Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2015 Jul 16:6:723.
doi: 10.3389/fmicb.2015.00723. eCollection 2015.

In vitro interaction of Stenotrophomonas maltophilia with human monocyte-derived dendritic cells

Emanuela Roscetto  1 , Laura Vitiello  2 , Rosa Muoio  1 , Amata A Soriano  1 , Vita D Iula  1 , Antonio Vollaro  3 , Eliana De Gregorio  1 , Maria R Catania  1
Affiliations

In vitro interaction of Stenotrophomonas maltophilia with human monocyte-derived dendritic cells

Emanuela Roscetto et al. Front Microbiol. .

Abstract

Stenotrophomonas maltophilia is increasingly identified as an opportunistic pathogen in immunocompromised, cancer and cystic fibrosis (CF) patients. Knowledge on innate immune responses to S. maltophilia and its potential modulation is poor. The present work investigated the ability of 12 clinical S. maltophilia strains (five from CF patients, seven from non-CF patients) and one environmental strain to survive inside human monocyte-derived dendritic cells (DCs). The effects of the bacteria on maturation of and cytokine secretion by DCs were also measured. S. maltophilia strains presented a high degree of heterogeneity in internalization and intracellular replication efficiencies as well as in the ability of S. maltophilia to interfere with normal DCs maturation. By contrast, all S. maltophilia strains were able to activate DCs, as measured by increase in the expression of surface maturation markers and proinflammatory cytokines secretion.

Keywords: DC maturation markers; cystic fibrosis; cytokines secretion; innate immune response; opportunistic pathogen.

PubMed Disclaimer

Figures

FIGURE 1
FIGURE 1
Interactions of S. maltophilia strains with iDCs. White and gray bar graphs indicate CFUs recovered by iDCs after 1 h and 18 h of infection, respectively. *p < 0.05. Each bar indicates the mean value ± standard deviation of at least three independent experiments in triplicate.
FIGURE 2
FIGURE 2
DC infection assays. (A) Entry Index (EI). Bar graphs shown the percentage internalization of S. maltophilia strains after 1 h of infection with DCs. (B) Intracellular Replication Index (RI). Bar graphs shown the percentage survival of S. maltophilia strains after 18 h of infection within DCs. Each bar indicates the mean value ± standard deviation of at least three independent experiments in triplicate.
FIGURE 3
FIGURE 3
Stenotrophomonas maltophilia strains induce dendritic cells maturation. Bar graphs shown the fold change in CD80 (A) and CD86 (B) expression after 18 h of incubation. CD86 and CD80 expression on DCs was measured by flow cytometry. The mean fluorescence intensity (MFI) reflects the upregulation of molecule on cell surface. Each bar indicates the mean ± standard deviation of three independent experiments. *p < 0.05. Medium: iDCs uninfected.
FIGURE 4
FIGURE 4
Stenotrophomonas maltophilia strains induce cytokines production by dendritic cells. Bar graphs shown the production of IL-12 (A) and TNFα (B) by dendritic cells after incubation with the S. maltophilia strains. IL-12 and TNFα expression by DCs was measured by ELISA and flow cytometry, respectively. Each bar indicates mean ± standard deviation of at three independent experiments. All the bacterial strains induced the production of TNFα and IL-12 by DCs (p < 0.001). Medium: iDCs uninfected.
See this image and copyright information in PMC

References

    1. Acosta-Rodriguez E. V., Napolitani G., Lanzavecchia A., Sallusto F. (2007). Interleukins 1β and 6 but not transforming growth factor- β are essential for the differentiation of interleukin 17-producing human T helper cells. Nat. Immunol. 8, 942–949. 10.1038/ni1496 - DOI - PubMed
    1. Brooke J. S. (2012). Stenotrophomonas maltophilia: an emerging global opportunistic pathogen. Clin. Microbiol. Rev. 25, 2–41. 10.1128/CMR.00019-11 - DOI - PMC - PubMed
    1. Brooke J. S. (2014). New strategies against Stenotrophomonas maltophilia: a serious worldwide intrinsically drug-resistant opportunistic pathogen. Expert Rev. Anti Infect. Ther. 12, 1–4. 10.1586/14787210.2014.864553 - DOI - PubMed
    1. Bueno S. M., Riquelme S., Riedel C. A., Kalergis A. M. (2012). Mechanisms used by virulent Salmonella to impair dendritic cell function and evade adaptive immunity. Immunology 137, 28–36. 10.1111/j.1365-2567.2012.03614.x - DOI - PMC - PubMed
    1. Chang Y. T., Lin C. Y., Lu P. L., Lai C. C., Chen T. C., Chen C. Y., et al. (2014). Stenotrophomonas maltophilia bloodstream infection: comparison between community-onset and hospital-acquired infections. J. Microbiol. Immunol. Infect. 47, 28–35. 10.1016/j.jmii.2012.08.014 - DOI - PubMed

LinkOut - more resources