Macrophage-mediated inflammatory responses impair mucosal barrier components and promote goblet cell loss during Eimeria tenella infection in chickens.

The present study aimed to investigate the role of macrophages in regulating intestinal epithelial barrier integrity during the early stages of Eimeria tenella infection in chickens. The intestinal mucosal barrier, comprising tight junction proteins and mucus-producing goblet cells, plays a critical role in protecting against pathogen invasion. However, the influence of innate immune cells, particularly macrophages, on mucosal barrier components during coccidial infection remains unclear. To examine this, chicks were treated with ι-carrageenan to induce suppression of macrophage-associated responses during E. tenella infection. This was supported by the reduced expression of macrophage markers (MHC-II and CD80) in the spleen, cecal tonsils, and cecum. Histopathological analysis revealed that the ι-carrageenan-treated chicks exhibited significantly lower lesion scores than the infected controls. Notably, the goblet cell numbers were better preserved in the ι-carrageenan-treated chicks, whereas the infected controls showed a marked reduction in the number of goblet cells at 3 and 5 days post-infection. Gene expression analysis demonstrated elevated levels of pro-inflammatory cytokines (interleukin-1β and interferon-γ) and inducible nitric oxide synthase in the infected controls, indicating enhanced inflammatory responses. Contrarily, inhibition of macrophage-related responses attenuated inflammatory signaling in the ι-carrageenan-treated group. Additionally, increased expression of MUC5AC and SAM pointed domain containing ETS transcription factor (SPDEF) were observed in the ι-carrageenan-treated chicks, suggesting enhanced goblet cell-associated responses in the mucosal barrier. Overall, these findings suggest that modulation of macrophage-associated responses is associated with preservation of goblet cells and attenuation of barrier-related pathological changes during E. tenella infection.