Table 2.

Comparison of intestinal immunity, microbial diversity and microbiota-related interactions within the murine hosts and the mosquito vectors during intestinal parasitic infections.

Comparison	Mouse	Mosquito
Mechanical barriers	Mucus layer, enriched in mucin glycoproteins, permanently lining the intestinal epithelial layer as a shield from direct exposure to external stimuli and invading microorganisms. Commensal microbiota supports mucus secretion and maintenance.	Semipermeable peritrophic matrix (PM) composed of chitin and glycoproteins, lining the entire larval gut. In adult females, PM is secreted in the midgut upon blood feeding, which induces significant microbial proliferation in the midgut. Commensal microbiota stimulates peritrophic matrix synthesis.
Intestinal microbial diversity	Higher complexity and species diversity. Compositional changes occur subject to environmental and dietary changes like breastfeeding or gastrointestinal infections. Exhibits overall less drastic compositional shifts during lifespan of host. Dominant bacterial groups include Enterobacter, Lactobacillus, Bifidobacteria, Bacteroides, Clostridia, Ruminococcus.	Lower complexity and species diversity. High fluctuation in diversity and species abundance observed throughout the development and after blood meal uptake. Exhibits drastic compositional shifts during vector development. Dominant bacterial groups include Enterobacter, Serratia, Pantoea, Asaia, Aeromonas, Pseudomonas, Bacillus.
Microbial fingerprint during parasitic infections	Numerous studies have demonstrated significant alterations of intestinal microbial communities during infections with protozoan parasites (eg. Giardia lamblia and Toxoplasma gondii), as well as during nematode infections with Heligmosomoides polygyrus or Trichuris muris.	Not enough evidence of Plasmodium influence on midgut microbial communities, possibly due to limited time spent by the parasite in the midgut lumen.
Microbial priming of immune defenses against parasitic infections	Segmented filamentous bacteria (family Clostridiales) are known potent inducers of intestinal Th17 responses, key for host protection against Giardia infection.	Midgut microbiota is a potent inducer of IMD/NF-κB pathway. Basal activity of IMD is regulated by the midgut microbiome, and bacterial proliferation after blood feeding further enhances pathway activation. The microbiota-dependent activation of the IMD pathway impacts within-mosquito development of Plasmodium falciparum.
	Lactobacilli induce intestinal Treg responses during infection with H. polygyrus, but not during T. muris infection, and correlate with higher worm burdens	Enterobacter isolates have direct plasmodicidal activity. They produce ROS that kills Plasmodium ookinetes. Soluble factors of Serratia marcescens and motility of some Serratia strains impact development of P. berghei ookinetes.
	Clostridia can induce suppressive Treg responses via short-chain fatty acid production during H. polygyrus infection	Although understudied, immune activation after blood feeding is linked to oxidative stress. Blood feeding increases hydrogen peroxide levels and ROS detoxification responses. Moreover, inhibition of ROS leads to lethal systemic bacterial infections.
	γ-Proteobacteria, among the most abundant commensal bacteria in mice, contribute to intestinal immunopathology during T. gondii infection via activation of neutrophils and ROS-producing inflammatory monocytes	γ-Proteobacteria is the most abundant class of bacteria in mosquitoes. It limits mosquito vector competence for Plasmodium transmission by inducing the IMD pathway and probably other as yet unknown mechanisms.