Metabolic and adaptive immune responses induced in mice infected with tissue-dwelling nematode Trichinella zimbabwensis

Abstract

Tissue-dwelling helminths are known to induce intestinal and systemic inflammation accompanied with host compensatory mechanisms to counter balance nutritional and metabolic deficiencies. The metabolic and immune responses of the host depend on parasite species and tissues affected by the parasite. This study investigated metabolic and immuno-inflammatory responses of mice infected with tissue-dwelling larvae of Trichinella zimbabwensis and explored the relationship between infection, metabolic parameters and Th1/Th17 immune responses. Sixty (60) female BALB/c mice aged between 6 to 8 weeks old were randomly assigned into T. zimbabwensis-infected and control groups. Levels of Th1 (interferon-γ) and Th17 (interleukin-17) cytokines, insulin and blood glucose were determined as well as measurements of body weight, food and water intake. Results showed that during the enteric phase of infection, insulin and IFN-γ levels were significantly higher in the Trichinella infected group accompanied with a reduction in the trends of food intake and weight loss compared with the control group. During systemic larval migration, trends in food and water intake were significantly altered and this was attributed to compensatory feeding resulting in weight gain, reduced insulin levels and increased IL-17 levels. Larval migration also induced a Th1/Th17 derived inflammatory response. It was concluded that T. zimbabwensis alters metabolic parameters by instigating host compensatory feeding. Furthermore, we showed for the first time that non-encapsulated T. zimbabwensis parasite plays a role in immunomodulating host Th1/Th17 type responses during chronic infection.

Keywords: Enteric phase; Insulin; Larval migration; Th1 and Th17; Trichinella zimbabwensis.

Fig. 1

Mean number of intestinal adult worms (AW) and counts of ML larvae per gram of muscle (lpg) recovered from BALB/c mice infected with Trichinella zimbabwensis. Levels of significant differences (* P<0.05; ** P<0.01, and *** P<0.001) were obtained by comparing the parasite loads in the infected and control groups.

Fig. 2

Graph showing trend of food intake of mice in the infected and control groups during the experimentation period of 30 days. Levels of significant differences (* P<0.05; ** P<0.01, and *** P<0.001) were obtained by comparing the infected and control groups.

Fig. 3

Graph showing trends of water intake of mice in the infected and control groups during the experimentation period of 30 days. Levels of significant differences (* P<0.05; ** P<0.01, and *** P<0.001) were obtained by comparing the infected and control groups.

Fig. 4

Graph showing changes in mice body weight during the course of Trichinella zimbabwensis infection. Levels of significant differences (* P<0.05; ** P<0.01, and *** P<0.001) were obtained by comparing the infected and control groups.

Fig. 5

Levels of insulin in mice during the course of Trichinella zimbabwensis infection. Levels of significant differences (* P<0.05; ** P<0.01, and *** P<0.001) were obtained by comparing the infected and control groups.

Fig. 6

Levels of Interferon gamma (IFN-γ) cytokine concentration during the course of Trichinella zimbabwensis infection. Levels of significant differences (* P<0.05; ** P<0.01, and *** P<0.001) were obtained by comparing the infected and control groups.

Fig. 7

Levels of Interleukin-17 (IL-17) cytokine concentration during the course of Trichinella zimbabwensis infection. Levels of significant differences (* P<0.05; ** P<0.01, and *** P<0.001) were obtained by comparing the infected and control groups.