PMID- 12540575
OWN - NLM
STAT- MEDLINE
DCOM- 20030226
LR  - 20210526
IS  - 0019-9567 (Print)
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Linking)
VI  - 71
IP  - 2
DP  - 2003 Feb
TI  - Phagocytic activity and monocyte chemotactic protein expression by pulmonary 
      macrophages in persistent pulmonary cryptococcosis.
PG  - 930-6
AB  - The mechanisms by which Cryptococcus neoformans persists in an immunocompetent 
      host are not well understood. Using a rat model of persistent infection, we 
      investigated the ability of pulmonary macrophages (PuM) to phagocytize C. 
      neoformans and produce monocyte chemotactic protein 1 (MCP-1) as a function of 
      the length of time of infection and opsonin. The ability of macrophages to affect 
      serum-mediated phagocytosis varied over the course of infection and was dependent 
      on CD11b/c and CD18 expression. Infection resulted in increased MCP-1 levels 
      within the lung, though the actual amounts varied over the course of infection. 
      Immunohistochemical studies localized MCP-1 expression to macrophages and 
      epithelioid cells. Enhanced production of MCP-1 by PuM from infected rats was 
      confirmed by ex vivo studies. Induction of MCP-1 following serum-mediated 
      phagocytosis was observed for PuM from both infected and noninfected rats and 
      depended on the interaction of C. neoformans with CD11b/c and CD18. Specific 
      antibody was more efficient than serum in promoting phagocytosis and consistently 
      elicited more MCP-1. The relative amount of MCP-1 produced in association with 
      phagocytosis was similar for PuM at all lengths of time of infection. Decreased 
      MCP-1 production was observed for PuM obtained from older rats, including 
      long-term (8 to 10 months)-infected and age-matched controls, suggesting that 
      aging may affect the production of MCP-1 by PuM in response to cryptococcal 
      infection. In summary, our results show that macrophages are an important source 
      of MCP-1 during pulmonary cryptococcosis and that MCP-1 production is actively 
      regulated during infection. Furthermore, we find that phagocytosis of C. 
      neoformans can serve as an important stimulus for MCP-1 production by PuM, though 
      the efficiency of this process is dependent on the opsonin type and may be 
      affected by aging.
FAU - He, Wu
AU  - He W
AD  - Department of Pediatrics, Albert Einstein College of Medicine, Bronx, New York 
      10461, USA.
FAU - Casadevall, Arturo
AU  - Casadevall A
FAU - Lee, Sunhee C
AU  - Lee SC
FAU - Goldman, David L
AU  - Goldman DL
LA  - eng
GR  - AI01300/AI/NIAID NIH HHS/United States
GR  - AI33774/AI/NIAID NIH HHS/United States
GR  - R01 AI033774/AI/NIAID NIH HHS/United States
GR  - R01 HL059842/HL/NHLBI NIH HHS/United States
GR  - AI3342/AI/NIAID NIH HHS/United States
GR  - HL-59842-01/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (CD11b Antigen)
RN  - 0 (CD11c Antigen)
RN  - 0 (Chemokine CCL2)
SB  - IM
MH  - Animals
MH  - CD11b Antigen/metabolism
MH  - CD11c Antigen/metabolism
MH  - Chemokine CCL2/*metabolism
MH  - Chronic Disease
MH  - Cryptococcosis/immunology
MH  - Cryptococcus neoformans/*immunology
MH  - Disease Models, Animal
MH  - Lung/immunology/microbiology
MH  - Lung Diseases, Fungal/*immunology
MH  - Macrophages, Alveolar/*immunology/microbiology
MH  - Male
MH  - *Phagocytosis
MH  - Rats
MH  - Rats, Inbred F344
PMC - PMC145381
EDAT- 2003/01/24 04:00
MHDA- 2003/02/27 04:00
PMCR- 2003/02/01
CRDT- 2003/01/24 04:00
PHST- 2003/01/24 04:00 [pubmed]
PHST- 2003/02/27 04:00 [medline]
PHST- 2003/01/24 04:00 [entrez]
PHST- 2003/02/01 00:00 [pmc-release]
AID - 1151 [pii]
AID - 10.1128/IAI.71.2.930-936.2003 [doi]
PST - ppublish
SO  - Infect Immun. 2003 Feb;71(2):930-6. doi: 10.1128/IAI.71.2.930-936.2003.