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Regulation of Granulocyte Responses in the Blood and Peritoneal Cavity of CBA and B10 Mice During an Acute Inflammation
Author(s) -
Sluiter W.,
ElzengaClaasen I.,
HemsbergenOomens L.W.M.,
Kleyvan Andel A.,
Dissel J.T.,
Furth R.
Publication year - 1987
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.42.6.653
Subject(s) - granulocytosis , granulocyte , peritoneal cavity , inflammation , biology , immunology , granulocyte colony stimulating factor , ratón , bone marrow , peritonitis , immune system , chemotherapy , genetics , anatomy
The regulatory mechanisms that determine the course of an inflammation induced by an intraperitoneal injection of kaolin were investigated in Listeria‐susceptible CBA and Listeria‐resistant B10 mice. The magnitude of the granulocyte inflammatory response in the peritoneal cavity was high in B10 mice (area under the curve; AUC 0‐48 h : 210.9 × 10 6 granulocytes/mouse × h) and lower in CBA mice AUC 0‐48 h : 136.8 × 10 6 granulocytes/mouse × h), whereas the reverse was seen for the granulocyte response in the peripheral blood (AUC 0‐48 h = 30.5 and 80.7 × 10 6 granulocytes/mouse × h, respectively). With respect to the presence of humoral factors that affect the number of granulocytes in the circulation, sera of both mouse strains sampled 24 h after the kaolin injection had granulocytosis‐inducing effect in CBA recipient mice and did not induce a response in the B10 recipient mice. This divergent sensitivity to serum factors inducing granulocytosis is consistent with the difference in the blood granulocyte response of B10 and CBA mice but does not explain the divergent inflammatory responses in the peritoneal cavity. Computer simulation showed that at least two factors must be taken into consideration to explain the differences in the inflammatory response, i.e., a factor regulating the release of granulocytes from the bone marrow and a factor governing the rate of granulocyte efflux from the site of inflammation.