当前位置： SCI文献检索 > CYTOKINE期刊下所有文献 > Human neutrophils produce IL-12, IL-10, PGE2 and LTB4 in response to Paracoccidioides brasiliensis. Involvement of TLR2, mannose receptor and dectin-1.

Human neutrophils produce IL-12, IL-10, PGE2 and LTB4 in response to Paracoccidioides brasiliensis. Involvement of TLR2, mannose receptor and dectin-1.

Abstract：

:The functions of phagocytic cells against pathogens are initiated by the interaction between membrane receptors and molecular structures which compose the cell wall of these microorganisms. Thus our study aimed to identify the neutrophil receptors involved in the recognition of different strains of Paracoccidioides brasiliensis and the consequent modulation of immune response through the production of cytokines and inflammatory mediators. Neutrophils did not produce TNF-alfa in response to both strains. However, these cells produce IL-12, mainly in response to Pb 265, with participation of TLR2 and dectin-1. These cells also produce L-10, whose levels were higher for Pb 18 with involvement of TLR2 and MR and only TLR2 for Pb 265. The production of PGE2 and LTB4 was detected similarly for the two strains. For PGE2, MR and dectin-1 were involved, while in relation to LTB4, none of them. In summary, we demonstrated that neutrophils have a dynamic role during host immune response to P. brasiliensis, since in addition to their role as effector cells of innate immunity; they have the capacity to modulate innate and adaptative immune response against this fungus by producing cytokines and lipidic mediators. This modulation may be toward a pró- or anti-inflammatory pattern in a dependence of P. brasiliensis strains and PRR involved in fungus recognition by these cells.

journal_name

Cytokine

journal_title

Cytokine

authors

Balderramas HA,Penitenti M,Rodrigues DR,Bachiega TF,Fernandes RK,Ikoma MR,Dias-Melicio LA,Oliveira SL,Soares ÂM

doi

10.1016/j.cyto.2014.02.004

subject

Has Abstract

pub_date

2014-05-01 00:00:00

pages

36-43

issue

1

eissn

1043-4666

issn

1096-0023

pii

S1043-4666(14)00046-5

journal_volume

67

pub_type

杂志文章

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