FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2346706608> ?p ?o ?g. }

• W2346706608 endingPage "9905" @default.
• W2346706608 startingPage "9894" @default.
• W2346706608 abstract "Innate immunity plays a central role in resolving infections by pathogens. Host survival during plague, caused by the Gram-negative bacterium Yersinia pestis, is favored by a robust early innate immune response initiated by IL-1β and IL-18. These cytokines are produced by a two-step mechanism involving NF-κB-mediated pro-cytokine production and inflammasome-driven maturation into bioactive inflammatory mediators. Because of the anti-microbial effects induced by IL-1β/IL-18, it may be desirable for pathogens to manipulate their production. Y. pestis type III secretion system effectors YopJ and YopM can interfere with different parts of this process. Both effectors have been reported to influence inflammasome caspase-1 activity; YopJ promotes caspase-8-dependent cell death and caspase-1 cleavage, whereas YopM inhibits caspase-1 activity via an incompletely understood mechanism. However, neither effector appears essential for full virulence in vivo. Here we report that the sum of influences by YopJ and YopM on IL-1β/IL-18 release is suppressive. In the absence of YopM, YopJ minimally affects caspase-1 cleavage but suppresses IL-1β, IL-18, and other cytokines and chemokines. Importantly, we find that Y. pestis containing combined deletions of YopJ and YopM induces elevated levels of IL-1β/IL-18 in vitro and in vivo and is significantly attenuated in a mouse model of bubonic plague. The reduced virulence of the YopJ-YopM mutant is dependent on the presence of IL-1β, IL-18, and caspase-1. Thus, we conclude that Y. pestis YopJ and YopM can both exert a tight control of host IL-1β/IL-18 production to benefit the bacteria, resulting in a redundant impact on virulence. Innate immunity plays a central role in resolving infections by pathogens. Host survival during plague, caused by the Gram-negative bacterium Yersinia pestis, is favored by a robust early innate immune response initiated by IL-1β and IL-18. These cytokines are produced by a two-step mechanism involving NF-κB-mediated pro-cytokine production and inflammasome-driven maturation into bioactive inflammatory mediators. Because of the anti-microbial effects induced by IL-1β/IL-18, it may be desirable for pathogens to manipulate their production. Y. pestis type III secretion system effectors YopJ and YopM can interfere with different parts of this process. Both effectors have been reported to influence inflammasome caspase-1 activity; YopJ promotes caspase-8-dependent cell death and caspase-1 cleavage, whereas YopM inhibits caspase-1 activity via an incompletely understood mechanism. However, neither effector appears essential for full virulence in vivo. Here we report that the sum of influences by YopJ and YopM on IL-1β/IL-18 release is suppressive. In the absence of YopM, YopJ minimally affects caspase-1 cleavage but suppresses IL-1β, IL-18, and other cytokines and chemokines. Importantly, we find that Y. pestis containing combined deletions of YopJ and YopM induces elevated levels of IL-1β/IL-18 in vitro and in vivo and is significantly attenuated in a mouse model of bubonic plague. The reduced virulence of the YopJ-YopM mutant is dependent on the presence of IL-1β, IL-18, and caspase-1. Thus, we conclude that Y. pestis YopJ and YopM can both exert a tight control of host IL-1β/IL-18 production to benefit the bacteria, resulting in a redundant impact on virulence. Manipulation of interleukin-1β and interleukin-18 production by Yersinia pestis effectors YopJ and YopM and redundant impact on virulence.Journal of Biological ChemistryVol. 291Issue 31PreviewVOLUME 291 (2016) PAGES 9894–9905 Full-Text PDF Open Access" @default.
• W2346706608 created "2016-06-24" @default.
• W2346706608 creator A5011977345 @default.
• W2346706608 creator A5034107890 @default.
• W2346706608 creator A5057997189 @default.
• W2346706608 creator A5066698549 @default.
• W2346706608 creator A5077091911 @default.
• W2346706608 creator A5082765204 @default.
• W2346706608 creator A5087535749 @default.
• W2346706608 date "2016-05-01" @default.
• W2346706608 modified "2023-10-11" @default.
• W2346706608 title "Manipulation of Interleukin-1β and Interleukin-18 Production by Yersinia pestis Effectors YopJ and YopM and Redundant Impact on Virulence" @default.
• W2346706608 cites W1864325817 @default.
• W2346706608 cites W1882905539 @default.
