PMID- 26819497
OWN - NLM
STAT- MEDLINE
DCOM- 20160920
LR  - 20181113
IS  - 1466-1861 (Electronic)
IS  - 0962-9351 (Print)
IS  - 0962-9351 (Linking)
VI  - 2015
DP  - 2015
TI  - Resistance to P. brasiliensis Experimental Infection of Inbred Mice Is Associated 
      with an Efficient Neutrophil Mobilization and Activation by Mediators of 
      Inflammation.
PG  - 430525
LID - 10.1155/2015/430525 [doi]
LID - 430525
AB  - Paracoccidioidomycosis (PCM) is a systemic fungal infection, endemic in Brazil, 
      that leads to severe morbidity and even mortality if not correctly treated. 
      Patients may respond differently to PCM depending on the pattern of the acquired 
      immune response developed. The onset of protective immune response is notably 
      mediated by neutrophils (PMN) that play an important role through directly 
      killing the fungi and also by interacting with other cell types to modulate the 
      acquired protective immune response that may follow. In that way, this study 
      aimed to present and compare different experimental models of PCM 
      (intraperitoneal and subcutaneous) regarding PMN production and maturation inside 
      femoral bone marrow and also PMN infiltration in peritoneal and subcutaneous 
      exudates of resistant and susceptible mice. We also assessed the fungal colony 
      forming units and the levels of soluble inflammatory mediators (LTB4, KC, IFN-gamma, 
      GM-CSF, and IL-10) inside subcutaneous air-pouches to compare the efficiency of 
      the PMN present at this site in relation to the two main neutrophil functions: 
      initial lysis of the invading pathogen and modulation of the acquired immune 
      response. P. brasiliensis inoculated intraperitoneally was able to disseminate to 
      the bone marrow of susceptible mice, causing a more marked alteration of PMN 
      production and maturation than that observed after resistant mice infection by 
      the same route. Subcutaneous air-pouch inoculation of P. brasiliensis elicited a 
      controlled and limited infection that produced a PMN-rich exudate, thus favoring 
      the study of the interaction between the fungus and the neutrophils. Susceptible 
      mice produced higher numbers of PMN; however, these cells were less effective in 
      killing the fungi. Inflammatory cytokines were more pronounced in resistant mice, 
      which supports their PCM raised resistance.
FAU - Sperandio, Felipe Fornias
AU  - Sperandio FF
AD  - Instituto de Ciencias Biomedicas, Universidade Federal de Alfenas (UNIFAL), 
      Brazil.
FAU - Fernandes, Gisele Pesquero
AU  - Fernandes GP
AD  - Setor de Ciencias da Saude, Universidade Federal do Parana (UFPR), Brazil.
FAU - Mendes, Ana Carolina Silverio Cerqueira
AU  - Mendes AC
AD  - Instituto de Ciencias Biomedicas, Universidade Federal de Alfenas (UNIFAL), 
      Brazil.
FAU - Bani, Giulia Maria de Alencar Castro
AU  - Bani GM
AD  - Instituto de Ciencias Biomedicas, Universidade Federal de Alfenas (UNIFAL), 
      Brazil.
FAU - Calich, Vera Lucia Garcia
AU  - Calich VL
AD  - Instituto de Ciencias Biomedicas, Universidade de Sao Paulo (USP), Brazil.
FAU - Burger, Eva
AU  - Burger E
AD  - Instituto de Ciencias Biomedicas, Universidade Federal de Alfenas (UNIFAL), 
      Brazil.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20151224
PL  - United States
TA  - Mediators Inflamm
JT  - Mediators of inflammation
JID - 9209001
RN  - 0 (IL10 protein, mouse)
RN  - 0 (Inflammation Mediators)
RN  - 130068-27-8 (Interleukin-10)
SB  - IM
MH  - Animals
MH  - Bone Marrow/pathology
MH  - *Cell Movement
MH  - Inflammation Mediators/*physiology
MH  - Interleukin-10/physiology
MH  - Male
MH  - Mice
MH  - *Neutrophil Activation
MH  - Neutrophils/cytology/*immunology
MH  - Paracoccidioides
MH  - Paracoccidioidomycosis/*immunology/pathology
PMC - PMC4706933
EDAT- 2016/01/29 06:00
MHDA- 2016/09/22 06:00
PMCR- 2015/12/24
CRDT- 2016/01/29 06:00
PHST- 2015/07/03 00:00 [received]
PHST- 2015/10/21 00:00 [revised]
PHST- 2015/10/25 00:00 [accepted]
PHST- 2016/01/29 06:00 [entrez]
PHST- 2016/01/29 06:00 [pubmed]
PHST- 2016/09/22 06:00 [medline]
PHST- 2015/12/24 00:00 [pmc-release]
AID - 10.1155/2015/430525 [doi]
PST - ppublish
SO  - Mediators Inflamm. 2015;2015:430525. doi: 10.1155/2015/430525. Epub 2015 Dec 24.