Lung macrophages from bacille Calmette–Guérin-vaccinated guinea pigs suppress T cell proliferation but restrict intracellular growth of<i>M. tuberculosis</i>after recombinant guinea pig interferon-γ activation

Jeevan, Amminikutty; Majorov, Konstantin; Sawant, Kirti V.; Cho, H.; McMurray, David N.

doi:10.1111/j.1365-2249.2007.03425.x

Cited by 16 publications

(40 citation statements)

References 49 publications

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Section: Innate Immune Responses To Bcg Vaccinationmentioning

confidence: 96%

“…Other supporting ex vivo studies indicate that AMs from BCG-vaccinated guinea pigs challenged with M.tb express significantly less IL-10 and more IL-12p40, compared to unvaccinated controls (45). This same study reported an elevated expression of MHC II on peritoneal macrophages from BCG-vaccinated guinea pigs (45). Thus, based on our current understanding of the requirements for mycobacterial immunity; immunity induced by the BCG vaccine results in responses to M.tb at the early phase of infection that directly impact macrophage function.…”

Section: Innate Immune Responses To Bcg Vaccinationmentioning

confidence: 96%

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Immune Responses to Bacillus Calmette–Guérin Vaccination: Why Do They Fail to Protect against Mycobacterium tuberculosis?

2017

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Mycobacterium tuberculosis (M.tb), the causative agent of tuberculosis (TB), is the current leading cause of death due to a single infectious organism. Although curable, the broad emergence of multi-, extensive-, extreme-, and total-drug resistant strains of M.tb has hindered eradication efforts of this pathogen. Furthermore, computational models predict a quarter of the world’s population is infected with M.tb in a latent state, effectively serving as the largest reservoir for any human pathogen with the ability to cause significant morbidity and mortality. The World Health Organization has prioritized new strategies for improved vaccination programs; however, the lack of understanding of mycobacterial immunity has made it difficult to develop new successful vaccines. Currently, Mycobacterium bovis bacillus Calmette–Guérin (BCG) is the only vaccine approved for use to prevent TB. BCG is highly efficacious at preventing meningeal and miliary TB, but is at best 60% effective against the development of pulmonary TB in adults and wanes as we age. In this review, we provide a detailed summary on the innate immune response of macrophages, dendritic cells, and neutrophils in response to BCG vaccination. Additionally, we discuss adaptive immune responses generated by BCG vaccination, emphasizing their specific contributions to mycobacterial immunity. The success of future vaccines against TB will directly depend on our understanding of mycobacterial immunity.

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Section: Innate Immune Responses To Bcg Vaccinationmentioning

confidence: 96%

Section: Innate Immune Responses To Bcg Vaccinationmentioning

confidence: 96%

Immune Responses to Bacillus Calmette–Guérin Vaccination: Why Do They Fail to Protect against Mycobacterium tuberculosis?

2017

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“…For example, suppression of lung T‐cell proliferation to purified protein derivative (PPD) occurred in co‐cultures of lung macrophages from M. tuberculosis ‐infected mice 25 . Previously, we have reported that alveolar macrophages (AMøs) as well as lung tissue macrophages (LMøs) obtained from BCG‐vaccinated guinea pigs suppressed the proliferation of lung T cells to PPD while peritoneal macrophages (PMøs) induced robust proliferation 26 . However, the effect of BCG vaccination on the responses of lung cells from M. tuberculosis ‐infected guinea pigs has not been studied.…”

Section: Introductionmentioning

confidence: 99%

Expression of interferon‐γ and tumour necrosis factor‐α messenger RNA does not correlate with protection in guinea pigs challenged with virulent Mycobacterium tuberculosis by the respiratory route

