PMID- 14568960
OWN - NLM
STAT- MEDLINE
DCOM- 20040130
LR  - 20190516
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 171
IP  - 9
DP  - 2003 Nov 1
TI  - The phenotype of inflammatory macrophages is stimulus dependent: implications for 
      the nature of the inflammatory response.
PG  - 4816-23
AB  - Many diseases are characterized by inflammatory reactions involving both the 
      innate and adaptive arms of the immune system. Thioglycolate medium (TM) 
      injection into the peritoneal cavity has long been used as a stimulus for 
      eliciting inflammatory macrophages for study and for determining the importance 
      of a particular mediator in inflammation. However, the response to this irritant 
      may not be relevant to many inflammatory diseases. Therefore, we have developed 
      an Ag-specific peritonitis model using methylated BSA (mBSA) as the stimulus. 
      Priming mice intradermally with mBSA in adjuvant and boosting 14 days later, 
      followed by an i.p. challenge with mBSA after an additional 7 days, led to an 
      inflammatory reaction equivalent in magnitude to that induced with TM as judged 
      by the number of exudate cells. The inflammatory macrophages elicited by the mBSA 
      protocol differed, being smaller and less vacuolated than TM-elicited 
      macrophages. Also, macrophages from 4-day mBSA-induced exudates expressed more 
      MHC class II than TM-induced exudates, were able to stimulate allogeneic T 
      lymphocytes, and upon in vitro stimulation with LPS secreted greater levels of 
      IL-6 and IL-1beta. Macrophages from 4-day TM-induced exudates, on the other hand, 
      expressed Ly6C and ER-MP58, immature myeloid markers. The inflammatory response 
      elicited using the Ag mBSA may be more relevant for studying the inflammatory 
      responses in many diseases, such as those of autoimmune origin and those 
      involving an acquired immune response.
FAU - Cook, Andrew D
AU  - Cook AD
AD  - Arthritis and Inflammation Research Center, Department of Medicine, and 
      Cooperative Research Center for Chronic Inflammatory Diseases, University of 
      Melbourne, Parkville, Victoria, Australia. adcook@unimelb.edu.au
FAU - Braine, Emma L
AU  - Braine EL
FAU - Hamilton, John A
AU  - Hamilton JA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Antigens, Surface)
RN  - 0 (Epitopes)
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (Integrins)
RN  - 0 (Thioglycolates)
RN  - 0 (methylated bovine serum albumin)
RN  - 27432CM55Q (Serum Albumin, Bovine)
SB  - IM
MH  - Animals
MH  - Antigens, Surface/analysis
MH  - Ascitic Fluid/immunology/pathology
MH  - Cell Count
MH  - Cell Lineage/immunology
MH  - Disease Models, Animal
MH  - Eosinophils/chemistry/immunology/pathology
MH  - Epitopes/administration & dosage/immunology
MH  - Histocompatibility Antigens Class II/biosynthesis
MH  - Immunity, Active/immunology
MH  - *Immunophenotyping/methods
MH  - Injections, Intraperitoneal
MH  - Integrins/biosynthesis
MH  - Lymphocyte Culture Test, Mixed
MH  - Macrophages, Peritoneal/chemistry/*immunology/*pathology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Peritoneal Cavity/pathology
MH  - Peritonitis/*immunology/metabolism/*pathology
MH  - Serum Albumin, Bovine/administration & dosage/immunology
MH  - Thioglycolates/administration & dosage
EDAT- 2003/10/22 05:00
MHDA- 2004/01/31 05:00
CRDT- 2003/10/22 05:00
PHST- 2003/10/22 05:00 [pubmed]
PHST- 2004/01/31 05:00 [medline]
PHST- 2003/10/22 05:00 [entrez]
AID - 10.4049/jimmunol.171.9.4816 [doi]
PST - ppublish
SO  - J Immunol. 2003 Nov 1;171(9):4816-23. doi: 10.4049/jimmunol.171.9.4816.