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Peripheral Blood Eosinophilia in Guinea‐pigs following Implantation of Anaphylactic Guinea‐pig and Human Lung
Author(s) -
Parish W. E.,
Coombs R. R. A.
Publication year - 1968
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1968.tb06994.x
Subject(s) - eosinophil , eosinophilia , medicine , guinea pig , anaphylaxis , lung , histamine , immunology , peritoneal cavity , pathology , allergy , asthma , surgery
S ummary . Samples of anaphylactic guinea‐pig lung implanted in the peritoneal cavity of normal guinea‐pigs induced an eosinophilia in the peripheral blood 24 hours later; samples of normal, non‐anaphylactic lung caused only a slight rise in the number of eosinophils. Samples of diaphragm from guinea‐pigs killed by anaphylaxis stimulated a smaller increase of eodnophils in the recipients than that caused by lung, but diaphragm taken from normal animals depressed the eosinophil count of the recipients to zero. The eosinophil‐stimulating factor was present in cell‐free extracts of anaphylactic lungs tested by intraperitoneal injection, though it was unable to diffuse through Millipore membranes in vivo . Antigen‐antibody complexes prepared in vitro , and sensitized tissue treated with antigen, stimulated an eosinophilia in normal guinea‐pigs, and such complexes are believed to be the eosinophil‐stimulating factor in anaphylactic lung. Intraperitoneal injections of 2 and 20 μ g . histamine were followed by an eosinophilia in the peripheral blood 3–6 hours later. However, histamine does not appear to be the eosinophil‐stimulating factor in post‐mortem anaphylactic tissue. Fresh human lung from infants dying suddenly from unexplained causes, possibly an anaphylactic cot death, implanted in the peritoneal cavity of normal guinea‐pigs depressed the eosinophil counts, though not completely and to a lesser extent than lung from infants dying of other causes, which depressed the eosinophil counts to zero. This test in guinea‐pigs is not reliable evidence of anaphylaxis in post‐mortem tissue and therefore cannot be used to put to a crucial test the hypothesis that cot death may result from anaphylaxis. Nevertheless, there was some indirect evidence for an eosinophil‐stimulating factor in the lungs of all of four cot‐death cases, and this was absent from the lungs of all of three infants dying of other causes; this is slight evidence, more in favour of the anaphylactic hypothesis than against it.