Tumor necrosis factor alpha (TNFalpha) promotes growth of virulent Mycobacterium tuberculosis in human monocytes iron-mediated growth suppression is correlated with decreased release of TNFalpha from iron-treated infected monocytes.

Byrd, Thomas F.

doi:10.1172/jci119436

Cited by 81 publications

(72 citation statements)

References 56 publications

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“…6b). Formation of infected cellular aggregates has been previously reported during MDM monolayer infection with M. abscessus rough variants, as well as with virulent M. tuberculosis (Byrd, 1997;Byrd & Lyons, 1999). The complemented strain did not differ in terms of replication over 24 h compared to wild-type; however, by 48 h intracellular replication had begun to occur (Fig.…”

Section: S Dmmpl4b Has Acquired the Ability To Replicate In Human mentioning

confidence: 64%

“…In addition, nuclear counts in replicate wells were determined, and c.f.u. standardized to 10 5 nuclei to account for any differences in monocyte number in the different monolayers, as has been described previously (Byrd, 1997). Replicate monolayers treated in the same fashion were fixed with PBS/4 % paraformaldehyde and photographed with a Nikon TE1 2000 U phase-contrast microscope.…”

Section: Methodsmentioning

confidence: 99%

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Deletion of the mmpL4b gene in the Mycobacterium abscessus glycopeptidolipid biosynthetic pathway results in loss of surface colonization capability, but enhanced ability to replicate in human macrophages and stimulate their innate immune response

et al. 2011

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Mycobacterium abscessus is considered to be the most virulent of the rapidly growing mycobacteria. Generation of bacterial gene knockout mutants has been a useful tool for studying factors that contribute to virulence of pathogenic bacteria. Until recently, the optimal genetic approach to generation of M. abscessus gene knockout mutants was not clear. Based on the recent identification of genetic recombineering as the preferred approach, a M. abscessus mutant was generated in which the gene mmpL4b, critical to glycopeptidolipid synthesis, was deleted. Compared to the previously well-characterized parental strain 390S, the mmpL4B deletion mutant had lost sliding motility and the ability to form biofilm, but acquired the ability to replicate in human macrophages and stimulate macrophage Toll-like receptor 2. This study demonstrates that deletion of a gene associated with expression of a cell-wall lipid can result in acquisition of an immunostimulatory, invasive bacterial phenotype and has important implications for the study of M. abscessus pathogenesis at the cellular level.

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Section: S Dmmpl4b Has Acquired the Ability To Replicate In Human mentioning

confidence: 64%

Section: Methodsmentioning

confidence: 99%

Deletion of the mmpL4b gene in the Mycobacterium abscessus glycopeptidolipid biosynthetic pathway results in loss of surface colonization capability, but enhanced ability to replicate in human macrophages and stimulate their innate immune response

et al. 2011

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“…At 2, 4 and 7 days, culture supernates and cell lysates were plated separately on 7H11 agar, and values were added together to give total c.f.u. per well at each time point (Byrd, 1997). For Rv-D981, supernate c.f.u.…”

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confidence: 99%

“…in monocyte lysates were compared, and when c.f.u. in monocyte lysates were corrected for the number of monocytes remaining adherent at each time point (data not shown The viability of infected monocyte monolayers and the number of nuclei per well was also determined at each time point as described by Byrd (1997). Monocyte monolayers were >98 % viable in all groups at 2 and 4 days, with viability decreasing to a mean of 87 %, 69 % and 96 % in H37Rv, Rv-D981 and Rv-D981C, respectively, at 7 days.…”

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confidence: 99%

Evidence for complex interactions of stress-associated regulons in an mprAB deletion mutant of Mycobacterium tuberculosis

