Nonspecific and immune-specific up-regulation of cytokines in rabbit dermal tuberculous (BCG) lesions

Sugisaki, Katsunori; Dannenberg, Arthur M.; Abe, Yasuharu; Tsuruta, Junji; Su, Wei; Said, Waheeda; Li, Feng; Yoshimura, Teizo; Converse, Paul J.; Mounts, Phoebe

doi:10.1002/jlb.63.4.440

Cited by 33 publications

(26 citation statements)

References 45 publications

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“…Nevertheless, the ear represents a comparatively different immune compartment, with relatively fewer lymphoid cells, and there is likely to be a balance in the level of bacterial replication and clearance in the ear, with the clearance attributable to either bacterial death and phagocytic clearance or phagocytic transport or draining of live bacteria to the local draining lymph nodes. Indeed, the abundant CD15 + neutrophil population observed in blister fluid (Figure 1 F ) is consistent with data from animal models of intradermal BCG infection in which neutrophils were shown to be induced by BCG in the skin and engineer the induction of T cells through their interactions with dendritic cells [19, 20]. …”

Section: Discussionsupporting

confidence: 86%

A Human Challenge Model for Mycobacterium tuberculosis Using Mycobacterium bovis Bacille Calmette-Guérin

Minassian

Satti

Poulton

et al. 2012

The Journal of Infectious Diseases

106

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(See the editorial commentary by Dockrell, on pages .)Background. There is currently no safe human challenge model of Mycobacterium tuberculosis infection to enable proof-of-concept efficacy evaluation of candidate vaccines against tuberculosis. In vivo antimycobacterial immunity could be assessed using intradermal Mycobacterium bovis bacille Calmette-Guérin (BCG) vaccination as a surrogate for M. tuberculosis infection.Methods. Healthy BCG-naive and BCG-vaccinated volunteers were challenged with intradermal BCG. BCG load was quantified from skin biopsy specimens by polymerase chain reaction (PCR) and culture colony-forming units. Cellular infiltrate was isolated by suction blisters and examined by flow cytometry. Prechallenge immune readouts were correlated with BCG load after challenge.Results. In BCG-naive volunteers, live BCG was detected at the challenge site for up to 4 weeks and peaked at 2 weeks. Infiltration of mainly CD15+ neutrophils was observed in blister fluid. In previously BCG-vaccinated individuals, PCR analysis of skin biopsy specimens reflected a degree of mycobacterial immunity. There was no significant correlation between BCG load after challenge and mycobacterial-specific memory T cells measured before challenge by cultured enzyme-linked immunospot assay.Conclusions. This novel experimental human challenge model provides a platform for the identification of correlates of antimycobacterial immunity and will greatly facilitate the rational down-selection of candidate tuberculosis vaccines. Further evaluation of this model with BCG and new vaccine candidates is warranted.

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Section: Discussionsupporting

confidence: 86%

A Human Challenge Model for Mycobacterium tuberculosis Using Mycobacterium bovis Bacille Calmette-Guérin

Minassian

Satti

Poulton

et al. 2012

The Journal of Infectious Diseases

106

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“…Increased expression and secretion of chemokines (including IL-8, macrophage-inflammatory protein-1␣, and RANTES) have been demonstrated in bronchoalveolar lavage fluids from humans with active pulmonary tuberculosis (24,25), murine pulmonary granulomas (26), and dermal DTH responses in Mycobacterium bovis bacillus Calmette-Guerin-infected rabbits (27). Interestingly, Rhoades et al found significant differences in chemokine mRNA levels from mice infected with either CSU22 or CSU46, two clinical isolates of M. tuberculosis, compared with mice infected with M. tuberculosis Erdman (26).…”

Section: Discussionmentioning

confidence: 99%

Infection of B Cell-Deficient Mice with CDC 1551, a Clinical Isolate ofMycobacterium tuberculosis: Delay in Dissemination and Development of Lung Pathology

Bosio

Gardner

Elkins

2000

The Journal of Immunology

139

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Long-term survival of mice infected with Mycobacterium tuberculosis is dependent upon IFN-γ and T cells, but events in early phases of the immune response are not well understood. In this study, we describe a role for B cells during early immune responses to infection with a clinical isolate of M. tuberculosis (CDC 1551). Following a low-dose infection with M. tuberculosis CDC 1551, similar numbers of bacteria were detected in the lungs of both B cell knockout (IgH 6−, BKO) and C57BL/6J (wild-type) mice. However, despite comparable bacterial loads in the lungs, less severe pulmonary granuloma formation and delayed dissemination of bacteria from lungs to peripheral organs were observed in BKO mice. BKO mice reconstituted with naive B cells, but not those given M. tuberculosis-specific Abs, before infection developed pulmonary granulomas and dissemination patterns similar to wild-type animals. Further analysis of lung cell populations revealed greater numbers of lymphocytes, especially CD8+ T cells, macrophages, and neutrophils in wild-type and reconstituted mice than in BKO mice. Thus, less severe lesion formation and delayed dissemination of bacteria found in BKO mice were dependent on B cells, not Abs, and were associated with altered cellular infiltrate to the lungs. These observations demonstrate an important, previously unappreciated, role for B cells during early immune responses to M. tuberculosis infections.

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“…When the bacteria were heat-killed, they lost the ability to induce liquefaction and the granulomas they induced were also smaller than those caused by live mycobacteria. BCG, H37Ra and M. smegmatis could induce nonspecific inflammatory molecules such as MCP-1, IL-8, etc., in 1-3 days, 16 so mononuclear cells can be attracted and activated, and the bacteria could be destroyed if the bacterial number is small. The undestroyed bacteria will survive in granuloma or macrophages, and stimulate specific immunity, and enough number of mycobacteria could induce caseous necrosis, liquefaction or ulcer.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of mycobacterial virulence using rabbit skin liquefaction model

et al. 2010

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Nonspecific and immune-specific up-regulation of cytokines in rabbit dermal tuberculous (BCG) lesions

Cited by 33 publications

References 45 publications

A Human Challenge Model for Mycobacterium tuberculosis Using Mycobacterium bovis Bacille Calmette-Guérin

A Human Challenge Model for Mycobacterium tuberculosis Using Mycobacterium bovis Bacille Calmette-Guérin

Infection of B Cell-Deficient Mice with CDC 1551, a Clinical Isolate ofMycobacterium tuberculosis: Delay in Dissemination and Development of Lung Pathology

Evaluation of mycobacterial virulence using rabbit skin liquefaction model

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