. Therefore, the antigen modulating activity of cytokines can thoroughly affect the biological behavior of normal and neoplastic cells. As described here, most of the modulating effects of cytokines on different cell surface structures and the functional consequences of antigenic modulation can be verified in human malignant melanoma cells.



1988 ◽  
Vol 18 (5) ◽  
pp. 767-772 ◽  
Author(s):  
Thomas Miethke ◽  
Ruth Schmidberger ◽  
Klaus Heeg ◽  
Steven Gillis ◽  
Hermann Wagner


2018 ◽  
Vol 115 (40) ◽  
pp. 10106-10111 ◽  
Author(s):  
Emily C. Hollenbeck ◽  
Alexandra Antonoplis ◽  
Chew Chai ◽  
Wiriya Thongsomboon ◽  
Gerald G. Fuller ◽  
...  

UropathogenicEscherichia coli(UPEC) are the major causative agents of urinary tract infections, employing numerous molecular strategies to contribute to adhesion, colonization, and persistence in the bladder niche. Identifying strategies to prevent adhesion and colonization is a promising approach to inhibit bacterial pathogenesis and to help preserve the efficacy of available antibiotics. This approach requires an improved understanding of the molecular determinants of adhesion to the bladder urothelium. We designed experiments using a custom-built live cell monolayer rheometer (LCMR) to quantitatively measure individual and combined contributions of bacterial cell surface structures [type 1 pili, curli, and phosphoethanolamine (pEtN) cellulose] to bladder cell adhesion. Using the UPEC strain UTI89, isogenic mutants, and controlled conditions for the differential production of cell surface structures, we discovered that curli can promote stronger adhesive interactions with bladder cells than type 1 pili. Moreover, the coproduction of curli and pEtN cellulose enhanced adhesion. The LCMR enables the evaluation of adhesion under high-shear conditions to reveal this role for pEtN cellulose which escaped detection using conventional tissue culture adhesion assays. Together with complementary biochemical experiments, the results support a model wherein cellulose serves a mortar-like function to promote curli association with and around the bacterial cell surface, resulting in increased bacterial adhesion strength at the bladder cell surface.



2020 ◽  
Vol 21 (23) ◽  
pp. 9092
Author(s):  
Waheed Ur Rahman ◽  
Adriana Osickova ◽  
Nela Klimova ◽  
Jinery Lora ◽  
Nataliya Balashova ◽  
...  

The Gram-negative coccobacillus Kingella kingae is increasingly recognized as an important invasive pediatric pathogen that causes mostly bacteremia and skeletal system infections. K. kingae secretes an RtxA toxin that belongs to a broad family of the RTX (Repeats in ToXin) cytotoxins produced by bacterial pathogens. Recently, we demonstrated that membrane cholesterol facilitates interaction of RtxA with target cells, but other cell surface structures potentially involved in toxin binding to cells remain unknown. We show that deglycosylation of cell surface structures by glycosidase treatment, or inhibition of protein N- and O-glycosylation by chemical inhibitors substantially reduces RtxA binding to target cells. Consequently, the deglycosylated cells were more resistant to cytotoxic activity of RtxA. Moreover, experiments on cells expressing or lacking cell surface integrins of the β2 family revealed that, unlike some other cytotoxins of the RTX family, K. kingae RtxA does not bind target cells via the β2 integrins. Our results, hence, show that RtxA binds cell surface oligosaccharides present on all mammalian cells but not the leukocyte-restricted β2 integrins. This explains the previously observed interaction of the toxin with a broad range of cell types of various mammalian species and reveals that RtxA belongs to the group of broadly cytolytic RTX hemolysins.



1987 ◽  
Vol 169 (8) ◽  
pp. 3792-3800 ◽  
Author(s):  
R Lamed ◽  
J Naimark ◽  
E Morgenstern ◽  
E A Bayer


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