In the past Maria Cristina Gagliardi has collaborated on articles with Elisabetta Iona. One of their most recent publications is Maturation of human dendritic cells induced by the adjuvant cholera toxin: role of cAMP on chemokine receptor expression. Which was published in journal Vaccine.

More information about Maria Cristina Gagliardi research including statistics on their citations can be found on their Copernicus Academic profile page.

Maria Cristina Gagliardi's Articles: (3)

Maturation of human dendritic cells induced by the adjuvant cholera toxin: role of cAMP on chemokine receptor expression

AbstractCholera toxin (CT) is a very effective adjuvant for mucosal vaccination. It binds to cells through its B subunit and induces intracellular increase of cAMP through the A subunit. We previously showed that CT induces maturation of human dendritic cells (DCs) and this may account for its adjuvant property. Here, we investigated the role of the A subunit on DCs maturation by using forskolin, a cAMP inducer. The results show that although cAMP does not stimulate full maturation of DCs it induces upregulation of the chemokine receptors CXCR4 and CCR7.

Bacillus Calmette-Guérin shares with virulent Mycobacterium tuberculosis the capacity to subvert monocyte differentiation into dendritic cell: implication for its efficacy as a vaccine preventing tuberculosis

AbstractThe only available vaccine against tuberculosis (TB) is Bacillus Calmette-Guérin (BCG) whose efficacy in preventing pulmonary tuberculosis is however controversial. Here, we show that BCG infection of monocytes causes their differentiation into mature dendritic cells (DCs) lacking CD1 molecules expression, coupled with suboptimal up-regulation of HLA class II, CD80 and CD40 molecules and a marked unresponsiveness to lipopolysaccharide stimulation. In addition, alloreactive naïve T lymphocytes primed by these subverted DCs did not undergo defined functional polarization, as witnessed by their inability to produce IFN-γ. Since efficient antigen presentation and IFN-γ production by mycobacterial-specific T lymphocytes are required for protection against Mycobacterium tuberculosis, our data might provide additional explanation for the low efficacy of BCG vaccination.

Original articleInfection of human THP-1 cells with dormant Mycobacterium tuberculosis

AbstractDormant, non-replicating Mycobacterium tuberculosis H37Rv strain cultured in hypoxic conditions was used to infect THP-1 cells. CFUs counting, Kinyoun staining and electron microscopy showed that dormant bacilli infected THP-1 cells at a rate similar to replicating M. tuberculosis, but failed to grow during the first 6 days of infection. The absence of growth was specific to the intracellular compartment, as demonstrated by efficient growth in liquid medium. Quantification of β-actin mRNA recovered from infected cells showed that, in contrast with log-phase bacteria, infection with dormant bacilli determined a reduced THP-1 cell death. Gene expression of intracellular non-replicating bacteria showed a pattern typical of a dormant state. Intracellular dormant bacteria induced the activation of genes associated to a proinflammatory response in THP-1 cells. Though, higher levels of TNFα, IL-1β and IL-8 mRNAs compared to aerobic H37Rv infected cells were not paralleled by increased cytokine accumulation in the supernatants. Moreover, dormant bacilli induced a higher expression of inducible cox-2 gene, accompanied by increased PGE2 secretion. Overall, our data describe a new model of in vitro infection using dormant M. tuberculosis that could provide the basis for understanding how non-replicating bacilli survive intracellularly and influence the maintenance of the hypoxic granuloma.

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