Elevated Levels of Serum Macrophage Migration Inhibitory Factor in Patients with Pulmonary Tuberculosis

Yamada, Gen; Shijubo, Noriharu; Takagi-Takahashi, Yoko; Nishihira, Jun; Mizue, Yuka; Kikuchi, Kokichi; Abe, Shosaku

doi:10.1006/clim.2002.5255

Cited by 32 publications

(24 citation statements)

References 24 publications

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“…Although this model has been crucial in elucidating the role of other cytokines in the innate immune response against M. tuberculosis (12), it would be of value to confirm the effect of MIF in another important in vitro model of innate immune response, such as the one that uses the cocultures of both lymphocytes and monocytes (30). However, the in vivo observations that MIF acts as an immune effector in the early stages of pulmonary granulomas in mice (19,21), and the recently reported findings of high levels of MIF in serum in patients with pulmonary tuberculosis (32), substantially support the concept that MIF is involved in host defense mechanisms against M. tuberculosis.…”

mentioning

confidence: 72%

Macrophage Migration Inhibitory Factor Reduces the Growth of VirulentMycobacterium tuberculosisin Human Macrophages

Oddo¹,

Calandra²,

Bucala

et al. 2005

Infect Immun

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Macrophage migration inhibitory factor (MIF) is a key mediator of the innate immune system and plays a crucial role in the host response to bacterial infections. Its role in immunity to intracellular pathogens has not been well studied. Here, we show that MIF released by infected human macrophages inhibits the growth of virulent Mycobacterium tuberculosis.Macrophages (M) are involved in the innate immune response to Mycobacterium tuberculosis (16). The ability of the host response to increase the mycobactericidal activity of M is important for the development of an early effective response and for the containment of M. tuberculosis infection. The infection of M with M. tuberculosis induces the release of early proinflammatory cytokines, like tumor necrosis factor alpha (TNF-␣) and interleukin-1␤ (24). However, at least in humans, the exact mechanisms by which cytokines act to contain mycobacterial growth remain unclear (17). Macrophage migration inhibitory factor (MIF) was first discovered as a proinflammatory T-cell cytokine (5, 14) but was then shown to be released in substantial quantities by M as well (8). MIF has recently emerged as a key effector molecule of the innate immune responses against bacteria (3,7,9,10,22,25,26) as well as intracellular pathogens (2,18,20,29). In the present study, we provide evidence for an important role for MIF in the innate immune response against M. tuberculosis. MIF is released by human M after incubation with M. tuberculosis antigens or infection with virulent M. tuberculosis. MIF induction by M was determined in parallel experiments by incubating cells with immunogenic M. tuberculosis antigens or with a virulent M. tuberculosis strain (H37Rv).Human M were derived from blood monocytes obtained from healthy volunteers and prepared by centrifugation over a Ficoll-Hypaque (Seromed, Biochrom, Berlin, Germany) gradient followed by a fibronectin adherence step. Monocytes were resuspended in RPMI 1640 (Life Technologies, Gaithersburg, MD) with 2 mM L-alanyl-L-glutamine (Life Technologies) and 10% fetal calf serum (PAA, Linz, Austria) and plated at 5 ϫ 10 5 cells/well on 24-well Falcon Primaria plates (Becton Dickinson, Lincoln Park, NJ).Recognition of mycobacterial products is a crucial step of the host defense response. Host-mycobacterial interactions are primarily mediated by antigens that are found on the M. tuberculosis cell wall. These particularly include lipoarabinomannan (LAM) (31) and 19-kDa lipoprotein (6). ManLAM (derived from the virulent Erdman M. tuberculosis strain) and purified M. tuberculosis 19-kDa lipoprotein were a kind gift from John T. Belisle (Department of Microbiology, Colorado State University, Fort Collins, CO). ManLAM was solubilized in phosphate-buffered saline. Lipopolysaccharide (LPS) contamination was Ͻ5 ng/mg as determined by Limulus assay.H37Rv (American Type Culture Collection, Manassas, VA) was used as the virulent M. tuberculosis strain. Mycobacteria were grown as previously described (23). M were infected for 12 and 24 h with a suspension of ...

