Happy to share new work from #theonlylabever, lead by the phenomenal @sltai.bsky.social - who developed a tool to study the biology of ILC3s, identifying their role in controlling CSF2-dependent myeloid cells. 🤗
@mucosalimmunol.bsky.social @societymucosalimm.bsky.social
OA: doi.org/10.1016/j.mu...

HBD.

Happy 🇨🇦 day! 😘

I am very thankful to all our fantastic collaborators and members of #theonlylabever for their hard work and important contributions! It a privilege to work with you 😘

12) In summary, we demonstrate a gut commensal protozoan-driven gut-lung axis that impacts the outcome or respiratory diseases.

10) Can protozoan colonization be beneficial to respiratory bacterial infection? Eosinophils in the lungs of T.mu+ mice show greater degranulation following M.tb, infection, delaying the systemic dissemination of M.tb into the periphery, indicating respiratory shielding by a gut protozoan commensal.

9) When challenged, asthma manifests with a striking severity in animals colonized with T.mu. Interestingly, protozoa DNA traits are also found in patients with severe asthma, suggesting a disease exacerbating effect mediated by colonization with protozoa commensals.

8) Which signals are needed to maintain this immune tripartite network? B cell-derived ICOSL OX40-OX40L interaction and T cell-derived IL-2 are critical to mediate iILC2 and eosinophil accumulation in response to intestinal protozoan colonization.

7) We observed the accumulation of ILC2s with B cells and T cells in the lungs of T.mu colonized mice, suggesting a possible immune tripartite network upstream of airway eosinophilia.

6) Surprisingly, T.mu-mediated iILC2 and eosinophilia in the lung require B and T cells. Only when protozoan commensal and iILC2, B cells and T cells come together is eosinophilia installed in the lung, suggesting an adaptive regulation of innate immune cells.

5) We then demonstrate that iILC2s egress from the gut in response to S1P/S1PR4 to accumulate in the lungs of T.mu+ mice.

4) iILC2s have been suggested to originate from the gut in response to IL-25. We used photo-conversion to formally demonstrate that gut-derived iILC2 accumulate in the lungs of T.mu colonized mice.

3) ILC2s are a major sources of IL-5 in the lung of T.mu+ mice, but here, ILC2s compose of natural ILC2 and inflammatory (i)ILC2s. iILC2s in the lungs of T.mu+ mice express high levels of IL-5, OX40L and ICOS implicating potential interactions with the adaptive immune system.

2) T.mu promotes tuft cell-derived IL-25 explaining high IL-5 levels in the gut. However, alarmin production in the lung remained unchanged in the lung, despite high IL-5 production in this organ. Is the IL-5 source in the lung the same as in the gut?

1) Animals colonized by the gut protozoa Tritrichomonas musculis (T.mu) show elevated numbers of bone marrow eosinophil precursors and eosinophils with higher expression of mucosal homing markers CCR3 and a4b7 integrin. Gut and lung eosinophils consequently elevate.

Ever wondered how gut microbes control immune responses at extra-intestinal locations?
Here #theonlylabever reports how a gut protozoan commensal shapes pulmonary immunity to exacerbate asthma and limit the dissemination of mycobacteria.
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