The incidences of multiple sclerosis have risen worldwide, yet neither the trigger nor efficient treatment is known. Some research is dedicated to looking for treatment by parasites, mainly by helminths. However, little is known about the effect of helminths that infect the nervous system. Therefore, we chose the neurotropic avian schistosome Trichobilharzia regenti, which strongly promotes M2 polarization and tissue repair in the central nervous system, and we tested its effect on the course of experimental autoimmune encephalomyelitis (EAE) in mice. Surprisingly, the symptoms of EAE tended to worsen after the infection with T. regenti. The infection did not stimulate tissue repair, as indicated by the similar level of demyelination. Eosinophils heavily infiltrated the infected tissue, and the microglia number increased as well. Furthermore, splenocytes from T. regenti-infected EAE mice produced more interferon (IFN)-γ than splenocytes from EAE mice after stimulation with myelin oligodendrocyte glycoprotein. Our research indicates that the combination of increased eosinophil numbers and production of IFN-γ tends to worsen the EAE symptoms. Moreover, the data highlight the importance of considering the direct effect of the parasite on the tissue, as the migrating parasite may further tissue damage and make tissue repair even more difficult.

Infection with the parasitic nematode Strongyloides stercoralis is characteristic for tropical and subtropical regions of the world, but autochthonous cases have been reported in European countries as well. Here we present the first nation-wide survey of S. stercoralis seroprevalence in Croatian individuals presenting with eosinophilia, and evaluate the fraction of positive microscopy rates in stool specimens of seropositive individuals. In our sample of 1407 patients tested between 2018 and 2021, the overall prevalence of strongyloidiasis was 9.31%, with significantly higher rates in those older than 60 years of age (P = 0.005). Of those, one-quarter (25.95%) were also positive following microscopy examination of faeces after using the merthiolate–iodine–formaldehyde concentration method. Our findings reinforce the notion of endemic strongyloidiasis transmission in Croatia, particularly in older individuals, and highlight the need to consider the presence of S. stercoralis in patients with eosinophilia.

Human autochthonous infections with the trematode Paragonimus kellicotti are increasingly being reported in North America, but the true prevalence and geographic distribution are unknown. Ingestion of raw crayfish is reported in most human cases, typically in the context of alcohol intoxication. Risk of infection varies depending on what part of the crayfish is ingested as metacercariae of P. kellicotti (>50% mature to adults) localize to the heart and pericardium of the crayfish. Reported human cases have manifested primarily in otherwise healthy young adults presenting with severe eosinophilic pneumonia, pleuritis, systemic symptoms, dermatologic lesions and cerebral involvement. However, it is likely that many infections go unreported due to lack of awareness, mild illness or the absence of rapid commercially available diagnostic tests. Promising advances have been made related to novel diagnostic targets. Conservation of these antigen targets among at least four Paragonimus species could make these antigens viable for diagnostic testing of P. kellicotti specifically as well as other Paragonimus species, but additional studies and funding investments are required. Public and physician awareness may have improved due to targeted education campaigns, but ongoing activities to raise awareness are needed, particularly in areas where cases have not been frequently reported to date.

The secondary response of eosinophilia has been studied in mice infected with A. suum. In mice infected orally with 1000 A. suum eggs, larvae disappeared from the body within two weeks after infection. The number of peripheral blood eosinophils decreased to the pre-infection level within eight weeks. A typical secondary response of IgG antibody production to egg antigen was found after reinfection with 1000 eggs. The number of peripheral blood eosinophils increased more rapidly after reinfection than after the primary infection. However, the peak number of eosinophils after reinfection was similar to that after primary infection, and the long-lasting characteristics of eosinophilia after reinfection did not differ from those after primary infection. These results suggest that the secondary response of eosinophilia is characterized by a rapid increase in the number of eosinophils in A. suum-reinfected mice.

A marked strain variation in eosinophilia following oral infection with Toxocara canis eggs was observed in mice. Mutual radiation chimeras between high and low responder mice in terms of eosinophilia were made and compared with the respective donor and recipient for eosinophilia after the infection. As a result, the degree and time course of eosinophilia in chimeric mice were similar to those in donors. The result suggested that genes which regulate inheritance of the trait, marked eosinophilia in T. canis-infected mice, might be expressed in bone marrow derived cells.

The genetic influences upon host variation in eosinophilia and resistance to helminth infection, and the relationship between these parameters, was investigated in 9 inbred and 3 hybrid strains of mice infected with Mesocestoides corti. Blood, bone marrow, spleen and peritoneal fluid eosinophilia were far higher in SJL mice than in any other inbred strain. SWR, NIH, C3H and BALB/c mice were high responders to M. corti whereas CBA and 3 congenic strains sharing the B10 background (C57BL/10, B10.S, B10.G) were low responders. Some of the genes for high eosinophil responsiveness appeared to be dominant, as F1 hybrids from high and low response parental strains were intermediate to high in response to infection. SJL and NIH strains were highly susceptible to infection with M. corti, larval burdens at 21 days after infection with 100 tetrathyridia being considerably higher (>1000) than all other strains. BALB/c (≃ 700 larvae) were designated susceptible, SWR (>400 larvae) were resistant and the BIO congenics (<400 larvae) were highly resistant. Genes influencing resistance also appeared to be dominant, as F1 hybrids between resistant and susceptible parental strains were intermediate to resistant on infection. The overall response patterns indicate a direct correlation between susceptibility to infection and high eosinophil responsiveness, but this relationship is not consistent in all strains.