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confidence: 72%

Macrophage Migration Inhibitory Factor Reduces the Growth of VirulentMycobacterium tuberculosisin Human Macrophages

Oddo¹,

Calandra²,

Bucala

et al. 2005

Infect Immun

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“…MIF has been reported to be elevated in both serum and bronchoalveolar lavage fluid in patients with pulmonary TB (35,40). MIF genotype and serum levels were investigated in 133 HIV-negative patients whose sera were obtained from the US Centers for Disease Control and Prevention (CDC) Tuberculosis Trials Consortium (TBTC) Study 22 (41).…”

Section: Resultsmentioning

confidence: 99%

Macrophage migration inhibitory factor (MIF) is a critical mediator of the innate immune response to Mycobacterium tuberculosis

Das

Koo²,

Kim

et al. 2013

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

110

112

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Significance Failure of the host immune system to control infection with Mycobacterium tuberculosis is a major determinant of tuberculosis (TB) disease. In this work, we examined the role of macrophage migration inhibitory factor (MIF), a cytokine that is encoded in a functionally polymorphic locus in humans, in TB. We found genetic low expressers of MIF to be enriched in a population of patients with HIV and disseminated TB. From our work in cellular and mouse models, we propose a key mechanism by which MIF regulates bacterial recognition as the first step in triggering inflammatory pathways to enable mycobacterial control.

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“…Another single article was not included in the meta-analysis because it was not designed as a case-control study. Finally, 11 eligible articles 12, 18–27 were included in the current meta-analysis. Nine of the 11 included articles were in English 12, 18–24, 27 and two were in Chinese 25, 26 .…”

Section: Resultsmentioning

confidence: 99%

“…More recently, studies have found the MIF may played a vital role in the pathogenesis of infectious diseases, such as sepsis and Gram-negative bacterial infection 11 . Furthermore, significantly higher MIF concentrations were observed in patients with pulmonary tuberculosis (PTB) than in the healthy population 12 . In vitro , MIF has also been found to play an important role in restraining virulent Mtb growth 13 .…”

Section: Introductionmentioning

confidence: 99%

Association between the MIF-173G/C Polymorphism and Serum MIF levels with Pulmonary Tuberculosis: A Meta-analysis

Xiang

Yan

Qin

et al. 2017

Sci Rep

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Many studies have indicated that Macrophage migration inhibitory factor (MIF)-173G/C gene polymorphisms are associated with susceptibility to pulmonary tuberculosis (PTB). Additionally, some studies have suggested that there are higher levels of serum MIF in patients with PTB than the controls. However, the results of these studies were underpowered. The current study aimed to precisely evaluate the association between the MIF-173G/C polymorphism and serum MIF concentrations with PTB. Therefore, a systematic literature search was preformed to identify studies involving the indicated association. Eleven articles (1316 cases and 1272 controls) were included in the study. The results indicated that the MIF-173G/C polymorphism was significantly associated with PTB susceptibility, especially in Asians. Interestingly, the results further detected that circulating MIF levels were significantly higher in patients with PTB than in healthy controls, but this was only the case among Asians. Moreover, the statistical significance was also similar to that of the high quality group. The present study indicated that the MIF-173G/C polymorphism may contribute to the development of PTB. Furthermore, significantly higher serum MIF levels were observed in PTB patients than in controls, which further indicated that the MIF may play an important role in PTB progression, particularly in Asians.

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Elevated Levels of Serum Macrophage Migration Inhibitory Factor in Patients with Pulmonary Tuberculosis

Cited by 32 publications

References 24 publications

Macrophage Migration Inhibitory Factor Reduces the Growth of VirulentMycobacterium tuberculosisin Human Macrophages

Macrophage Migration Inhibitory Factor Reduces the Growth of VirulentMycobacterium tuberculosisin Human Macrophages

Macrophage migration inhibitory factor (MIF) is a critical mediator of the innate immune response to Mycobacterium tuberculosis

Association between the MIF-173G/C Polymorphism and Serum MIF levels with Pulmonary Tuberculosis: A Meta-analysis

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