Cytokines and the Koch phenomenon

Rook, G.A.W.; Attiyah, R. Al

doi:10.1016/0041-3879(91)90019-o

Cited by 92 publications

(35 citation statements)

References 32 publications

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“…The results showed that in all animals intradermal inoculation of CFP-10 caused a drop in the rectal temperature of approximately ϳ4°C (Fig. 4), which is consistent with both TNF-␣ and tuberculin shocks (13,17,23). No rectal temperature change was observed in infected guinea pigs skin tested with either saline, Mtb 39, or PPD (not shown).…”

Section: Resultssupporting

confidence: 63%

Skin Test Performed with Highly PurifiedMycobacterium tuberculosisRecombinant Protein Triggers Tuberculin Shock in Infected Guinea Pigs

et al. 2005

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Tuberculin shock due to inoculation of Mycobacterium tuberculosis antigens in patients with tuberculosis is a serious syndrome originally described over 100 years ago by Robert Koch. Here, we present experimental evidence that a single M. tuberculosis recombinant protein, CFP-10, triggers this syndrome. Intradermal inoculation of CFP-10 elicits in M. tuberculosis-infected mice high levels of serum tumor necrosis factor alpha and causes tuberculin shock in infected guinea pigs characterized by hypothermia and death within 6 to 48 h after the antigen inoculation. Autopsies of these animals revealed intense polycythemia and hemorrhagic patches in the lung parenchyma, a pathological observation consistent with tuberculin shock. These results point to the possible occurrence of tuberculin shock in sensitive individuals inoculated with highly purified M. tuberculosis recombinant proteins as vaccine candidates or skin test reagents.

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Section: Resultssupporting

confidence: 63%

Skin Test Performed with Highly PurifiedMycobacterium tuberculosisRecombinant Protein Triggers Tuberculin Shock in Infected Guinea Pigs

et al. 2005

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“…The former was related to a typical Th1 mechanism and induced nonnecrotic granulomas, while the latter was related to a Th2 mechanism and, thus, was responsible for the intragranulomatous necrosis generated by M. tuberculosis infection, which was considered to be negative. The Th2 response should be counterbalanced in order to control the infection better and to avoid the development of TB (21,31). The comparison of IFN-␥/IL-4 ratios measured by different techniques after the FIG.…”

Section: Discussionmentioning

confidence: 99%

Induction of a Specific Strong Polyantigenic Cellular Immune Response after Short-Term Chemotherapy Controls Bacillary Reactivation in Murine and Guinea Pig Experimental Models of Tuberculosis

Guirado

Gil

Cáceres

et al. 2008

Clin Vaccine Immunol

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RUTI is a therapeutic vaccine that is generated from detoxified and liposomed Mycobacterium tuberculosis cell fragments that has demonstrated its efficacy in the control of bacillus reactivation after short-term chemotherapy. The aim of this study was to characterize the cellular immune response generated after the therapeutic administration of RUTI and to corroborate the lack of toxicity of the vaccine. Mouse and guinea pig experimental models were infected with a low-dose M. tuberculosis aerosol. RUTI-treated animals showed the lowest bacillary load in both experimental models. RUTI also decreased the percentage of pulmonary granulomatous infiltration in the mouse and guinea pig models. This was not the case after Mycobacterium bovis BCG treatment. Cellular immunity was studied through the characterization of the intracellular gamma interferon (IFN-␥)-producing cells after the splenocytes' stimulation with M. tuberculosis-specific structural and growth-related antigens. Our data show that the difference between the therapeutic administration of BCG and RUTI resides mainly in the stronger activation of IFN-␥ ؉ CD4 ؉ cells and CD8 ؉ cells against tuberculin purified protein derivative, ESAT-6, and Ag85B that RUTI generates. Both vaccines also triggered a specific immune response against the M. tuberculosis structural antigens Ag16kDa and Ag38kDa and a marked mRNA expression of IFN-␥, tumor necrosis factor, interleukin-12, inducible nitric oxide synthase, and RANTES in the lung. The results show that RUTI's therapeutic effect is linked not only to the induction of a Th1 response but also to the stimulation of a quicker and stronger specific immunity against structural and growth-related antigens that reduces both the bacillary load and the pulmonary pathology.