Genetic influences upon host variation in eosinophilia and resistance to helminth infection, and the relationship between these parameters, were investigated in 7 inbred and 1 hybrid strains of mice infected with Trichinella spiralis. Clear strain-dependent variations were observed in the maximum peripheral blood, bone marrow and spleen eosinophilia attained in infected animals. SWR, NIH and SJL strains of mice all gave high responses to infection; four congenic strains sharing the B10 background (C57BL10 [B10], B10.S, B10.G and B10.BR) were low responders. Some of the genes for high responsiveness appeared to be dominant, as F1 hybrids from high- and low-response phenotype parental strains showed intermediate to high responses to infection. Intestinal eosinophilia showed no correlation with either peripheral blood or bone marrow responses (NIH and B10 strains having similar levels of eosinophil response in gut tissue) and was unrelated to the level of resistance to infection. Whereas NIH were highly resistant, with adult worm burdens at 13 days post-infection and muscle larval burdens at 35 days post-infection significantly lower than all other strains, B10 were quite susceptible, retaining substantial worm burdens at day 13 and harbouring large numbers of muscle larvae. Measurements of the level of the eosinophilopoietic cytokine IL-5 in sera during infection showed that the two strains differed in the kinetics of release but not in their absolute capacity to produce this cytokine. NIH mice released high levels during a primary infection, B10 released high levels during a secondary infection. The relationship between eosinophilia and resistance and the differences seen between responses in different body compartments are discussed in terms of genetically determined influences operating at the levels of T helper cell populations, T cell cytokines and bone-marrow precursor cell populations.

Oral administration of raffinose, a naturally occurring indigestible oligosaccharide, has reportedly ameliorated atopic dermatitis in human subjects although the mechanism is unknown. The present study investigated the effect of dietary raffinose on allergen-induced airway eosinophilia in ovalbumin-sensitised Brown Norway rats as an atopic disease model. Brown Norway rats were immunised by subcutaneous injection with ovalbumin on day 0 and fed either a control diet or the diet supplemented with raffinose (50 g/kg diet). The rats were exposed to aerosolised ovalbumin on day 20, and broncho-alveolar lavage fluid was obtained on the next day. The number of eosinophils in the fluid was significantly lower in the rats fed the raffinose diet than in those fed the control diet. Dietary raffinose significantly reduced IL-4 and IL-5 mRNA levels in lung tissue and tended to lower ovalbumin-specific Ig E levels. Suppression of eosinophilia by dietary raffinose was still observed in caecectomised and neomycin-administered rats, suggesting little contribution by the colonic bacteria to the effect of raffinose. Intraperitoneal administration of raffinose also suppressed eosinophilia. Significant concentrations of raffinose were detected in portal venous and abdominal arterial plasma after the intragastric administration of raffinose. Overall, the findings suggest that dietary raffinose ameliorates allergic airway eosinophilia at least partly via post-absorptive mechanisms in Brown Norway rats.

The effects of dietary protein and zinc restrictions on Heligmosomoides polygyrus were compared following primary and challenge infection in female BALB/c mice fed either control (24%), marginal (7%) or low (3%) protein combined with either high or low zinc (60 or 3 mg Zn/kg diet). Dietary protein restriction (3%) resulted in significantly lower body weight gain. As well, blood urea nitrogen (BUN) significantly decreased with decreasing dietary protein level. However, neither plasma albumin concentration nor relative thymus or spleen weights were reduced. Marginal zinc deficiency was confirmed by significantly lower tibia and liver zinc concentration, but food intake, body weight gain, relative thymus and spleen weights, and alkaline phosphatase activity were not altered. On day 29 post-primary infection, worm burdens were significantly higher in mice fed either marginal or low protein and in mice fed a low zinc diet, while parasite egg output was significantly higher in mice fed both low protein and low zinc diets. Immune status was compromised in mice fed low protein (significantly lower serum IgG1 and lower eosinophilia), and in mice fed low zinc diet (significantly lower eosinophilia). Early in the infection, IgE titres were elevated in mice fed low protein or low zinc, but IgE titres declined to levels lower than the control diet groups after 14–21 days. On day 29 post-challenge infection, worm burdens and parasite egg output were significantly higher in mice fed low protein, whereas the other groups had expelled almost all parasites. Dietary restriction had no effect on serum IgE. Significantly reduced serum IgG1 titres and eosinophilia in mice fed 3% protein supported the view that low dietary protein but not low zinc increased host susceptibility to H. polygyrus by compromising host immune function following reinfection in immunized mice.

In areas where malaria is endemic, helminthic infections, caused by intestinal or filarial parasites, commonly coexist with malaria in the same individual. This study investigates the course of Plasmodium berghei malaria infection in CBA/J mice inoculated with irradiated attenuated 3rd-stage larvae (L3) of Brugia pahangi. Peripheral eosinophil counts, serum IgE levels and cytokine production revealed that the filarial antigen induced T-helper type 2 (Th2) cell predominance in these mice, which protected them against the development of cerebral malaria. These mice significantly prolonged their survival, compared with the control mice after P. berghei infection. All of the mice not inoculated with irradiated L3 died within 12 days with acute neurological manifestations unrelated to the level of parasitaemia after infection of P. berghei. Conversely, most of the inoculated mice lived more than 3 weeks following infection with P. berghei, dying in the fourth week of severe anaemia and overwhelming parasitaemia. This suggests that Th2-dominant responses lead to the downregulation of susceptibility to murine cerebral malaria.