The many faces of the YopM effector from plague causative bacterium Yersinia pestis and its implications for host immune modulation
V Soundararajan, N Patel, V Subramanian… - Innate …, 2011 - journals.sagepub.com
The Yersinia outer protein (Yop) M effector from the Yersinia pestis bacterium is well-known
for being a critical virulence determinant; however, structural insight vis-à-vis its role in Y …
for being a critical virulence determinant; however, structural insight vis-à-vis its role in Y …
Host Lipid Manipulation by Intracellular Bacteria: Moonlighting for Immune Evasion
N Challagundla, D Phadnis, A Gupta… - The Journal of …, 2023 - Springer
Lipids are complex organic molecules that fulfill energy demands and sometimes act as
signaling molecules. They are mostly found in membranes, thus playing an important role in …
signaling molecules. They are mostly found in membranes, thus playing an important role in …
Tetraacylated Lipopolysaccharide of Yersinia pestis Can Inhibit Multiple Toll-Like Receptor–Mediated Signaling Pathways in Human Dendritic Cells
MV Telepnev, GR Klimpel, J Haithcoat… - The Journal of …, 2009 - academic.oup.com
Background Yersinia pestis, the causative agent of plague, showed a temperature-
dependent change in lipid A composition, with a reduced degree of acylation when bacteria …
dependent change in lipid A composition, with a reduced degree of acylation when bacteria …
Enzymatic modification of lipid A by ArnT protects Bordetella bronchiseptica against cationic peptides and is required for transmission
Pathogen transmission cycles require many steps: initial colonization, growth and
persistence, shedding, and transmission to new hosts. Alterations in the membrane …
persistence, shedding, and transmission to new hosts. Alterations in the membrane …
Mutually constructive roles of Ail and LPS in Yersinia pestis serum survival
The outer membrane is a key virulence determinant of gram‐negative bacteria. In Yersinia
pestis, the deadly agent that causes plague, the protein Ail and lipopolysaccharide (LPS) 6 …
pestis, the deadly agent that causes plague, the protein Ail and lipopolysaccharide (LPS) 6 …
Substrates of the Plasminogen Activator Protease of Yersinia pestis
AJ Caulfield, WW Lathem - Advances in Yersinia Research, 2012 - Springer
The plasminogen activator protease (Pla) of Yersinia pestis is a critical virulence
determinant in the progression of both bubonic and pneumonic plague. A member of the …
determinant in the progression of both bubonic and pneumonic plague. A member of the …
Poly-N-Acetylglucosamine Expression by Wild-Type Yersinia pestis Is Maximal at Mammalian, Not Flea, Temperatures
P Yoong, C Cywes-Bentley, GB Pier - MBio, 2012 - Am Soc Microbiol
Numerous bacteria, including Yersinia pestis, express the poly-N-acetylglucosamine
(PNAG) surface carbohydrate, a major component of biofilms often associated with a specific …
(PNAG) surface carbohydrate, a major component of biofilms often associated with a specific …
Type 3 secretion system induced leukotriene B4 synthesis by leukocytes is actively inhibited by Yersinia pestis to evade early immune recognition
A Brady, KR Sheneman, AR Pulsifer, SL Price… - Plos …, 2024 - journals.plos.org
Subverting the host immune response to inhibit inflammation is a key virulence strategy of
Yersinia pestis. The inflammatory cascade is tightly controlled via the sequential action of …
Yersinia pestis. The inflammatory cascade is tightly controlled via the sequential action of …
Deletion of Braun lipoprotein gene (lpp) and curing of plasmid pPCP1 dramatically alter the virulence of Yersinia pestis CO92 in a mouse model of pneumonic …
SL Agar, J Sha, WB Baze, TE Erova… - …, 2009 - microbiologyresearch.org
Deletion of the murein (Braun) lipoprotein gene, lpp, attenuates the Yersinia pestis CO92
strain in mouse models of bubonic and pneumonic plague. In this report, we characterized …
strain in mouse models of bubonic and pneumonic plague. In this report, we characterized …
Lipid A 3′-O-deacylation by Salmonella outer membrane enzyme LpxR modulates the ability of lipid A to stimulate Toll-like receptor 4
K Kawasaki, M Teramoto, R Tatsui… - … and Biophysical Research …, 2012 - Elsevier
Modification of lipopolysaccharides, including the membrane anchor portion lipid A, is
essential for bacterial adaptation to its host. We examined whether lipid A 3′-O-deacylation …
essential for bacterial adaptation to its host. We examined whether lipid A 3′-O-deacylation …