title: Yersinia pestis activates both IL-1β and IL-1 receptor antagonist to modulate lung inflammation during pneumonic plague.
abstract: Pneumonic plague is the most rapid and lethal form of Yersinia pestis infection. Increasing evidence suggests that Y. pestis employs multiple levels of innate immune evasion and/or suppression to produce an early "pre-inflammatory" phase of pulmonary infection, after which the disease is highly inflammatory in the lung and 100% fatal. In this study, we show that IL-1β/IL-18 cytokine activation occurs early after bacteria enter the lung, and this activation eventually contributes to pulmonary inflammation and pathology during the later stages of infection. However, the inflammatory effects of IL-1β/IL-1-receptor ligation are not observed during this first stage of pneumonic plague. We show that Y. pestis also activates the induction of IL-1 receptor antagonist (IL-1RA), and this activation likely contributes to the ability of Y. pestis to establish the initial pre-inflammatory phase of disease.
authors.affiliation: Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America; Department of Biology, North Carolina Central University, Durham, North Carolina, United States of America.
authors.forename: Vijay
authors.initials: V
authors.lastname: Sivaraman
authors.affiliation: Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
authors.forename: Roger D
authors.initials: RD
authors.lastname: Pechous
authors.affiliation: Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
authors.forename: Nikolas M
authors.initials: NM
authors.lastname: Stasulli
authors.forename: Kara R
authors.initials: KR
authors.lastname: Eichelberger
authors.affiliation: Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
authors.forename: Edward A
authors.initials: EA
authors.lastname: Miao
authors.affiliation: Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
authors.forename: William E
authors.initials: WE
authors.lastname: Goldman
mesh_terms: D000818:Animals; D006801:Humans; D053583:Interleukin-1beta / Q000378:metabolism*; D051379:Mice; D010930:Plague / Q000276:immunology*; D011014:Pneumonia / Q000382:microbiology* / Q000473:pathology; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors / Q000276:immunology* / Q000378:metabolism*; D015010:Yersinia pestis / Q000276:immunology*
chemical_list: D053583:Interleukin-1beta; D017472:Receptors, Interleukin-1