A naturally occurring strain (Anga-Mali) was identified in mosquitoes of the complex collected in the Malian villages of Dangassa and Kenieroba. Phylogenetic analysis of the nucleotide sequence of two 16S rRNA regions showed thatAnga-Mali clusters with strains from supergroup A and has the highest homology to a strain isolated from cat fleas (). Anga-Mali is different from two strains previously reported in from Burkina Faso (Anga_VK5_STP and Anga_VK5_3.1a). Quantitative analysis of and sporozoite infection in field-collected mosquitoes indicates that the prevalence and intensity of sporozoite infection is significantly lower in -infected females. The presence of in females from a laboratory (, M form) colony experimentally infected with (NF54 strain) gametocyte cultures slightly enhanced oocyst infection. However, infection significantly reduced the prevalence and intensity of sporozoite infection, as observed in the field. This indicates that Anga-Mali infection does not limit early stages of infection in the mosquito, but it has a strong deleterious effect on sporozoites and reduces malaria transmission.

Immune priming in Anopheles gambiae is mediated by the systemic release of a hemocyte differentiation factor (HDF), a complex of lipoxin A4 bound to Evokin, a lipid carrier. HDF increases the proportion of circulating granulocytes and enhances mosquito cellular immunity. Here, we show that Evokin is present in hemocytes and fat-body cells, and messenger RNA (mRNA) expression increases significantly after immune priming. The double peroxidase (DBLOX) enzyme, present in insects but not in vertebrates, is essential for HDF synthesis. DBLOX is highly expressed in oenocytes in the fat-body tissue, and these cells increase in number in primed mosquitoes. We provide direct evidence that the histone acetyltransferase AgTip60 (AGAP001539) is also essential for a sustained increase in oenocyte numbers, HDF synthesis, and immune priming. We propose that oenocytes may function as a population of cells that are reprogrammed, and orchestrate and maintain a broad, systemic, and long-lasting state of enhanced immune surveillance in primed mosquitoes.

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Succinate produced by the commensal protistTritrichomonas musculis(T. mu) stimulates chemosensory tuft cells, resulting in intestinal type 2 immunity. Tuft cells express the succinate receptor SUCNR1, yet this receptor does not mediate anti-helminth immunity nor alter protist colonization. Here, we report that microbial-derived succinate increases Paneth cell numbers and profoundly alters the antimicrobial peptide (AMP) landscape in the small intestine. Succinate was sufficient to drive this epithelial remodeling, but not in mice lacking tuft cell chemosensory components required to detect this metabolite. Tuft cells respond to succinate by stimulating type 2 immunity, leading to interleukin-13-mediated epithelial and AMP expression changes. Moreover, type 2 immunity decreases the total number of mucosa-associated bacteria and alters the small intestinal microbiota composition. These findings demonstrate that a single metabolite produced by commensals, likeT. mu, can markedly shift the intestinal AMP profile and suggest that tuft cells utilize SUCNR1 to modulate bacterial homeostasis.