Dynamic production of tumour necrosis factor‐α (TNF‐α) messenger RNA, intracellular and extracellular TNF‐α by murine macrophages and possible association with protein tyrosine phosphorylation of STAT1α and ERK2 as an early signal

Zheng, Zhi-Ming; Specter, Steven

doi:10.1046/j.1365-2567.1996.513591.x

Cited by 18 publications

(6 citation statements)

References 36 publications

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“…Finally, since CHX blocked Tat-induced TNF-· production in THP-1 cells, this pathway is dependent on TNF-· mRNA translation. Although the TNF-· converting enzyme [57,58] activity was not examined here, the finding that Tatinduced TNF-· production is dependent on mRNA translation is in agreement with other studies which show that TNF-· production closely coincides with mRNA production [59]. Given the specificity of the action of Tat on macrophages, it is likely that Tat-induced TNF-· synthesis may be a membrane receptor-mediated event.…”

Section: Discussionsupporting

confidence: 90%

HIV-1 Tat Molecular Diversity and Induction of TNF-α: Implications for HIV-Induced Neurological Disease

Mayne

Bratanich

Chen

et al. 1998

Neuroimmunomodulation

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Activation and infection by HIV-1 of glial cells and infiltrating macrophages are cardinal features of AIDS-related neurological disease. Tumor necrosis factor-α (TNF-α) is released by these cell types, and increased TNF-α mRNA and protein levels are associated with the development and severity of HIV-induced neurological disease. HIV-1 proteins have been implicated in HIV neuropathogenesis including Tat which has been shown to be a potent inducer of TNF-α. We review our data showing the induction of TNF-α by Tat in primary human fetal astrocytes, human peripheral blood mononuclear cells, macrophages, and astrocytic and macrophage cell lines. TNF-α induction was NF-κB dependent and was eliminated by inhibiting protein kinase A, phospholipase C and protein tyrosine kinase activity. In addition, we examined the molecular diversity of the tat genome in the brains of HIV-infected patients from different HIV-1 clades. Comparison of matched brain- and spleen-derived tat sequences indicated that homology among brain-derived clones was greater than that between the brain- and spleen-derived clones. The brain-derived tat sequences were markedly heterogeneous in regions which influence viral replication and intracellular transport. Future studies using Tat, encoded by different sequences, will be necessary to determine the functional significance of tat molecular diversity. Nonetheless, these studies suggest that Tat is an important inducer of TNF-α production and thus may play a key role in the pathogenesis of HIV-related neurological disease.

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Section: Discussionsupporting

confidence: 90%

HIV-1 Tat Molecular Diversity and Induction of TNF-α: Implications for HIV-Induced Neurological Disease

Mayne

Bratanich

Chen

et al. 1998

Neuroimmunomodulation

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“…Several studies have reported a link between TNF-␣ production and MAPK activation (31,32,40,41,57,61). Recently, Ruckdeschel et al (46) suggested a correlation between the inhibition of TNF-␣ release and the inhibition of ERK1/2, p38, and JNK MAPK activities in macrophages infected by Y. enterocolitica.…”

Section: Discussionmentioning

confidence: 99%

Role of YopP in Suppression of Tumor Necrosis Factor Alpha Release by Macrophages duringYersiniaInfection

