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. 2019 Jul 25;11(8):681. doi: 10.3390/v11080681

Figure 1.

Figure 1

Regulation of different immune mechanisms by intestinal microbiota in AIV, IBDV, MDV, and NDV virus infected broiler chickens. (A) Collinsella, Faecalibacterium, Oscillibacter, Holdemanella, Pseudoflavonifractor, Anaerotruncus, Butyricoccus, and Bifidobacterium enhance the IFN-α, IFN-β, and IL-22 secretions, which control the virus replication by degrading the virus nucleus, as well as virus replication genes, and repair mucosal tissue damage. (B) Bacteroides, Candidatus, SMB53, Parabacteroides, Lactobacillus, Paenibacillus, Enterococcus, and Streptococcus spp. promote the antimicrobial peptides such as MUC, TFF, ZO, and tight junction proteins comprised of claudins, occludin, and zona occludens mRNA expressions and inhibit pathobiont colonization and translocation and suppress inflammation. (C) Clostridium XlVa and Firmicutes induce the T regulatory cells, which produce anti-inflammatory cytokines and suppress inflammation. (D) Faecalibacterium and Blautia spp. enhance butyrate succinate and lactate production, which provide energy and reduce inflammation. (E) Cluster XI, Salmonella, Escherichia, and Shigella are pathobionts. These pathogens decrease IFN-α, IFN-β, and IL-22 antimicrobial peptides such as MUC, TFF, ZO, and tight junction proteins comprised of claudins, occludin, and zona occludens mRNA expressions, increase the IFN- γ, IL-17A secretions that cause the mucosal inflammation, tissue damage Increased virus replication and fecal shedding. (F) Desulfovibrionaceae produce hydrogen sulfides and produce inflammation of mucosa. (G) Vampirovibrio, Clostridium cluster XIVb, and genus Ruminococcus induce the proinflammatory cytokines IL-6 and IL-1B, which produce GIT inflammation and leads to increased viral replication. (H) Salmonella typhimurium, Campylobacter jejuni decrease viral specific IgG and IgA production, which results in more viral shedding.