Elevation of cytokines and antibodies in guinea pigs experimentally infected with Tunga penetrans

Aim: Tungiasis caused by Tunga penetrans is a neglected tropical disease that majorly affects children, the elderly and persons living with disabilities in rural homes in sub-Saharan Africa. The disease is characterized by swelling and inflammation symptoms, especially on the hands and feet. However, it is unclear whether inflammatory responses induced by T. penetrans may be associated with alterations of cytokine and antibody profiles. The study evaluated the immunological changes: cytokine and antibody profiles of experimentally raised guinea pigs exposed to T. penetrans. Methods: A total of 24 guinea pigs were experimented on; 16 were exposed to T. penetrans while 8 were controls. Blood samples were collected before and after exposure. Enzyme-linked immunosorbent assay (ELISA) technique was used to quantify cytokines and antibodies. Data analysis was performed using GraphPad Prism 10.4. Results: At day 10 of post-infection, guinea pigs showed significant elevation (p < 0.05) of pro-inflammatory cytokines, tumor necrosis factor alpha (TNF-α) (235 pg/mL), and interferon gamma (IFN-γ) (425 pg/mL) in the serum. Anti-inflammatory cytokine had a delayed elevation, with interleukin-4 (IL-4) peaking to 357 pg/mL by day 15, while IL-10 rose to 367 pg/mL by day 15 of post-infection. Total systemic circulating levels of antibodies in serum were significantly elevated (p < 0.05), with immunoglobulin E (IgE) elevating to 232 ng/mL while IgG peaking at 272 ng/mL on day 15 post-infection. Conclusions: Pro-inflammatory cytokines elevated during the early stages of infection may serve as early markers for the infection, and their potential role in the pathogenesis of tungiasis needs to be explored further. The study has established that IgE and IgG are important antibodies that are produced in response to tungiasis, and their efficacy in controlling the infection needs to be further explored for potential alleviation of severe forms of the infection.