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Quantification, dynamics, and mechanisms of pulmonary inflammatory response around schistosomula of Schistosoma
Abstract:
The inflammatory response around schistosomula injected into the lungs of uninfected mice and mice infected with Schistosoma mansoni was quantified. In uninfected mice, the inflammatory response started at 1 hour and peaked at 6 days, whereas in the infected mice, the inflammatory response was accelerated and peaked at 24 hours. This latter inflammatory reaction was 1.5 times greater than the 6-day reaction found in uninfected controls. Neutrophils and mononuclear cells were seen around schistosomula impacted into the pulmonary microvasculature by 1 hour; later, however, eosinophils constituted the predominant cell. This augmented inflammatory response was detected in mice infected with S mansoni first at 4 weeks after injection and peaked at 12 weeks. The augmented response correlated with acquired resistance as assayed by the recovery of the organisms from the lungs 4 days after challenge. Augmented inflammatory reaction and increased protection was induced by subcutaneous sensitization with dead schistosomula or eggs but not by cercariae or adult worms. Adoptive transfer of serum but not lymphoid cells from 12-15 week-infected mice resulted in augmented inflammation and enhanced resistance in recipient normal animals. The serum activity was absorbed by both schistosomula and eggs and was shown to reside in the fraction containing IgG1.
Insights
Mice infected with Schistosoma mansoni show an accelerated and amplified inflammatory response in the lungs. This enhanced immune reaction, mediated by serum IgG1, confers resistance against subsequent parasite challenge.
Area of Science:
- Immunology
- Parasitology
- Pulmonary Medicine
Background:
- Schistosomiasis is a significant global health concern caused by parasitic flatworms.
- The host immune response to Schistosoma mansoni infection, particularly in the lungs, is complex and not fully understood.
- Understanding the inflammatory kinetics and protective mechanisms is crucial for developing effective interventions.
Purpose of the Study:
- To quantify and characterize the inflammatory response in mouse lungs following Schistosoma mansoni infection.
- To investigate the correlation between the augmented inflammatory response and acquired resistance.
- To identify the components of the immune system responsible for the enhanced inflammatory reaction and protection.
Main Methods:
- Intranasal injection of schistosomula into naive and Schistosoma mansoni-infected mice.
- Quantification of inflammatory cell infiltration (neutrophils, mononuclear cells, eosinophils) in lung tissue.
- Assessment of acquired resistance through parasite recovery assays.
- Evaluation of immune mediators via adoptive serum and lymphoid cell transfer experiments.
- Immunoglobulin G1 (IgG1) isolation and characterization.
Main Results:
- Infection with Schistosoma mansoni accelerated and amplified the pulmonary inflammatory response, peaking at 24 hours compared to 6 days in naive mice.
- The augmented inflammatory response correlated with increased resistance to parasite challenge.
- Subcutaneous sensitization with dead schistosomula or eggs, but not adult worms or cercariae, induced both augmented inflammation and protection.
- Adoptive transfer of serum from infected mice, but not lymphoid cells, conferred enhanced inflammation and resistance to naive recipients.
- The protective serum activity was attributed to IgG1 antibodies that bound to both schistosomula and eggs.
Conclusions:
- Schistosoma mansoni infection elicits a potent, accelerated inflammatory response in the lungs.
- Acquired resistance is mediated by serum factors, primarily IgG1 antibodies, which are induced by schistosomula and eggs.
- This study elucidates key immunological mechanisms underlying host defense against Schistosoma mansoni, highlighting the role of antibody-mediated inflammation.