Urogenital schistosomiasis is associated with signatures of microbiome dysbiosis in Nigerian adolescents

Abstract

Urogenital schistosomiasis is a neglected tropical disease caused by the parasite Schistosoma haematobium, which resides in the vasculature surrounding the urogenital system. Previous work has suggested that helminthic infections can affect the intestinal microbiome, and we hypothesized that S. haematobium infection could result in an alteration of immune system-microbiota homeostasis and impact the composition of the gut microbiota. To address this question, we compared the fecal microbiomes of infected and uninfected schoolchildren from the Argungu Local Government Area of Kebbi State, Nigeria, detecting significant differences in community composition between the two groups. Most remarkably, we observed a decreased abundance of Firmicutes and increased abundance of Proteobacteria – a shift in community structure which has been previously associated with dysbiosis. More specifically, we detected a number of changes in lower taxa reminiscent of inflammation-associated dysbiosis, including decreases in Clostridiales and increases in Moraxellaceae, Veillonellaceae, Pasteurellaceae, and Desulfovibrionaceae. Functional potential analysis also revealed an enrichment in orthologs of urease, which has been linked to dysbiosis and inflammation. Overall, our analysis indicates that S. haematobium infection is associated with perturbations in the gut microbiota and may point to microbiome disruption as an additional consequence of schistosome infection.

Gut microbiota signatures in Schistosoma japonicum infection-induced liver cirrhosis patients

“…Additionally, even at the genus level, no major changes were detected, indicating that in our context, there is no gut dysbiosis in S. japonicum infection-induced liver cirrhosis patients. This result is somehow unexpected and different from other studies that have reported gut dysbiosis in the context of human schistosomiasis (e.g., those caused by S. mansoni and S. haematobium) [20,21,22,23,24]. Additionally, in vivo studies have reported Schistosoma infection-related alterations in gut microbial composition.…”

“…Different studies focused on different Schistosoma spp. that have different organ tropisms: e.g., S. mansoni and S. japonicum target the gut and liver, while S. haematobium targets the bladder and the urogenital system [20,21,22,24]. Importantly, the notion that S. haematobium infection was equally associated with human gut dysbiosis suggests that potential alterations of intestinal microbial communities in the context of schistosomiasis are probably a consequence of infection-induced systemic immune responses (and not of local events).…”

“…Importantly, the notion that S. haematobium infection was equally associated with human gut dysbiosis suggests that potential alterations of intestinal microbial communities in the context of schistosomiasis are probably a consequence of infection-induced systemic immune responses (and not of local events). In fact, some studies suggest this [20,21,22]. For instance, mesenteric lymph node cells isolated from mice infected with S. mansoni (dysbiotic) responded differently compared to the ones isolated from controls: higher interleukin (IL)-4, IL-10, and IL-17 secretion, together with lower interferon-γ production [22].…”

“…Indeed, the infection status may also condition the results. Human studies have mainly targeted adolescents [20] or children [24], and consequently, the early phase of infection. Additionally, the most commonly used mouse model of schistosomiasis in microbiome studies evaluated acute infection -less than 8 weeks post-challenge according to the model characterization [49,50,51].…”

“…Recent studies using not only animal models but also human clinical samples have demonstrated a clear relationship between gut microbiota alterations and Schistosoma spp. infection [20,21,22,23,24,25]. However, no study has explored the relationship between gut microbiota and S. japonicum infectioninduced liver cirrhosis; the potential role of gut microbiota alterations in disease onset and progression is still unclear.…”