🙌🏼🙌🏼 @heran.bsky.social

We then administered TNF or IL-1 🫁 themselves, one week prior to #SARSCoV2 infection and both can confer this anti-viral state! Head explode TNF or IL-1 protection was Ifnar1-independent! 🤯6/9

How do we know what inflammatory pathways can limit viral replication early in the lungs? We checked for ourselves and screened many KO mice in our favorite pathways…Turns out that besides IFNs, and their needed #PRRs TNF signaling is required, but IL-1 itself is not! 5/9

All the preconditioning stimuli and pathogens we tested provided sustained IFN-activation of lung epithelial subsets (targets for viral replication) possibly contributing to enhanced control of #SARSCoV2 upon exposure. Interestingly, TLR conditioning required both IFNAR1 and IL1R1 (🤩) 4/9

Recently resolved pulmonary bacterial or viral infection, underlying allergic asthma-like disease or even one-time admins of TLR ligands to the lung all potently limited #SARSCoV2 replication in the 🫁 3/9

Best #Nikolaus 🎅! Our paper on how the 🫁 microenvironment can shape #innate immunity against #viruses is out @sciimmunology.bsky.social This was a herculean effort brilliantly led by @pauljbaker.bsky.social who singlehandedly established the model in the lab during the pandemic. 🧪 #Immunosky 1/9

Post a pic for some zen

@gpollara.bsky.social gave a brilliant seminar on the role of #IL-6 in tuberculosis today at the VALIDATE seminar series!
Turns out this may all be context dependent, and fits beautifully with what we proposed in our „Tipping-point“ model of TB disease and innate cytokines

Finally we decided to try if TNF or IL-1 🫁administration alone, one week prior to #SARSCOV2 infection can also create this heightened anti-viral state. Well, yes, they totally can, and so far it seems IFN-independent! 7/10

How do we know what inflammatory pathways can limit viral replication early in the lungs? We checked for ourselves and screened many KO mice in our favorite pathways…Turns out that besides IFNs, and their needed #PRRs TNF signaling is required, but IL-1 itself is not! 6/10

The diverse preconditioning stimuli and pathogens sustained IFN-activation of different epithelial subsets (targets for viral replication) likely contributing to enhanced innate control of #SARSCOV2. Interestingly, TLR conditioning required both IFNAR1 and IL1R1 (🥰) 5/10

One week after pulmonary TLR administration, the #TRM macrophages were still metabolically altered and activated, and in the case of #IM substantially expanded; we think IM may not be directly involved in protection (check out preprint), but #AMs are still contenders…4/10

Recently resolved pulmonary bacterial or viral infection, underlying allergic asthma-like disease or even one-time admins of TLR ligands to the lung all potently limited #SARSCOV2 replication in the 3/10