2015
DOI: 10.7555/jbr.29.20150077
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Serum IL-1β and IL-18 correlate with ESR and CRP in multidrug-resistant tuberculosis patients

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Cited by 13 publications
(8 citation statements)
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“… 21 Here, in the vitreous of unique clinical patients, we show for the first time, to our knowledge, that there is an exacerbated inflammatory response of IL-10, IL-6, IL-8, IL-1β, and TNF-α in MDR-PA endophthalmitis compared with infection by S-PA, suggesting a possible relation between non-response to antibiotic treatment and inflammation-causing irreversible damage to the retina. 22 Our results are in concordance with findings in conditions such as MDR tuberculosis (MDR-TB), acute organ dysfunction, and bacteremia, in which IL-1β concentrations were found to be significantly higher in MDR-TB 23 and in MDR Escherichia coli and Klebsiella infections. 24 Additionally, Basingnaa et al 25 reported that the mean levels of IL-10 and TNF-α in MDR-TB cases were relatively higher compared with levels in drug-susceptible tuberculosis cases.…”
Section: Discussionsupporting
confidence: 89%
“… 21 Here, in the vitreous of unique clinical patients, we show for the first time, to our knowledge, that there is an exacerbated inflammatory response of IL-10, IL-6, IL-8, IL-1β, and TNF-α in MDR-PA endophthalmitis compared with infection by S-PA, suggesting a possible relation between non-response to antibiotic treatment and inflammation-causing irreversible damage to the retina. 22 Our results are in concordance with findings in conditions such as MDR tuberculosis (MDR-TB), acute organ dysfunction, and bacteremia, in which IL-1β concentrations were found to be significantly higher in MDR-TB 23 and in MDR Escherichia coli and Klebsiella infections. 24 Additionally, Basingnaa et al 25 reported that the mean levels of IL-10 and TNF-α in MDR-TB cases were relatively higher compared with levels in drug-susceptible tuberculosis cases.…”
Section: Discussionsupporting
confidence: 89%
“…However, while prior in vitro and mouse models have shown induction of IL-1β results in control of Mtb replication [ 6 , 26 ], we found TCA cycle remodeling and induction of IL-1β produced a distinctly proinflammatory phenotype in humans that was associated with increased bacterial burden and prolonged time to sputum culture conversion. Our findings are supported by independent human studies, which have consistently show elevated plasma concentrations of IL-1β in persons with pulmonary TB are correlated with markers of inflammation [ 28 ] and associated with greater extent of disease and cavitation on chest radiograph [ 19 , 29 ]. A possible explanation for these apparently discordant findings is that immunometabolic remodeling of macrophages evolves following infection with Mtb [ 30 ].…”
Section: Discussionsupporting
confidence: 86%
“…The observation that dysregulated IL-1β signaling occurs disproportionately in persons with MDR-TB has been reported previously [ 28 ], and inhaled IFN-α, which suppresses IL-1β production in pulmonary TB disease [ 34 ] has been studied as a potential treatment for refractory MDR-TB [ 35 ]. We hypothesize that the immunometabolic remodeling in the MDR-TB group in the present study was caused primarily by propagation of inflammatory signaling cascades resulting from prior, inadequate MDR-TB treatment.…”
Section: Discussionmentioning
confidence: 95%
“…However, a study demonstrated that activation of the TLR2/ NLRP3/IL-18 axis can protect against asthma [3], complicating the role of IL-18 in asthma. As IL-18 carries out its biological functions mainly through its receptor IL-18R [24], and IL-18BP is a potent endogenous neutralizing antagonist of IL-18, it is very likely that the role of IL-18 in atopic asthma is decided by the balance between IL-18, IL-18BP and IL-18R. We therefore examined expression of IL-18, IL-18BP and IL-18R in parallel in inflammatory cells of asthma.…”
Section: Discussionmentioning
confidence: 99%