Corneal Wounds May Heal Following Maggot Secretion and Excretion Therapy

Maggot therapy may reduce inflammatory cytokine production and promote corneal wound healing, according to a study published in Ocular Surface. These healing properties were consistent in both in vitro and in vivo models.  

Researchers cultured human corneal epithelial cells with maggot excretions and secretions (ES) and determined cell viability through a 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay. The team used quantitative polymerase chain reaction (qPCR) and enzyme-linked immunosorbent assay (ELISA) to determine the ability of the ES to modulate toll-like receptor (TLR)-induced IL-6 and IL-8 cytokine expression. Human corneal epithelial cells were evaluated in vitro, while a murine model was used to evaluate migration assay in vivo. Wounded corneas were imaged at the time of wounding and every 6 hours for 24 hours.

According to the report, maggot ES did not impair corneal epithelial cell viability up to 25μg/mL. Among the factors researchers evaluated, only the human beta defensin 2 (hBD-2) peptide was upregulated by 1.5μg/mL ES after 6hrs (P=.04). In human corneal epithelial cells, maggot ES reduced Poly I:C-induced IL-6 and IL-8 mRNA (P ≤.001) and protein (P ≤.0001) expression. Overall, the greatest in vitro migration effect was observed with 6.2μg/mL ES after 44hrs, indicated by a gap area of 53.3±3.7%  compared with the vehicle (500 μL of media) gap area (72.6±5.4%; P =.001). 

Analysis of the in vivo model revealed that wound area reduced significantly at 12 (P =.003) and 18 hours (P =.006) when treated with ES compared with a phosphate buffered saline solution. Overall, ES reduced the wounded area by 77% compared with the control solution.  

“Maggot ES accelerate wound healing rates in vitro and in vivo and suppress TLR-induced production of pro-inflammatory cytokines IL-8 and IL-6,” according to the researchers. “Anti-inflammatory effects of ES can be observed at low concentrations, are rapid (detectable within 6hrs) and are present when ES are added before, at the same time and most importantly after the inflammatory response has been initiated. These data directly point to a dual mechanism of action of ES in modulating wound healing by controlling inflammation and accelerating corneal wound closure.” 

Study limitations include a lack of testing on human participants.