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“…In vitro LAM has been shown to inhibit the proliferation of human T cells (20), scavenge oxygen free radicals, block the transcriptional activation of gamma interferon-inducible genes, inhibit protein kinase C activity (4), and alter cytokine expression by macrophages (2). LAM has also been implicated in fever induction, tissue necrosis (24), and lung cavity formation (5). Despite considerable evidence that LAM can function as an immunomodulator, there is no information available on the fate of LAM in vivo.…”

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confidence: 99%

Clearance and Organ Distribution ofMycobacterium tuberculosisLipoarabinomannan (LAM) in the Presence and Absence of LAM-Binding Immunoglobulin M

et al. 2000

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Lipoarabinomannan (LAM) is a component of the mycobacterial surface which has been associated with a variety of deleterious effects on immune system function. Despite the importance of LAM to the pathogenesis of mycobacterial infection, there is no information available on its fate in vivo. In this study, we determined the pharmacokinetics and tissue distribution of exogenously administered LAM in mice. For measurements of serum and tissue LAM concentrations, we developed an enzyme-linked immunosorbent assay which used monoclonal antibodies of different isotypes to capture and detect LAM at concentrations of >0.4 g/ml. Intravenous administration of LAM to mice resulted in transient serum levels with organ deposition in the spleen and in the liver. Immunohistochemical studies localized LAM to the spleen marginal zone macrophages and, to a lesser degree, to liver macrophages. When LAM was administered to mice previously given a LAM-binding immunoglobulin M (IgM), LAM was very rapidly cleared from circulation. In those mice, deposition of LAM in the spleen was significantly reduced while LAM deposition in the liver increased. Administration of LAM-binding IgM resulted in significant levels of IgM to LAM in bile consistent with an increased hepatobiliary excretion of LAM in the presence of specific antibody. Bile, liver extracts, and bile salts were found to rapidly inactivate the immunoreactivity of LAM. The results indicate that serum clearance and organ deposition of LAM in mice are affected by the presence of LAM-binding antibody and suggest a mechanism by which antibody could modify the course of mycobacterial infection.Lipoarabinomannan (LAM) is a mycobacterial envelope glycolipid (3) that has been implicated in the virulence and pathogenesis of Mycobacterium tuberculosis infection. In vitro LAM has been shown to inhibit the proliferation of human T cells (20), scavenge oxygen free radicals, block the transcriptional activation of gamma interferon-inducible genes, inhibit protein kinase C activity (4), and alter cytokine expression by macrophages (2). LAM has also been implicated in fever induction, tissue necrosis (24), and lung cavity formation (5). Despite considerable evidence that LAM can function as an immunomodulator, there is no information available on the fate of LAM in vivo. Another unexplored question is the role, if any, of LAMbinding antibody in altering the fate and tissue distribution in vivo. LAM is immunogenic and elicits antibody responses during natural mycobacterial infection (14, 29). There is evidence that some antibodies to M. tuberculosis may contribute to host defense (9). In this regard, a serum immunoglobulin G (IgG) response to LAM has been associated with reduced likelihood of M. tuberculosis dissemination in children (8).The liver and the spleen are important organs in the clearance of microbial products, and the presence of specific antibody can have profound effects on antigen clearance in vivo. For example, Cryptococcus neoformans glucuronoxylomannan (GXM) is deposited primari...

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Cytokines and the Koch phenomenon

Cited by 92 publications

References 32 publications

Skin Test Performed with Highly PurifiedMycobacterium tuberculosisRecombinant Protein Triggers Tuberculin Shock in Infected Guinea Pigs

Skin Test Performed with Highly PurifiedMycobacterium tuberculosisRecombinant Protein Triggers Tuberculin Shock in Infected Guinea Pigs

Induction of a Specific Strong Polyantigenic Cellular Immune Response after Short-Term Chemotherapy Controls Bacillary Reactivation in Murine and Guinea Pig Experimental Models of Tuberculosis

Clearance and Organ Distribution ofMycobacterium tuberculosisLipoarabinomannan (LAM) in the Presence and Absence of LAM-Binding Immunoglobulin M

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