CXCL10/IP-10 release is induced by incubation of whole blood from tuberculosis patients with ESAT-6, CFP10 and TB7.7

Rühwald, Morten; Bjerregaard-Andersen, Morten; Rabna, Paulo; Kofoed, Kristian; Eugen‐Olsen, Jesper; Ravn, Pernille

doi:10.1016/j.micinf.2007.02.021

Cited by 93 publications

(91 citation statements)

References 27 publications

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“…In addition, chemokines and their receptors, including IP-10, contribute to the formation and maintenance of granulomas in TB (33). IP-10 plays a role in M. tuberculosis infection, and several studies have shown that antigenstimulated IP-10 responses have a sensitivity similar to that of QFT-GIT for detecting active TB (12,13,34,35). Our results also showed a higher level of IP-10 in active TB patients, consistent with previously published studies; IP-10 can therefore serve as a potential diagnostic biomarker.…”

Section: Discussionsupporting

confidence: 91%

“…In addition to IFN-␥, many cytokines and chemokines have been investigated as potential biomarkers for M. tuberculosis infection and disease status (11)(12)(13)(14)(15)(16)(17)(18). The levels of several cytokines, including interleukin-6 (IL-6), IL-10, IL-15, chemokine (C-X-C) motif ligand (CXCL)/interferon gamma-inducible protein 10 (IP-10), and monocyte chemoattractant protein 2 (MCP-2), were significantly higher in TB patients than in healthy controls (7,11,(18)(19)(20)(21); although these finding suggest important roles for these factors in disease pathogenesis, they are not sufficient for diagnosing Citation Jeong YH, Hur Y-G, Lee H, Kim S, Cho J-E, Chang J, Shin SJ, Lee H, Kang YA, Cho S-N, Ha S-J.…”

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confidence: 99%

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Discrimination between Active and Latent Tuberculosis Based on Ratio of Antigen-Specific to Mitogen-Induced IP-10 Production

et al. 2015

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f Mycobacterium tuberculosis is the major causative agent of tuberculosis (TB). The gamma interferon (IFN-␥) release assay (IGRA) has been widely used to diagnose TB by testing cell-mediated immune responses but has no capacity for distinguishing between active TB and latent TB infection (LTBI). This study aims to identify a parameter that will help to discriminate active TB and LTBI. Whole-blood samples from 33 active TB patients, 20 individuals with LTBI, and 26 non-TB controls were applied to the commercial IFN-␥ release assay, QuantiFERON-TB Gold In-Tube, and plasma samples were analyzed for interleukin-2 (IL-2), IL-6, IL-8, IL-10, IL-13, tumor necrosis factor-alpha (TNF-␣), IFN-␥, monokine induced by IFN-␥ (MIG), interferon gamma inducible protein 10 (IP-10), interferon-inducible T cell alpha chemoattractant (I-TAC), and monocyte chemoattractant protein 1 (MCP-1) by using a commercial cytometric bead array. The Mycobacterium tuberculosis antigen-specific production of most of the assayed cytokines and chemokines was higher in the active TB than in the LTBI group. The mitogen-induced responses were lower in the active TB than in the LTBI group. When the ratio of TB-specific to mitogen-induced responses was calculated, IL-2, IL-6, IL-10, IL-13, TNF-␣, IFN-␥, MIG, and IP-10 were more useful in discriminating active TB from LTBI. In particular, most patients showed higher IP-10 production to Mycobacterium tuberculosis antigens than to mitogen at the individual level, and the ratio for IP-10 was the strongest indicator of active infection versus LTBI with 93.9% sensitivity and 90% specificity. In conclusion, the ratio of the TB-specific to the mitogen-induced IP-10 responses showed the most promising accuracy for discriminating active TB versus LTBI and should be further studied to determine whether it can serve as a biomarker that might help clinicians administer appropriate treatments. M ycobacterium tuberculosis, the major causative agent for tuberculosis (TB), is among the most successful human pathogens, infecting approximately 8.6 million people and leading to 1.3 million deaths each year (1). It is estimated that 2 billion people live with latent TB infection (LTBI) and are therefore a potential source of active TB (2, 3). Identifying LTBI is necessary in order to reduce the risk of development of the disease, while diagnosis of active TB can enable rapid treatment and disease control. To this end, diagnostic biomarkers that can accurately indicate disease status are needed (4, 5).There is presently no diagnostic gold standard for LTBI. Until recently, the tuberculin skin test (TST) involving the intracutaneous injection of purified protein derivative (PPD) into the forearm was the only available method for diagnosing LTBI. However, PPD cross-reacts with nontuberculous mycobacteria as well as with Mycobacterium bovis bacille Calmette-Guérin (BCG) vaccine and has poor sensitivity in immunocompromised patients (6). The interferon gamma (IFN-␥) release assay (IGRA) has been widely used in clinical practice a...

