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Phagocytosis of Leptospira by leukocytes from mice with different susceptibility to leptospirosis and possible role of chemokines.

Authors :
Silva PLD
Lauretti-Ferreira F
Caldas de Lima M
Lima SS
Covarrubias AE
De Franco M
Carvalho E
Ho PL
da Costa RMA
Martins EAL
Da Silva JB
Source :
BMC microbiology [BMC Microbiol] 2019 Jan 07; Vol. 19 (1), pp. 4. Date of Electronic Publication: 2019 Jan 07.
Publication Year :
2019

Abstract

Background: Leptospirosis is a widespread zoonosis caused by pathogenic prokaryotic microbes of the genus Leptospira. Although there are several reports in the literature, host-pathogen interaction is still poorly understood. The role of chemokine expression is important on the chemotaxis, activation and regulation of immune cells. Recent studies have shown that their expression profiles play an important role on the severity of leptospirosis outcome. We evaluated the phagocytosis of Leptospira by spleens cells from C3H/HeJ, C3H/HePas and BALB/c mouse strains, respectively susceptible, intermediate and resistant to leptospirosis, and by RAW 264.7 macrophages. Besides, we evaluated the effects of CCL2 treatment on the phagocytosis. The cells were incubated with or without CCL2 chemokine, and infected with virulent L. interrogans sv Copenhageni. Cells and culture supernatants were collected for subsequent analysis.<br />Results: The number of leptospires was higher in BALB/c cells, CCL2 pre-treated or only infected groups, when compared to C3H/HeJ and C3H/HePas cells. Indeed, CCL2 activation did not interfere in the phagocytosis of Leptospira. Expression of chemokines CXCL5 and CCL8 levels were significantly inhibited in infected BALB/c cells when compared to the non-infected control.<br />Conclusions: Higher ability to phagocytosis and early modulation of some chemokines correlated with the resistance to leptospirosis disease. Exposure to CCL2 did not interfere on phagocytosis of Leptospira in our experimental conditions, but acted in the modulation of chemokines expression during Leptospira infection.

Details

Language :
English
ISSN :
1471-2180
Volume :
19
Issue :
1
Database :
MEDLINE
Journal :
BMC microbiology
Publication Type :
Academic Journal
Accession number :
30616505
Full Text :
https://doi.org/10.1186/s12866-018-1371-9