The Interaction Between Giardiasis and Host Mucosal Immune System: A Review

Abstract

Giardia spp. is an intestinal protozoal parasite that infect humans and many different other mammalian hosts. The most significant clinical features of giardia infection are malabsorption and diarrhea. Giardia lamblia possesses the remarkable ability to continually alter its dominant surface antigen, known as the variant surface protein (VSP), allowing it to evade host immune detection. Infection with this protozoan trigger a strong adaptive immune response in both humans and animal models. It has long been established that significant amounts of parasite-specific IgA are produced following infection, with CD4+ T lymphocytes playing a pivotal role in stimulating IgA synthesis and contributing to the regulation of the infection. Although anti-VSP IgA antibodies in the gut have been demonstrated to influence the parasite’s antigenic switching, the extent to which local intestinal antibodies directly control Giardia colonization remains a subject of debate. The interface between the intestinal lumen and the epithelial lining serves as the primary attachment site for Giardia trophozoites, making it a critical zone for both the establishment of the parasite and the initiation of host immune defenses. This area thus represents a central battleground where host-pathogen interactions dictate the outcome of infection. This review will therefore focus on innate immune mechanisms and barrier integrity in giardiasis. The specific aims of this review are centered on elucidating the multifaceted interactions between Giardia and the host intestinal environment. First, the review seeks to characterize how Giardia disrupts epithelial junctional complexes and alters the cytoskeletal architecture, compromising intestinal barrier integrity. Second, it aims to examine the innate immune responses initiated by various cell types, including epithelial cells, macrophages, dendritic cells, and Paneth cells, in reaction to Giardia infection and its secreted molecules. Third, the review intends to analyze how these host–parasite interactions contribute to persistent barrier dysfunction and facilitate microbial translocation, which may exacerbate inflammatory outcomes. Finally, it explores potential therapeutic strategies that strengthen epithelial barrier function and modulate innate immune mechanisms to mitigate the pathological effects of giardiasis and promote mucosal homeostasis.