PMID- 29403476
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20191120
IS  - 1664-3224 (Print)
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 8
DP  - 2017
TI  - Contribution of IL-1RI Signaling to Protection against Cryptococcus neoformans 
      52D in a Mouse Model of Infection.
PG  - 1987
LID - 10.3389/fimmu.2017.01987 [doi]
LID - 1987
AB  - Interleukin-1 alpha (IL-1alpha) and interleukin-1 beta (IL-1beta) are pro-inflammatory 
      cytokines that are induced after Cryptococcus neoformans infection and activate 
      the interleukin-1 receptor type I (IL-1RI). To establish the role of IL-1RI 
      signaling in protection against cryptococcal infection, we analyzed wild-type 
      (WT) and IL-1RI-deficient (IL-1RI(-/-)) mice on the BALB/c background. 
      IL-1RI(-/-) mice had significantly reduced survival compared to WT mice after 
      intratracheal challenge with C. neoformans 52D. Microbiological analysis showed a 
      significant increase in the lung and brain fungal burden of IL-1RI(-/-) compared 
      to WT mice beginning at weeks 1 and 4 postinfection, respectively. Histopathology 
      showed that IL-1RI(-/-) mice exhibit greater airway epithelial mucus secretion 
      and prominent eosinophilic crystals that were absent in WT mice. Susceptibility 
      of IL-1RI(-/-) mice was associated with significant induction of a Th2-biased 
      immune response characterized by pulmonary eosinophilia, M2 macrophage 
      polarization, and recruitment of CD4(+) IL-13(+) T cells. Expression of 
      pro-inflammatory [IL-1alpha, IL-1beta, TNFalpha, and monocyte chemoattractant protein 1 
      (MCP-1)], Th1-associated (IFNgamma), and Th17-associated (IL-17A) cytokines was 
      significantly reduced in IL-1RI(-/-) lungs compared to WT. WT mice also had 
      higher expression of KC/CXCL1 and sustained neutrophil recruitment to the lung; 
      however, antibody-mediated depletion of these cells showed that they were 
      dispensable for lung fungal clearance. In conclusion, our data indicate that 
      IL-1RI signaling is required to activate a complex series of innate and adaptive 
      immune responses that collectively enhance host defense and survival after C. 
      neoformans 52D infection in BALB/c mice.
FAU - Shourian, Mitra
AU  - Shourian M
AD  - Division of Experimental Medicine, McGill University, Montreal, QC, Canada.
AD  - Meakins-Christie Laboratories, McGill University, Montreal, QC, Canada.
FAU - Ralph, Ben
AU  - Ralph B
AD  - Program in Infectious Diseases and Immunology in Global Health, Centre for 
      Translational Biology, The Research Institute of the McGill University Health 
      Center (RI-MUHC), Montreal, QC, Canada.
AD  - Department of Microbiology and Immunology, McGill University, Montreal, QC, 
      Canada.
FAU - Angers, Isabelle
AU  - Angers I
AD  - Meakins-Christie Laboratories, McGill University, Montreal, QC, Canada.
AD  - Program in Translational Research in Respiratory Diseases, Department of Critical 
      Care, The Research Institute of the McGill University Health Center (RI-MUHC), 
      Montreal, QC, Canada.
FAU - Sheppard, Donald C
AU  - Sheppard DC
AD  - Program in Infectious Diseases and Immunology in Global Health, Centre for 
      Translational Biology, The Research Institute of the McGill University Health 
      Center (RI-MUHC), Montreal, QC, Canada.
AD  - Department of Microbiology and Immunology, McGill University, Montreal, QC, 
      Canada.
AD  - Department of Medicine, McGill University, Montreal, QC, Canada.
FAU - Qureshi, Salman T
AU  - Qureshi ST
AD  - Division of Experimental Medicine, McGill University, Montreal, QC, Canada.
AD  - Meakins-Christie Laboratories, McGill University, Montreal, QC, Canada.
AD  - Program in Translational Research in Respiratory Diseases, Department of Critical 
      Care, The Research Institute of the McGill University Health Center (RI-MUHC), 
      Montreal, QC, Canada.
AD  - Department of Medicine, McGill University, Montreal, QC, Canada.
LA  - eng
PT  - Journal Article
DEP - 20180119
PL  - Switzerland
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
PMC - PMC5780350
OTO - NOTNLM
OT  - Cryptococcus neoformans
OT  - cytokines
OT  - fungal pneumonia
OT  - interleukin-1
OT  - interleukin-1 receptor
OT  - lung inflammation
OT  - lymphocyte differentiation
OT  - macrophage polarization
EDAT- 2018/02/07 06:00
MHDA- 2018/02/07 06:01
PMCR- 2017/01/01
CRDT- 2018/02/07 06:00
PHST- 2017/09/25 00:00 [received]
PHST- 2017/12/21 00:00 [accepted]
PHST- 2018/02/07 06:00 [entrez]
PHST- 2018/02/07 06:00 [pubmed]
PHST- 2018/02/07 06:01 [medline]
PHST- 2017/01/01 00:00 [pmc-release]
AID - 10.3389/fimmu.2017.01987 [doi]
PST - epublish
SO  - Front Immunol. 2018 Jan 19;8:1987. doi: 10.3389/fimmu.2017.01987. eCollection 
      2017.