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Friend virus-induced inhibition of eosinophil granulocyte exudation in mice
Abstract:
Exudation of eosinophil polymorphonuclear leukocytes (E-PMN) in response to tetanus toxoid (TT) was studied in DBA/2HaD mice with erythroleukemia induced by Friend virus (FV). The inhibition of exudation that developed was independent of increased levels of serum corticosteroids and occurred in surgically adrenalectomized mice. Thus it was independent of steroid-induced effects on E-PMN. The accumulation of neutrophil polymorphonuclear leukocytes (N-PMN) in TT-induced exudates was unaltered. Furthermore, N-PMN exudation in response to other inflammatory stimuli was similarly unimpaired in virus-infected mice, which confirmed the specificity of the inhibition for E-PMN. The virus entity in the FV complex responsible for the effect was not identified. Friend murine leukemia virus, the indigenous helper virus for the defective spleen focus-forming virus, alone, was incapable of inducing the inhibition. It is possible that the lack of participation of E-PMN in TT-induced immune inflammatory exudates in FV-infected mice reflects an unresponsiveness that contributes to the development and progression of leukemia in FV-infected mice.
Insights
Friend virus (FV) infection specifically inhibits eosinophil polymorphonuclear leukocyte (E-PMN) exudation in mice. This impairment, independent of corticosteroids, may contribute to leukemia development.
Area of Science:
- Immunology
- Virology
- Hematology
Background:
- Eosinophil polymorphonuclear leukocytes (E-PMN) play a role in immune responses.
- Friend virus (FV) complex causes erythroleukemia in mice.
- Understanding immune cell behavior during viral infections is crucial.
Purpose of the Study:
- To investigate the effect of Friend virus (FV) infection on eosinophil polymorphonuclear leukocyte (E-PMN) exudation.
- To determine if FV-induced inhibition of E-PMN is corticosteroid-dependent.
- To explore the potential link between impaired E-PMN response and leukemia progression.
Main Methods:
- Studied E-PMN exudation in response to tetanus toxoid (TT) in FV-infected DBA/2HaD mice.
- Utilized surgically adrenalectomized mice to assess corticosteroid independence.
- Compared neutrophil polymorphonuclear leukocyte (N-PMN) exudation to confirm E-PMN specificity.
Main Results:
- FV infection significantly inhibited E-PMN exudation in response to TT.
- The inhibition was independent of serum corticosteroids and adrenalectomy.
- Neutrophil polymorphonuclear leukocyte (N-PMN) exudation remained unaltered, indicating specificity for E-PMN.
Conclusions:
- Friend virus (FV) infection specifically impairs eosinophil polymorphonuclear leukocyte (E-PMN) inflammatory response.
- This E-PMN unresponsiveness may contribute to the development and progression of FV-induced erythroleukemia.
- The specific viral component responsible for this immunomodulation requires further identification.