• W2346706608 cites W1967725137 @default.
• W2346706608 cites W1968946043 @default.
• W2346706608 cites W1971915082 @default.
• W2346706608 cites W1972169896 @default.
• W2346706608 cites W1976143672 @default.
• W2346706608 cites W1987645931 @default.
• W2346706608 cites W1995781465 @default.
• W2346706608 cites W1998591058 @default.
• W2346706608 cites W2001366460 @default.
• W2346706608 cites W2009423065 @default.
• W2346706608 cites W2014477644 @default.
• W2346706608 cites W2014748534 @default.
• W2346706608 cites W2023221600 @default.
• W2346706608 cites W2024293665 @default.
• W2346706608 cites W2024591203 @default.
• W2346706608 cites W2028145763 @default.
• W2346706608 cites W2032897380 @default.
• W2346706608 cites W2034561711 @default.
• W2346706608 cites W2049930535 @default.
• W2346706608 cites W2052164279 @default.
• W2346706608 cites W2055408817 @default.
• W2346706608 cites W2060782009 @default.
• W2346706608 cites W2067910103 @default.
• W2346706608 cites W2073678899 @default.
• W2346706608 cites W2076286334 @default.
• W2346706608 cites W2080827095 @default.
• W2346706608 cites W2084244470 @default.
• W2346706608 cites W2085414634 @default.
• W2346706608 cites W2089003246 @default.
• W2346706608 cites W2093688663 @default.
• W2346706608 cites W2093815300 @default.
• W2346706608 cites W2095645811 @default.
• W2346706608 cites W2097298997 @default.
• W2346706608 cites W2101472578 @default.
• W2346706608 cites W2105425697 @default.
• W2346706608 cites W2107849257 @default.
• W2346706608 cites W2110324427 @default.
• W2346706608 cites W2115792196 @default.
• W2346706608 cites W2123769162 @default.
• W2346706608 cites W2132225065 @default.
• W2346706608 cites W2132868108 @default.
• W2346706608 cites W2137211177 @default.
• W2346706608 cites W2137270024 @default.
• W2346706608 cites W2145638464 @default.
• W2346706608 cites W2145912774 @default.
• W2346706608 cites W2146045163 @default.
• W2346706608 cites W2146258738 @default.
• W2346706608 cites W2146888187 @default.
• W2346706608 cites W2148581259 @default.
• W2346706608 cites W2149231090 @default.
• W2346706608 cites W2155184228 @default.
• W2346706608 cites W2165832942 @default.
• W2346706608 cites W2167092302 @default.
• W2346706608 cites W2171511755 @default.
• W2346706608 cites W2172282307 @default.
• W2346706608 cites W2194029163 @default.
• W2346706608 cites W2209731801 @default.
• W2346706608 cites W2210680772 @default.
• W2346706608 doi "https://doi.org/10.1074/jbc.m115.697698" @default.
• W2346706608 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4965588" @default.
• W2346706608 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27474778" @default.
• W2346706608 hasPublicationYear "2016" @default.
• W2346706608 type Work @default.
• W2346706608 sameAs 2346706608 @default.
• W2346706608 citedByCount "27" @default.
• W2346706608 countsByYear W23467066082016 @default.
• W2346706608 countsByYear W23467066082017 @default.
• W2346706608 countsByYear W23467066082018 @default.
• W2346706608 countsByYear W23467066082019 @default.
• W2346706608 countsByYear W23467066082020 @default.
• W2346706608 countsByYear W23467066082021 @default.
• W2346706608 countsByYear W23467066082022 @default.
• W2346706608 countsByYear W23467066082023 @default.
• W2346706608 crossrefType "journal-article" @default.
• W2346706608 hasAuthorship W2346706608A5011977345 @default.
• W2346706608 hasAuthorship W2346706608A5034107890 @default.
• W2346706608 hasAuthorship W2346706608A5057997189 @default.
• W2346706608 hasAuthorship W2346706608A5066698549 @default.
• W2346706608 hasAuthorship W2346706608A5077091911 @default.
• W2346706608 hasAuthorship W2346706608A5082765204 @default.
• W2346706608 hasAuthorship W2346706608A5087535749 @default.
• W2346706608 hasBestOaLocation W23467066081 @default.
• W2346706608 hasConcept C104317684 @default.
• W2346706608 hasConcept C130211564 @default.

• next