Assessment of the intestinal immune response in Giardia duodenalis experimentally infected rats using quantitative real-time PCR

Abstract

Background: Giardia duodenalis is a well-known intestinal parasite. The host immune response needs much effort to be clarified. Objective: Evaluation of the transcriptional level of a panel of cytokines in intestinal tissue and assessing the correlation between these levels and cyst count. Material and Methods: An experimental G. duodenalis infection was conducted in a rat model composed of twentyfive laboratory-bred, parasite-free male albino rats, divided into 10 for control group and 15 for infected group. Samples from intestinal tissues were collected to investigate interferon gamma (IFN-γ), tumor necrosis factor alpha (TNF-α), interleukin-4 (IL-4) and interleukin-10 (IL-10) using quantitative real-time (qRT)-PCR. Results: The gene expression levels of IFN-γ showed up-regulation on day 7 post-infection (p.i) and reached the peak on day 14 p.i which coincided with the peak of the cyst output. The peak of the expression level of TNF-α, IL-4, and IL-10 was on day 7 p.i. The correlation between cyst count and relative gene expression of pro-inflammatory cytokines showed a strong positive correlation. IL-10 relative gene expression level was moderately correlated, while IL-4 relative gene expression level was weakly correlated. Conclusion: Results indicate that this infection triggers a mixed type of immune response with predominant participation of the pro-inflammatory cytokines. The balance between the pro-inflammatory and the anti-inflammatory cytokines is important in defining infection outcome.

The Effect of Tumor Necrosis Factor Alpha Antagonist (Adalimumab) on Giardiasis in Mice

“…Muñoz-Cruz et al (2018) reported the TNF-role in the early control of giardiasis, by significantly released by mast cells on infection time. Mahmoud et al (2018) found that peak up-regulation of gene expression of TNF-inal tissue was 7 th dpi. Zhao et al (2022) showed that mRNA levels of TNF--1, & IL-6 transcription and protein expression were significantly higher in giardiasis than controls.…”

Evaluation of immune response and haematological parameters in infected male albino rats by giardiasis

“…However, the mechanisms of host defence used to regulate Giardia infections are not fully understood 8 . The mechanisms of innate immunity involve antimicrobial peptide (AMP) production, nitric oxide (NO), phagocytosis of macrophage, lymphocyte development and dendritic cell (DC) migration to the site of infection 9 . Paneth cells and other cells secrete AMPs that can destroy trophozoites 4 .…”

“…Also, Li et al 12 stated that the immune response induced by Giardia infection in BALB/c mice included that IL‐4, IL‐5 and IL‐10 cytokines as well as IgG and IgE antibodies. IL‐4 is important to boost Th2 and to inhibit Th1 differentiation, and increased IL‐10 synthesis during infection may counterbalance inflammatory responses 9 . As a potent anti‐inflammatory cytokine, IL‐10 has been shown to suppress IFN‐γ‐induced macrophage killing ability against intra‐ and extracellular parasites and to avoid immune‐mediated degradation of the host tissue in reaction to infectious agents 24 …”

“…8 The mechanisms of innate immunity involve antimicrobial peptide (AMP) production, nitric oxide (NO), phagocytosis of macrophage, lymphocyte development and dendritic cell (DC) migration to the site of infection. 9 Paneth cells and other cells secrete AMPs that can destroy trophozoites. 4 NO production is a crucial component of the innate immune response because it is toxic to many pathogens and can prevent the reproduction of G. lamblia trophozoites and the processes of encystation and excystation.…”

“…IL-4 is important to boost Th2 and to inhibit Th1 differentiation, and increased IL-10 synthesis during infection may counterbalance inflammatory responses. 9 As a potent anti-inflammatory cytokine, IL-10 has been shown to suppress IFNγ-induced macrophage killing ability against intra-and extracellular parasites and to avoid immune-mediated degradation of the host tissue in reaction to infectious agents. 24 According to Dann et al, 25 who found a significant and selective increase in intestinal IL-17A in mice infected with G. muris and G. lamblia, with maximal expression after 2 weeks, the IL-17A response was triggered by Th17 cells in the lamina propria and innate immune cells in the epithelial compartment of the small intestine.…”