2009

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Summary Cytokine messenger RNA (mRNA) expression was investigated in the spleen and lung digest cells of bacillus Calmette–Guérin (BCG)‐vaccinated and non‐vaccinated guinea pigs following low‐dose, pulmonary exposure to virulent Mycobacterium tuberculosis. After purified protein derivative (PPD) stimulation, the levels of lung cell interferon‐γ (IFN‐γ), tumour necrosis factor‐α (TNF‐α) and spleen cell interleukin‐12 (IL‐12) p40 mRNAs were significantly increased in the non‐vaccinated M. tuberculosis‐infected guinea pigs compared to the BCG‐vaccinated guinea pigs. In contrast, the expression of anti‐inflammatory transforming growth factor‐β and IL‐10 mRNAs was significantly enhanced in the spleens of BCG‐vaccinated animals. Despite the presence of protective cytokine mRNA expression, the non‐vaccinated guinea pigs had significantly higher lung and spleen bacterial burdens. In contrast, BCG‐vaccinated guinea pigs controlled the bacterial multiplication in their lungs and spleens, indicating that both protective as well as anti‐inflammatory cytokine responses are associated with a reduction in bacteria. In addition, lung digest cells from non‐vaccinated guinea pigs contained a significantly higher percentage of neutrophils, CD3+ and CD8+ T cells, while the percentage of macrophages was increased in the BCG‐vaccinated animals. Total and purified lung digest T cells co‐cultured with lung macrophages (LMøs) proliferated poorly after PPD stimulation in both non‐vaccinated and BCG‐vaccinated animals while robust proliferation to PPD was observed when T cells were co‐cultured with peritoneal macrophages (PMøs). Macrophages within the lung compartment appear to regulate the response of T cells irrespective of the vaccination status in guinea pigs. Taken together, our results suggest that type I cytokine mRNA expression is not associated with vaccine‐induced protection in the low‐dose guinea pig model of tuberculosis.

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“…Lung infections, especially experimental paracoccidioidomycosis (PCMEx) [3][4][5], involve newly recruited CD11b + and CD23 + resident macrophages with potential immune disturbances for the host [6]. Several studies have implicated lung alveolar macrophages in the suppressive process of T-lymphocytes [7,8]. The mechanism by which pulmonary macrophages mediate the suppression of the T-lymphocytes proliferation in PCMEx is still unclear; however, it might involve soluble factors, either Th1/Th2 interleukins [9,10], CD23s [11], prostaglandins [12], regulatory T cells [13], antagonist of the IL receptors [14], accessory molecules, such as CD80 [15], CD86 [16], adhesion molecules [17][18][19][20] or genetic background of the host [21].…”

Section: Introductionmentioning

confidence: 99%

TGF-β and CD23 are involved in nitric oxide production by pulmonary macrophages activated by β-glucan from Paracoccidioides brasiliensis

Queiroz

Mattos

Silva

et al. 2009

Med Microbiol Immunol

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Pulmonary macrophages (PM), which are CD11b/CD18(+) and CD23(+), may be involved in the onset of inflammatory events caused by Paracoccidioides brasiliensis in the lungs. In the present study, we measured the nitric oxide (NO) and interleukin in PM production after intratracheal (i.t.) inoculation of an enriched beta-glucan cell wall fraction from P. brasiliensis (Fraction F1). BALB/c and C57/BL6 (B6) mice were i.t. treated with Fraction F1, and their PM were restimulated in vitro with LPS and interferon-gamma up to 14 days after treatment. Macrophages BALB/c mice produced less NO than PM from B6 mice. The lower NO production was caused by higher production of TGF-beta by pulmonary macrophages of BALB/c and was abrogated by anti-TGF-beta MoAb in vitro and in vivo. Other interleukins such as IL-10, IL-4 and a combination of IL-1, TNF-alpha and IL-6 were not involved in NO production induced by Fraction F1. Expression of CD11b increases and expression of CD23 decreases on PM of BALB/c mice after in vivo treatment whereas PM of B6 mice do not show a variation of their phenotype. Moreover, the ability of pulmonary macrophages to induce lymphocyte proliferation was reduced in mixed cultures of CD11b(+) or CD23(+) macrophages but was restored when lymphocytes were cultivated in the presence of NO inhibitor (L-NMMA). Thus, the results presented herein indicate that in BALB/c but not in B6 mice TGF-ss is strongly induced by Fraction 1 in PM in vivo and suppresses NO production. Low NO production by PM is associated with a change in CD11b/CD23 expression and with a high lymphocyte proliferative response. Thus, CD11b(+)/CD23(+) PM modulate NO and TGF-beta production in the pulmonary microenvironment.

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Lung macrophages from bacille Calmette–Guérin-vaccinated guinea pigs suppress T cell proliferation but restrict intracellular growth ofM. tuberculosisafter recombinant guinea pig interferon-γ activation

Cited by 16 publications

References 49 publications

Immune Responses to Bacillus Calmette–Guérin Vaccination: Why Do They Fail to Protect against Mycobacterium tuberculosis?

Immune Responses to Bacillus Calmette–Guérin Vaccination: Why Do They Fail to Protect against Mycobacterium tuberculosis?

Expression of interferon‐γ and tumour necrosis factor‐α messenger RNA does not correlate with protection in guinea pigs challenged with virulent Mycobacterium tuberculosis by the respiratory route

TGF-β and CD23 are involved in nitric oxide production by pulmonary macrophages activated by β-glucan from Paracoccidioides brasiliensis

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