Pang

Byrd³

et al. 2007

Microbiology

101

157

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Two-component systems are important constituents of bacterial regulatory networks. Results of this investigation into the role of the MprAB two-component system of Mycobacterium tuberculosis indicate that it is associated with the regulation of several stress-responsive regulons. Using a deletion mutant lacking portions of the response regulator, MprA, and the histidine kinase, MprB, it was demonstrated by real-time PCR, primer extension analyses and DNA microarrays that MprAB activates sigma factor genes sigE and sigB, under SDS stress and during exponential growth. SDS-inducible, MprA-dependent transcriptional start points were identified for mprA, sigE and sigB, and variations in distance between these points and MprA-binding sites suggest that MprA is involved in different mechanisms of promoter activation. Although most of the SigE regulon was downregulated in the deletion mutant, the cluster of genes Rv1129c, Rv1130 and Rv1131, which is associated with growth in monoctyes, was upregulated in the deletion mutant under SDS stress, and this upregulation was dependent upon atmospheric growth conditions. Multiple stress-associated genes of the DosR, SigD and IdeR regulons were also upregulated in the deletion mutant, during exponential growth and/or in the presence of SDS. Surprisingly, the deletion mutant had increased resistance to SDS compared to the parental strain, and enhanced growth in human peripheral blood monocytes, characteristics which may result from a loss of repression of stress-associated genes. INTRODUCTIONAs evidenced by its historical and current impact on human populations (Corbett & Raviglione, 2005;Zink et al., 2005), Mycobacterium tuberculosis is a highly successful pathogen. To withstand the challenges of aerosol transmission, growth within host macrophages, and prolonged encapsulation within lung granuloma, these organisms require the ability to respond to different types of stress. M. tuberculosis has 13 sigma factors (Cole et al., 1998), and DNA microarray analyses have shown the importance of several of these in regulating the changes in gene expression patterns associated with various stresses (Geiman et al., 2004;Manganelli et al., 2001Manganelli et al., , 2002. In addition to sigma factors, the response regulators of some two-component systems (TCSs) (Rison et al., 2005), such as DosR (Kendall et al., 2004;Park et al., 2003) and PhoP Perez et al., 2001;Walters et al., 2006), and other transcriptional regulators, such as IdeR (Dussurget et al., 1999;Manabe et al., 2005) and EmbR (Sharma et al., 2006), have been shown to modulate mycobacterial gene expression in response to particular stresses. However, in general, the mechanisms by which M. tuberculosis senses a particular stress, and activates the appropriate regulatory factor(s) while inhibiting others, are largely unknown. The GEO accession numbers for the array data associated with this paper are GSM155424-155447 (series record no. GSE6750).Four supplementary tables are available with the online version of this paper.Abbreviati...

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“…Nitric oxide has the ability to autoregulate its own production (38) and, by negative feedback, to counteract the excessive cytokine release. The continued presence of TNF-α has a growth-promoting effect on M tuberculosis (39). Hence, the negative stimulation by means of nitric oxide is necessary to decrease the proinflammatory state and, consequently, the amount of TNF-α.…”

Section: Discussionmentioning

confidence: 99%

Elevated N-terminal pro-brain natriuretic peptide in Mycobacterium tuberculosis pulmonary infection without myocardial dysfunction

Bar

Sayeh

Ignaszewski

2009

Canadian Journal of Cardiology

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Tumor necrosis factor alpha (TNFalpha) promotes growth of virulent Mycobacterium tuberculosis in human monocytes iron-mediated growth suppression is correlated with decreased release of TNFalpha from iron-treated infected monocytes.

Cited by 81 publications

References 56 publications

Deletion of the mmpL4b gene in the Mycobacterium abscessus glycopeptidolipid biosynthetic pathway results in loss of surface colonization capability, but enhanced ability to replicate in human macrophages and stimulate their innate immune response

Deletion of the mmpL4b gene in the Mycobacterium abscessus glycopeptidolipid biosynthetic pathway results in loss of surface colonization capability, but enhanced ability to replicate in human macrophages and stimulate their innate immune response

Evidence for complex interactions of stress-associated regulons in an mprAB deletion mutant of Mycobacterium tuberculosis

Elevated N-terminal pro-brain natriuretic peptide in Mycobacterium tuberculosis pulmonary infection without myocardial dysfunction

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