Pechous, Roger

Associate Professor

B.S. Biology University of Illinois at Urbana/Champaign
M.S. Biological Sciences Illinois State University
Ph.D Microbiology and Molecular Genetics Medical College of Wisconsin
Postdoc Dept. of Microbiology and Immunology, UNC at Chapel Hill

Phone:  252-744-2752
Fax:  252-744-3104
Email:  pechousr24@ecu.edu

 

Research

Our lab uses the bacterium Yersinia pestis, the causative agent of plague, to understand how bacteria overcome host innate immune responses to cause severe and lethal pneumonia. Y. pestis is responsible for at least 3 major pandemics in recorded history, including the Black Death of the Middle Ages. Pulmonary infection with Y. pestis results in primary pneumonic plague, a rapidly progressing necrotic pneumonia that is 100 % fatal if left untreated.

The progression of pneumonic plague is biphasic, with an early pre-inflammatory and a later pro-inflammatory disease phase. Early after infection Y. pestis evades and suppresses host immune responses and replicates to high numbers in the lung in the absence of disease symptoms or signs of inflammation.  This is followed by the abrupt shift to a pro-inflammatory state that sees the emergence of symptoms accompany massive neutrophil infiltration into the lung, the onset of a pro-inflammatory cytokine storm, and significant host-driven pulmonary damage that ultimately proves lethal.

We seek to identify bacterial factors that aid in establishing infection in the lung and limit host responsiveness. Further, we hope to define bacterial and host mediators that drive progression into a lethal pro-inflammatory stage in the lung. We use bacterial genetics coupled with cell culture, human ex vivo cell and tissue infection platforms, and a powerful mouse model of infection to characterize Y. pestis pathogenesis. Characterizing Y. pestis virulence factors and defining host innate immune pathways that are both suppressed and activated during pulmonary infection will help to understand why pneumonic plague is so lethal, and will inform treatment options for severe and lethal pneumonia caused by Y. pestis and other significant respiratory pathogens.

Select Publications

Yersinia pestis and pneumonic plague: Insight into how a lethal pathogen interfaces with innate immune populations in the lung to cause severe disease. Venugopal G, Pechous RD.Cell Immunol. 2024 Jul 10;403-404:104856. doi: 10.1016/j.cellimm.2024.104856. Online ahead of print.PMID: 39002222

An ex vivo human precision-cut lung slice platform provides insight into SARS-CoV-2 pathogenesis and antiviral drug efficacy. Pechous RD, Malaviarachchi PA, Banerjee SK, Byrum SD, Alkam DH, Ghaffarieh A, Kurten RC, Kennedy JL, Zhang X.J Virol. 2024 Jul 23;98(7):e0079424. doi: 10.1128/jvi.00794-24. Epub 2024 Jun 28.PMID: 38940558

Pulmonary Expression of Interleukin-17 Contributes to Neutrophil Infiltration into the Lungs during Pneumonic Plague. Theriot HM, Malaviarachchi PA, Scott MG, Appell KT, Banerjee SK, Pechous RD.Infect Immun. 2023 Jul 18;91(7):e0013123. doi: 10.1128/iai.00131-23. Epub 2023 Jun 20.PMID: 37338372

Treatment with Fluticasone Propionate Increases Antibiotic Efficacy during Treatment of Late-Stage Primary Pneumonic Plague. Crane SD, Banerjee SK, Pechous RD.Antimicrob Agents Chemother. 2022 Jan 18;66(1):e0127521. doi: 10.1128/AAC.01275-21. Epub 2021 Nov 15.PMID: 34780267

The Yersinia pestis GTPase BipA Promotes Pathogenesis of Primary Pneumonic Plague. Crane SD, Banerjee SK, Eichelberger KR, Kurten RC, Goldman WE, Pechous RD.Infect Immun. 2021 Jan 19;89(2):e00673-20. doi: 10.1128/IAI.00673-20. Print 2021 Jan 19.PMID: 33257531

A Dual Role for the Plasminogen Activator Protease During the Preinflammatory Phase of Primary Pneumonic Plague. Banerjee SK, Crane SD, Pechous RD.J Infect Dis. 2020 Jul 6;222(3):407-416. doi: 10.1093/infdis/jiaa094.PMID: 32128567

Intranasal Inoculation of Mice with Yersinia pestis and Processing of Pulmonary Tissue for Analysis. Pechous RD.Methods Mol Biol. 2019;2010:17-28. doi: 10.1007/978-1-4939-9541-7_2.PMID: 31177428

Modeling Pneumonic Plague in Human Precision-Cut Lung Slices Highlights a Role for the Plasminogen Activator Protease in Facilitating Type 3 Secretion. Banerjee SK, Huckuntod SD, Mills SD, Kurten RC, Pechous RD.Infect Immun. 2019 Jul 23;87(8):e00175-19. doi: 10.1128/IAI.00175-19. Print 2019 Aug.PMID: 31085709

With Friends Like These: The Complex Role of Neutrophils in the Progression of Severe Pneumonia. Pechous RD.Front Cell Infect Microbiol. 2017 May 1;7:160. doi: 10.3389/fcimb.2017.00160. eCollection 2017.PMID: 28507954

Pneumonic Plague: The Darker Side of Yersinia pestis. Pechous RD, Sivaraman V, Stasulli NM, Goldman WE.Trends Microbiol. 2016 Mar;24(3):190-197. doi: 10.1016/j.tim.2015.11.008. Epub 2015 Dec 14.PMID: 26698952

Spatially distinct neutrophil responses within the inflammatory lesions of pneumonic plague. Stasulli NM, Eichelberger KR, Price PA, Pechous RD, Montgomery SA, Parker JS, Goldman WE.mBio. 2015 Oct 13;6(5):e01530-15. doi: 10.1128/mBio.01530-15.PMID: 26463167

Illuminating Targets of Bacterial Secretion. Pechous RD, Goldman WE.PLoS Pathog. 2015 Aug 6;11(8):e1004981. doi: 10.1371/journal.ppat.1004981. eCollection 2015 Aug.PMID: 26247771

Yersinia pestis activates both IL-1β and IL-1 receptor antagonist to modulate lung inflammation during pneumonic plague. Sivaraman V, Pechous RD, Stasulli NM, Eichelberger KR, Miao EA, Goldman WE.PLoS Pathog. 2015 Mar 17;11(3):e1004688. doi: 10.1371/journal.ppat.1004688. eCollection 2015 Mar.PMID: 25781467

In vivo transcriptional profiling of Yersinia pestis reveals a novel bacterial mediator of pulmonary inflammation. Pechous RD, Broberg CA, Stasulli NM, Miller VL, Goldman WE.mBio. 2015 Feb 17;6(1):e02302-14. doi: 10.1128/mBio.02302-14.PMID: 25691593

Early host cell targets of Yersinia pestis during primary pneumonic plague. Pechous RD, Sivaraman V, Price PA, Stasulli NM, Goldman WE.PLoS Pathog. 2013;9(10):e1003679. doi: 10.1371/journal.ppat.1003679. Epub 2013 Oct 3.PMID: 24098126

My bibliography

https://www.ncbi.nlm.nih.gov/myncbi/10WrsmkfN5K/bibliography/public/