scholarly journals The role of transition metal transporters for iron, zinc, manganese, and copper in the pathogenesis of Yersinia pestis

Metallomics ◽  
2015 ◽  
Vol 7 (6) ◽  
pp. 965-978 ◽  
Author(s):  
Robert D. Perry ◽  
Alexander G. Bobrov ◽  
Jacqueline D. Fetherston
Keyword(s):  
Transition Metal ◽  
Yersinia Pestis ◽  
Causative Agent ◽  
Transport Systems ◽  
Metal Transporters ◽  
Pneumonic Plague ◽  
Transition Metal Transporters

Yersinia pestis, the causative agent of bubonic, septicemic and pneumonic plague, encodes a multitude of Fe transport systems.

scholarly journals Combinatorial Viral Vector-Based and Live Attenuated Vaccines without an Adjuvant to Generate Broader Immune Responses to Effectively Combat Pneumonic Plague

mBio ◽  
2021 ◽  
Author(s):  
Paul B. Kilgore ◽  
Jian Sha ◽  
Emily K. Hendrix ◽  
Vladimir L. Motin ◽  
Ashok K. Chopra
Keyword(s):  
Immune Responses ◽  
Yersinia Pestis ◽  
Causative Agent ◽  
Viral Vector ◽  
Human Pathogen ◽  
Pneumonic Plague ◽  
Content Type ◽  
Live Attenuated Vaccines ◽  
Tier 1

Yersinia pestis , the causative agent of plague, is a Tier-1 select agent and a reemerging human pathogen. A 2017 outbreak in Madagascar with >75% of cases being pneumonic and 8.6% causalities emphasized the importance of the disease.

scholarly journals Metal selectivity determinants in a family of transition metal transporters.

2018 ◽  
Vol 293 (1) ◽  
pp. 402-402
Author(s):  
Dorina Podar ◽  
Judith Scherer ◽  
Zeenat Noordally ◽  
Pawel Herzyk ◽  
Dietrich Nies ◽  
...  
Keyword(s):  
Transition Metal ◽  
Metal Transporters ◽  
Metal Selectivity ◽  
Transition Metal Transporters

scholarly journals A comprehensive study on the role of the Yersinia pestis virulence markers in an animal model of pneumonic plague

2011 ◽  
Vol 56 (2) ◽  
pp. 95-102 ◽  
Author(s):  
W. E. Kaman ◽  
S. Hawkey ◽  
D. van der Kleij ◽  
M. P. Broekhuijsen ◽  
N. J. Silman ◽  
...  
Keyword(s):  
Animal Model ◽  
Yersinia Pestis ◽  
Pneumonic Plague ◽  
Virulence Markers ◽  
Comprehensive Study

Transition metal transporters in rhizobia: tuning the inorganic micronutrient requirements to different living styles

Metallomics ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 735-755 ◽  
Author(s):  
Isidro Abreu ◽  
Paula Mihelj ◽  
Daniel Raimunda
Keyword(s):  
Transition Metal ◽  
Metal Transporters ◽  
Transition Metal Transporters

Transition metal transporters in rhizobia integrate the requirements of these micronutrients to the specific living styles.

scholarly journals Modification of the pulmonary MyD88 inflammatory response underlies the role of the Yersinia pestis pigmentation locus in primary pneumonic plague

2020 ◽  
Author(s):  
Rachel M. Olson ◽  
Miqdad O. Dhariwala ◽  
William J. Mitchell ◽  
Jerod A. Skyberg ◽  
Deborah M. Anderson
Keyword(s):  
Inflammatory Response ◽  
Yersinia Pestis ◽  
Lung Infection ◽  
Primary Response ◽  
Pneumonic Plague ◽  
Inflammatory Damage ◽  
Pulmonary Inflammatory Response ◽  
Short Time ◽  
Combined Data

Pneumonic plague, caused by Yersinia pestis, is a rapidly progressing bronchopneumonia involving focal bacterial growth, neutrophilic congestion, and alveolar necrosis. Within a short time after inhalation of Y. pestis, inflammatory cytokines are expressed via the Toll/IL1 adaptor myeloid differentiation primary response 88 (MyD88), which facilitates the primary lung infection. We previously showed that Y. pestis lacking the 102kb chromosomal pigmentation locus (pgm) are unable to cause inflammatory damage in the lungs, whereas the WT strain induces the toxic MyD88 pulmonary inflammatory response. In this work, we investigated the involvement of the pgm in skewing the inflammatory response during pneumonic plague. We show that the early MyD88-dependent and -independent cytokine responses to pgm- Y. pestis infection of the lungs are similar yet distinct from those that occur during pgm+ infection. Furthermore, we found that MyD88 was necessary to prevent growth of the iron-starved pgm- Y. pestis despite the presence of iron chelators lactoferrin and transferrin. However, while this induced neutrophil recruitment, there was no hyper-inflammatory response and pulmonary disease was mild without MyD88. In contrast, growth in blood and tissues progressed rapidly in the absence of MyD88, due to an almost total loss of serum IFNγ. We further show that the expression of MyD88 by myeloid cells is important to control bacteremia, but not the primary lung infection. The combined data indicate distinct roles for myeloid and non-myeloid MyD88, and suggest that expression of the pgm locus is necessary to skew the inflammatory response in the lungs to cause pneumonic plague.

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