"In vivo" leukocyte chemotaxis in experimental mice Schistosoma mansoni infection

Abstract

The "in vivo" chemotaxis was studied in C57B1/10 mice 10, 30, 50 and 60 days after a Schistosoma mansoni infection in comparison to a control group (uninfected mice). Staphylococcal protein A was injected into a connective tissue air pouch of control and experimental mice and the leukocyte chemotaxis was counted. A decrease in polymorphonuclear (PMN) leukocyte response was found in infected mice in comparison to the control group (p<0.05). The 10 day infected mice showed a decreased PMN leukocyte response respecting the control group (p<0.05) and this finding became more evident 30 and 50 days post-infection. Although the PMN leukocyte response of 60 day infected mice increased in comparison to 50 day infected animals, it was still significantly lower the control response. The mononuclear leukocyte response was not significantly different between infected or uninfected mice.

Systemic modulation of peripheral eosinophilia (air pouch model) in Schistosoma mansoni infection

“…Other additional mechanisms can contribute to explain the down-modulation in the acute phase: (1) massive and compartmentalized mobilization of blood eosinophils to organs that suffer egg embolism; (2) large release of soluble adhesion molecules to the circulation, blocking leukocyte-endothelial interactions (Evan Secor et al 1994); (3) compartmentalized response of the air pouch to egg stimulation. Using protein A-stimulated air pouch, Teixeira et al (1994) showed a decrease of polimorphonuclear migration in mice infected with S. mansoni, mainly in the acute phase of the infection. The same phenomenon was observed by Abath et al (1988), in acute Trypanosoma cruzi infected mice; and (4) alterations of eosinophil capabilities by soluble factors.…”

Enhanced Interleukin-12 and CD40 Ligand Activities but ReducedStaphylococcus aureusCowan 1-Induced Responses Suggest a Generalized and Progressively Impaired Type 1 Cytokine Pattern for Human Schistosomiasis

“…Nonetheless, defects in leukocyte chemotaxis in experimental schistosomiasis have been observed (39), although the reasons for these findings have not been investigated further. In this work, we report defects in type 1 cytokine expression following stimulation of WBC cultures with various T-cell-dependent and T-cell-independent stimuli and relate these deficiencies to the different clinical stages of human schistosomiasis infection.…”