Expression of immunological molecules by cardiomyocytes and inflammatory and interstitial cells in rat autoimmune myocarditis.
BACKGROUND
In a heart with myocarditis, there are cardiomyocytes, inflammatory cells, and non-inflammatory interstitial cells. Immunological molecules are thought to influence not only inflammatory cells but also cardiac function and remodeling. Whatever their origin, the cells they target and the intercellular crosstalk they mediate remain unclear. Here, we examined native gene expression of immunological molecules in normal and rat experimental autoimmune myocarditis (EAM) 18 and 90 days after immunization, using real time RT-PCR in cardiomyocytes, CD11b(+) cells, alphabetaT cells and non-cardiomyocytic non-inflammatory (NCNI) cells.


RESULTS
Cells were isolated by collagenase perfusion on a Langendorff apparatus and purified by passing through a stainless-steel sieve followed by magnetic bead column separation using appropriate monoclonal antibodies. Most immunological molecules were expressed in inflammatory cells. However, some were expressed in NCNI cells or cardiomyocytes. Interestingly, most of interleukin (IL)-10, monocyte chemoattractant protein (MCP)-1, or tumor necrosis factor (TNF)-alpha receptor were found in NCNI cells and most of fractalkine were found in NCNI cells and cardiomyocytes. Moreover, TNF-alpha significantly upregulated fractalkine and MCP-1 mRNA in cultivated cells from EAM hearts.


CONCLUSIONS
In the rat experimental myocarditis heart, inflammatory cells express many immunological molecules. Some of them are thought to influence NCNI cells or cardiomyocytes directly via receptors on these cell types. It is further suggested that fractalkine, IL-10, and MCP-1 expressed in NCNI cells or cardiomyocytes regulate inflammatory cells.
Yoshida
Tsuyoshi
T
Division of Cardiology, Niigata University Graduate School of Medical and Dental Science, Japan.
Hanawa
Haruo
H
Toba
Ken
K
Watanabe
Hiroshi
H
Watanabe
Ritsuo
R
Yoshida
Kaori
K
Abe
Satoru
S
Kato
Kiminori
K
Kodama
Makoto
M
Aizawa
Yoshifusa
Y
D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology*; D018932:Chemokine CCL2 / Q000032:analysis; D054428:Chemokine CX3CL1; D018925:Chemokines / Q000032:analysis*; D020523:Chemokines, CX3C / Q000032:analysis; D005347:Fibroblasts / Q000276:immunology; D005434:Flow Cytometry; D018960:Hyaluronan Receptors / Q000032:analysis; D007150:Immunohistochemistry / Q000379:methods; D016753:Interleukin-10 / Q000032:analysis; D008565:Membrane Proteins / Q000032:analysis; D009131:Muscle, Smooth, Vascular / Q000276:immunology; D009205:Myocarditis / Q000276:immunology*; D009206:Myocardium / Q000276:immunology / Q000473:pathology; D032383:Myocytes, Cardiac / Q000276:immunology*; D053495:Osteopontin; D051381:Rats; D011917:Rats, Inbred Lew; D017471:Receptors, Interferon / Q000032:analysis; D018124:Receptors, Tumor Necrosis Factor / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012795:Sialoglycoproteins / Q000032:analysis; D013601:T-Lymphocytes / Q000276:immunology*; D000096743:Interferon gamma Receptor
D018932:Chemokine CCL2; D054428:Chemokine CX3CL1; D018925:Chemokines; D020523:Chemokines, CX3C; D018960:Hyaluronan Receptors; D016753:Interleukin-10; D008565:Membrane Proteins; D053495:Osteopontin; D017471:Receptors, Interferon; D018124:Receptors, Tumor Necrosis Factor; D012795:Sialoglycoproteins; D000096743:Interferon gamma Receptor; C491766:Ccl2 protein, rat; C515540:Cx3cl1 protein, rat; C506897:Spp1 protein, rat