A new form of localized allergic encephalomyelitis featuring polymorphonuclear neutrophilic leukocytes.
Mononuclear inflammatory infiltrates are characteristic of experimental allergic encephalomyelitis (EAE). Localized EAE was produced in rats in a single day by passive transfer of living lymphoid cells from immunized donors to non-immunized recipients with thermal brain injuries. When the recipients were pretreated with cyclophosphamide 1 or 2 days before cell transfer, neutrophils in the EAE infiltrates notably increased and mononuclear leukocytes decreased. This neutrophilic form of EAE was produced with cells from donors immunized with whole neural tissue or purified myelin basic protein and with adjuvants of different types. This lesion could not be reproduced if the EAE cells were replaced by EAE serum or by irrelevantly immunized cells, or if their activity was foiled by specific "desensitization" or by use of histoincompatible recipients. The 2-day period during which cyclophosphamide prepared recipients for neutrophilic EAE coincided with a transient lymphopenia and relative neutrocytosis caused by the drug. The passive transfer system made it possible for the drug to unbalance the recipient's hemopoietic system without risking adverse effects on the donor cells. The rapid development of the localized form of EAE made it possible to produce lesions before the recipient's transient imbalance gave way to pancytopenia. The new form of EAE may be useful for investigating autoimmune diseases because the neutrophils which indicate the immunologic injury are instantly recognized as reactive recipient cells. Preexisting conventional (mononuclear) EAE prevented subsequent production of neutrophilic infiltrates. This inhibitory effect may be due to local blockade of vessels by mononuclear cells, a concept for which there is evidence. These considerations suggest that the exudation of neutrophils in the new form of EAE may be due to suppression by cyclophosphamide of the mononuclear component of the inflammatory reaction, with loss of its blockading and protective influence on the vessels.
D000477:Alkylating Agents / Q000494:pharmacology; D000818:Animals; D001921:Brain / Q000276:immunology; D002056:Burns / Q000276:immunology; D003520:Cyclophosphamide / Q000494:pharmacology*; D003609:Dactinomycin / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology; D004195:Disease Models, Animal; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology*; D004731:Endotoxins / Q000494:pharmacology; D005260:Female; D006168:Guinea Pigs; D007114:Immunization; D007116:Immunization, Passive; D008297:Male; D008854:Microscopy, Electron; D009504:Neutrophils / Q000276:immunology*; D051381:Rats
D000477:Alkylating Agents; D004731:Endotoxins; D003609:Dactinomycin; D003907:Dexamethasone; D003520:Cyclophosphamide