Aims/hypothesis Maggots of the blowfly Lucilia sericata are
used for the treatment of chronic wounds. As monocytes
may contribute to the excessive inflammatory responses in
such wounds, this study focussed on the effects of maggot
secretions on the pro-inflammatory activities of these cells.
Methods Freshly isolated monocytes were incubated
with a range of secretions for 1 h and then stimulated with
lipopolysaccharides (range 0–100 ng/ml) or lipoteichoic acid
(range 0–5μg/ml) for 18 h. The expression of cell surface
molecules, cytokine and chemokine levels in culture supernatants,
cell viability, chemotaxis, and phagocytosis and
killing of Staphylococcus aureus were measured.
Results Maggot secretions dose-dependently inhibited production
of the pro-inflammatory cytokines TNF-α, IL-
12p40 and macrophage migration inhibitory factor by
lipopolysaccharides- and lipoteichoic acid-stimulated
monocytes, while enhancing production of the antiinflammatory
cytokine IL-10. Expression of cell surface
receptors involved in pathogen recognition remained unaffected
by secretions. In addition, maggot secretions altered the
chemokine profile of monocytes by downregulating macrophage
inflammatory protein-1β and upregulating monocyte
chemoattractant protein-1 and IL-8. Nevertheless, chemotactic
responses of monocytes were inhibited by secretions.
Furthermore, maggot secretions did not affect phagocytosis
and intracellular killing of S. aureus by human monocytes.
Finally, secretions induced a transient rise in the intracellular
cyclic AMP concentration in monocytes and Rp-cyclic
AMPS inhibited the effects of secretions.
Conclusions/interpretation Maggot secretions inhibit the
pro-inflammatory responses of human monocytes through
a cyclic AMP-dependent mechanism. Regulation of the
inflammatory processes by maggots contributes to their
beneficial effects on chronic wounds.