Virus-helminth coinfection reveals a microbiota-independent mechanism of immunomodulation
Lisa C. Osborne,Laurel A. Monticelli,Timothy J. Nice,Tara E. Sutherland,Mark C. Siracusa,Matthew R. Hepworth,Vesselin T. Tomov,Dmytro Kobuley,Sara Tran,Kyle Bittinger,Aubrey Bailey,Alice Laughlin,Jean-Luc Boucher,E. John Wherry,Frederic D. Bushman,Judith E. Allen,Herbert W. Virgin,David Artis +17 more
TLDR
Data indicate that helminth-induced immunomodulation occurs independently of changes in the microbiota but is dependent on Ym1, a chitinase-like molecule that is associated with alternatively activated macrophages, which could partially restore antiviral immunity.Abstract:
The mammalian intestine is colonized by beneficial commensal bacteria and is a site of infection by pathogens, including helminth parasites. Helminths induce potent immunomodulatory effects, but whether these effects are mediated by direct regulation of host immunity or indirectly through eliciting changes in the microbiota is unknown. We tested this in the context of virus-helminth coinfection. Helminth coinfection resulted in impaired antiviral immunity and was associated with changes in the microbiota and STAT6-dependent helminth-induced alternative activation of macrophages. Notably, helminth-induced impairment of antiviral immunity was evident in germ-free mice, but neutralization of Ym1, a chitinase-like molecule that is associated with alternatively activated macrophages, could partially restore antiviral immunity. These data indicate that helminth-induced immunomodulation occurs independently of changes in the microbiota but is dependent on Ym1.read more
Citations
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Linking the Microbiota, Chronic Disease, and the Immune System
TL;DR: A review discusses recent findings suggesting that shifts in the microbiota may contribute to chronic disease via effects on the immune system through changes in microbiota-derived metabolites.
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Sequential Infection with Common Pathogens Promotes Human-like Immune Gene Expression and Altered Vaccine Response
Tiffany A. Reese,Kevin Bi,Amal Kambal,Ali Filali-Mouhim,Lalit K. Beura,Matheus Carvalho Bürger,Bali Pulendran,Rafick Pierre Sekaly,Stephen C. Jameson,David Masopust,W. Nicholas Haining,Herbert W. Virgin +11 more
TL;DR: Sequential infection altered pre- and post-vaccination gene expression, cytokines, and antibodies in blood and raises the possibility that mouse models of vaccination and immunity can be improved by selective microbial exposure of laboratory animals to mimic that of humans.
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Chitinase-like proteins promote IL-17-mediated neutrophilia in a tradeoff between nematode killing and host damage
Tara E. Sutherland,Nicola Logan,Dominik Rückerl,Alison A. Humbles,Stuart M. Allan,Venizelos Papayannopoulos,Brigitta Stockinger,Rick M. Maizels,Judith E. Allen +8 more
TL;DR: It is found that Ym1 and Ym2 induced the accumulation of neutrophils through the expansion of γδ T cell populations that produced interleukin 17 (IL-17), which suggested that regulation of IL-17 is an inherent feature of mouse CLPs.
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Tropism for tuft cells determines immune promotion of norovirus pathogenesis.
Craig B. Wilen,Sanghyun Lee,Lee-Yang Hsieh,Robert C. Orchard,Chandni Desai,Barry L. Hykes,Michael R. McAllaster,Dale R. Balce,Taylor Feehley,Jonathan R. Brestoff,Christina A. Hickey,Christine C. Yokoyama,Ya-Ting Wang,Donna A. MacDuff,Darren Kreamalmayer,Michael R. Howitt,Jessica A Neil,Ken Cadwell,Paul M. Allen,Scott A. Handley,Menno van Lookeren Campagne,Megan T. Baldridge,Herbert W. Virgin +22 more
TL;DR: It is found that type 2 cytokines, which induce tuft cell proliferation, promote MNoV infection in vivo, which provides insight into how the immune system and microbes can coordinately promote enteric viral infection.
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Opposing macrophage polarization programs show extensive epigenomic and transcriptional cross-talk
Viviana Piccolo,Alessia Curina,Marco Genua,Serena Ghisletti,Marta Simonatto,Arianna Sabò,Bruno Amati,Bruno Amati,Renato Ostuni,Gioacchino Natoli,Gioacchino Natoli +10 more
TL;DR: It is found that IFN-γ and IL-4 mutually inhibited the epigenomic and transcriptional changes induced by each cytokine alone, providing a core mechanistic framework for the integration of signals that control macrophage activation in complex environmental conditions.
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