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Section: Discussionsupporting

confidence: 91%

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confidence: 99%

Discrimination between Active and Latent Tuberculosis Based on Ratio of Antigen-Specific to Mitogen-Induced IP-10 Production

et al. 2015

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“…In contrast, antigen-stimulated production of CCL5, IL-4, G-CSF, IFN-α, and CXCL10 were greatly decreased over the course of intensive-phase therapy. Antigen-stimulated CXCL10 responses have been reported to be more sensitive than IFN-γ for the diagnosis of active tuberculosis (28), and these data suggest that this panel of analytes may also hold promise as antigen-stimulated biomarkers of treatment response. Resolution of thrombocytosis is another well-recognized phenomenon associated with tuberculosis treatment (29), and network analysis revealed this to be linked to a decrease in circulating CCL5 and antigen-stimulated CCL5 and IL-4 among patients in our study.…”

Section: Discussionmentioning

confidence: 92%

Vitamin D accelerates resolution of inflammatory responses during tuberculosis treatment

Coussens

Wilkinson

Hanifa

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

275

204

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Calcidiol, the major circulating metabolite of vitamin D, supports induction of pleiotropic antimicrobial responses in vitro. Vitamin D supplementation elevates circulating calcidiol concentrations, and thus has a potential role in the prevention and treatment of infection. The immunomodulatory effects of administering vitamin D to humans with an infectious disease have not previously been reported. To characterize these effects, we conducted a detailed longitudinal study of circulating and antigen-stimulated immune responses in ninety-five patients receiving antimicrobial therapy for pulmonary tuberculosis who were randomized to receive adjunctive high-dose vitamin D or placebo in a clinical trial, and who fulfilled criteria for per-protocol analysis. Vitamin D supplementation accelerated sputum smear conversion and enhanced treatment-induced resolution of lymphopaenia, monocytosis, hypercytokinaemia, and hyperchemokinaemia. Administration of vitamin D also suppressed antigen-stimulated proinflammatory cytokine responses, but attenuated the suppressive effect of antimicrobial therapy on antigenstimulated secretion of IL-4, CC chemokine ligand 5, and IFN-α. We demonstrate a previously unappreciated role for vitamin D supplementation in accelerating resolution of inflammatory responses during tuberculosis treatment. Our findings suggest a potential role for adjunctive vitamin D supplementation in the treatment of pulmonary infections to accelerate resolution of inflammatory responses associated with increased risk of mortality.adjunctive therapy | immunomodulation | antimicrobial peptides | matrix metalloproteinases | steroid hormones

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“…New diagnostic approaches are needed that allow for a more targeted identification of patients at risk to develop TB. This may involve modifications of in vitro immunodiagnostic assays such as the use of novel stimulatory antigens [15,164,165], alternative biomarkers other than IFN-c [166][167][168][169][170][171][172], variations in incubation time [173,174], the readout system [9,12,13,175,176] or the clinical specimen instead of blood [177][178][179]. In addition, both for the detection of LTBI with a risk of reactivation and for suspected active TB, a novel approach based on a whole blood transcriptional signature could provide a biomarker system with high discriminative potential [180].…”

Section: Improvements In the Diagnosis Of Ltbi In Transplant Candidatmentioning

confidence: 99%

The risk of tuberculosis in transplant candidates and recipients: a TBNET consensus statement

Bumbăcea

Arend

Eyüboğlu³

et al. 2012

Eur Respir J

228

268

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Tuberculosis (TB) is a possible complication of solid organ and hematopoietic stem cell transplantation. The identification of candidates for preventive chemotherapy is an effective intervention to protect transplant recipients with latent infection with Mycobacterium tuberculosis from progressing to active disease. The best available proxy for diagnosing latent infection with M. tuberculosis is the identification of an adaptive immune response by the tuberculin skin test or an interferon-c based ex vivo assay. Risk assessment in transplant recipients for the development of TB depends on, among other factors, the locally expected underlying prevalence of infection with M. tuberculosis in the target population. In areas of high prevalence, preventive chemotherapy for all transplant recipients may be justified without immunodiagnostic testing while in areas of medium and low prevalence, preventive chemotherapy should only be offered to candidates with positive M. tuberculosis-specific immune responses. The diagnosis of TB in transplant recipients can be challenging. Treatment of TB is often difficult due to substantial interactions between anti-TB drugs and immunosuppressive medications. This management guideline summarises current knowledge on the prevention, diagnosis and treatment of TB related to solid organ and hematopoietic stem cell transplantation and provides an expert consensus on questions where scientific evidence is still lacking. KEYWORDS: Guideline, management, Mycobacterium tuberculosis, transplantation, tuberculosis T uberculosis (TB) is caused by the pathogenic species of the Mycobacterium tuberculosis complex. Only a minority of individuals who develop an adaptive immune response following infection with M. tuberculosis will ever develop TB, with the actual risk depending on the extent to which the host immune system provides a successful or inadequate response [1,2]. Therefore, individuals with impaired immune response, such as solid organ transplant (SOT) and hematopoietic stem cell transplant (HSCT) recipients, are more prone to develop TB than immunocompetent persons. TB in transplant recipients is more frequent compared to the general population (estimates from the last decades state 20-74 times as frequent in SOT [3,4] and twice as frequent in HSCT [5]), and more often fatal (up to 31% in SOT [6] and up to 50% in HSCT recipients [7]), thus adding effectiveness to interventions for its prevention, even in the face of difficulties, with treatment related to adverse drug events and drug-drug interactions. Active TB in transplant recipients can result from latent infection with M. tuberculosis (LTBI) in the transplant candidate or in the donor tissue, or from de novo post-transplant infection. These various scenarios prompt for targeted pre-transplant screening of both recipient and, if possible, donors to allow focused management of recipients selected for preventive intervention in the pre-and/or posttransplant period. The term ''preventive chemotherapy'' is used to denote treatmen...

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CXCL10/IP-10 release is induced by incubation of whole blood from tuberculosis patients with ESAT-6, CFP10 and TB7.7

Cited by 93 publications

References 27 publications

Discrimination between Active and Latent Tuberculosis Based on Ratio of Antigen-Specific to Mitogen-Induced IP-10 Production

Discrimination between Active and Latent Tuberculosis Based on Ratio of Antigen-Specific to Mitogen-Induced IP-10 Production

Vitamin D accelerates resolution of inflammatory responses during tuberculosis treatment

The risk of tuberculosis in transplant candidates and recipients: a TBNET consensus statement

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