**4. Host-parasite communications through small molecules**

Mechanisms of tiny molecules, hormones, molecular cues, and metabolites, which are closely involved in intercellular communication, draw much attention. As an example, short-chain fatty acids (SCFAs, butyrate, acetate, and propionate), for example, which are commensal derivatives at the level that promote regulatory T cells, are not generated by mammalian organisms [60]; dysbiosis is thus considered harmful for the disruption of this path [61, 62]. Surprisingly, these chemicals can also be produced by helminths [63], implying that commensal bacteria can produce a significant amount of SCFAs [64].

Another tiny molecules produced by filarial parasites *B. malayi* and *Onchocerca volvulus*, as well as skin-invasive cercariae of *S. mansoni*, include prostaglandins D2 and E2 [65–67]. In addition to tiny chemicals and metabolites, helminths change small ligands derived from the host, such as acetylcholine (through acetylcholinesterase) [68], the enormous discussion of platelet-activating factor (PAF hydrolase [69]) and ATP (apyrase [70]), among many others, is beyond the scope of this paper.

### **5. Microbiome-mediated interactions**

In the gastrointestinal system, particularly, helminth parasites contribute their position with numerous microorganisms, predominantly numerous bacterial species recognized as microbiota [71–73]. Remarkably, helminth contamination depend on excessive range on the existence of these parasites: as an illustration, in the lack of caecal bacteria, *Trichuris* eggs do not mature in the gut [74]. The majority of microbiota study in mice infection with gut helminths have discovered important and sometimes comprehensive alterations in species arrangement, mainly within *Lactobacillus* populations and *Bacteroides* [71–73]. Newly, it was declared that BALB/c mice infected with *H. polygyrus* showed enlargement of the *L. taiwanensis* species, and the degree of colonization with this bacterium was found to be positively linked with both adult worm populations and Treg activation [75]. Surprisingly, mice administered *L. taiwanensis* before receiving *H. polygyrus* larvae were shown to be more susceptible to infection, implying that the bacteria and helminth species work together to promote infection.

It has also been suggested that the immune-modulating capabilities of helminth infection could be aided in part by altering the microbiome of the intestine. To date, fascinating research have shown that infected mice's intestinal contents (which comprise bacteria as well as a variety of host and parasite products) can lessen allergy symptoms when transmitted to recipient mice [64]. It will be interesting to investigate this consequence minutely and mostly if *L. taiwanensis*, specific bacteria is responsible.

Considerably, a recent study showed that fecal miRNAs produced from intestinal epithelial cells might influence the microbiome, possibly by interacting directly with bacterial genes [76]. Feasibly these miRNAs could potentially be found in extracellular vesicles, raising the possibility that the helminths and host both might modify the microbiome through this innovative mechanism, and indeed as stated below, that host exosomes might have an impact on the helminth organism, parasitizing the intestinal tract.

### **6. Host-helminth interaction is bi-directional process**

While this analysis has focused on how helminths communicate with the immune system of hosts, there are several enthralling examples of how helminths detection and response towards host immune state. Adult *N. brasiliensis* worms acclimate towards an immunized host through adjusting secreted acetylcholinesterase expression levels and isoforms, according to previous research [77]. All the more as of late, identification of cytokines from host, has been found in schistosomes, which need the existence of TNF from host to develop to laying of egg [78] and filarial parasites reacting towards high IL-5 levels present *in-vivo* by speeding up the development and off-spring formation [79]. Helminth receptor illustration is ready to ligate host cytokine was set up on account of *S. mansoni* TGF-β family receptor [80].

An appealing chance of extracellular vesicles from the host may offer of communications of network, which accelerates the helminth parasites, although it is still

#### *Helminths Derived Immune-Modulatory Molecules: Implications in Host-Parasite Interaction DOI: http://dx.doi.org/10.5772/intechopen.102927*

not proved that, parasites can directly receptive to vesicle-mediated signals. There are a developing literature representing the how host-derived extra-mobile vesicle effect against defense in opposition of pathogens. As an instance, in recipient infected cells, IFN-α, exosomes derived from stimulated cell could induce the antiviral activity and bound viral replication [81, 82]. Additionally, semen exosomes from human is associated in resistant to HIV-1 resulting their uptake into immature cells by reducing viral fitness [83]. Innate response towards protozoan parasite *Cryptosporidium parvum* is also established as an instance of exosome-mediated host defense. Activation of host epithelium through TLR mediation enhances the secretion of antimicrobial exosomes, which contains peptides that limits infection rate of pathogen in the intestinal environment [84]. The progress of a targeted host exosomes anti-pathogen response has also been examined the usage of a clinical setting, in which host exosomes collected from parasite antigen-primed dendritic cells encourage protection against various protozoan contaminations, counting *Toxoplasma gondii* infection [85] and *Leishmania major* [86].