1998

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The Yersinia plasmid-encoded Yop virulon enables extracellular adhering bacteria to deliver toxic effector proteins inside their target cells. It includes a type III secretion system (Ysc), at least two translocator proteins (YopB, YopD), and a set of intracellular Yop effectors (YopE, YopH, YopO, YopM, and YopP). Infection of macrophages with a wild-type strain leads to low levels of tumor necrosis factor alpha (TNF-α) release compared to infection with plasmid-cured strains, suggesting that the virulence plasmid encodes a factor impairing the normal TNF-α response of infected macrophages. This effect is correlated with the inhibition of the macrophage mitogen-activated protein kinase (MAPK) activities. To identify the Yop protein responsible for the suppression of TNF-α release, we infected J774A.1 and PU5-1.8 macrophages with a battery of knockout Yersinia enterocolitica mutants and we quantified the TNF-α released. Mutants affected in secretion (yscN), in translocation (yopB and yopD), or in synthesis of all the known Yop effectors (yopH,yopO, yopP, yopE, andyopM polymutants) were unable to block the TNF-α response of the macrophages. In contrast, single yopE,yopH, yopO, and yopM mutants behaved like the wild-type strain. A yopP mutant elicited elevated TNF-α release, and complementation of the yopPmutant or the yop effector polymutant strain withyopP alone led to a drop in TNF-α release. In addition, YopP was also responsible for the inhibition of the extracellular signal-regulated kinase2 (ERK2) and p38 MAPK activities. These results show that YopP is the Yop effector responsible for theYersinia-induced suppression of TNF-α release by infected macrophages.

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“…More recently, Ruckdeschel et al (289), working with the mouse monocyte-macrophage cell line J774A.1 and Y. enterocolitica, showed that a functional type III secretion machinery is required for the phenomenon to occur and suggested a correlation between this inhibition of TNF-␣ release and inhibition of the ERK1/2, p38, and JNK mitogenactivated protein kinase (MAPK) activities. Several reports already described a link between MAPK activation and TNF-␣ production (202,203,273,280,347,388). It has been shown recently both for Y. enterocolitica (39) and for Y. pseudotuberculosis (251) that the Yersinia-induced inhibition of TNF-␣ release requires not only the type III secretion apparatus but also a functional Yop translocation apparatus and the effector YopP (Y. enterocolitica)/YopJ (Y. pseudotuberculosis).…”

Section: Figmentioning

confidence: 99%

The Virulence Plasmid ofYersinia, an Antihost Genome

Cornelis

Boland

Boyd

et al. 1998

Microbiol Mol Biol Rev

719

324

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SUMMARY The 70-kb virulence plasmid enables Yersinia spp. (Yersinia pestis, Y. pseudotuberculosis, and Y. enterocolitica) to survive and multiply in the lymphoid tissues of their host. It encodes the Yop virulon, an integrated system allowing extracellular bacteria to disarm the cells involved in the immune response, to disrupt their communications, or even to induce their apoptosis by the injection of bacterial effector proteins. This system consists of the Yop proteins and their dedicated type III secretion apparatus, called Ysc. The Ysc apparatus is composed of some 25 proteins including a secretin. Most of the Yops fall into two groups. Some of them are the intracellular effectors (YopE, YopH, YpkA/YopO, YopP/YopJ, YopM, and YopT), while the others (YopB, YopD, and LcrV) form the translocation apparatus that is deployed at the bacterial surface to deliver the effectors into the eukaryotic cells, across their plasma membrane. Yop secretion is triggered by contact with eukaryotic cells and controlled by proteins of the virulon including YopN, TyeA, and LcrG, which are thought to form a plug complex closing the bacterial secretion channel. The proper operation of the system also requires small individual chaperones, called the Syc proteins, in the bacterial cytosol. Transcription of the genes is controlled both by temperature and by the activity of the secretion apparatus. The virulence plasmid of Y. enterocolitica and Y. pseudotuberculosis also encodes the adhesin YadA. The virulence plasmid contains some evolutionary remnants including, in Y. enterocolitica, an operon encoding resistance to arsenic compounds.

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Dynamic production of tumour necrosis factor‐α (TNF‐α) messenger RNA, intracellular and extracellular TNF‐α by murine macrophages and possible association with protein tyrosine phosphorylation of STAT1α and ERK2 as an early signal

Cited by 18 publications

References 36 publications

HIV-1 Tat Molecular Diversity and Induction of TNF-α: Implications for HIV-Induced Neurological Disease

HIV-1 Tat Molecular Diversity and Induction of TNF-α: Implications for HIV-Induced Neurological Disease

Role of YopP in Suppression of Tumor Necrosis Factor Alpha Release by Macrophages duringYersiniaInfection

The Virulence Plasmid ofYersinia, an Antihost Genome

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