Acute inflammation articles within Nature Communications

Featured

  • Article
    | Open Access

    Amphihelical antimicrobial peptides (AMPs) are bactericidal host defense factors, but their function as immunomodulators is emerging. Here the authors show that several AMPs organize DNA into periodic nanocrystals by self-assembling into superhelical protofibril scaffolds, which potentiates DNA sensing by TLR9.

    • Ernest Y. Lee
    • , Changsheng Zhang
    •  & Gerard C. L. Wong

  • Article
    | Open Access

    Diverse interactions between the nervous and immune systems have been shown, but specific mechanistic insights are still lacking. Here the authors show, using both mouse inflammation models and clinical correlation, that adrenergic nerve may ameliorate inflammation by inducing repulsive guidance molecule A signalling.

    • Andreas Körner
    • , Martin Schlegel
    •  & Valbona Mirakaj

  • Article
    | Open Access

    Urolithins are microbial metabolites derived from food polyphenols. Here, Singh et al. show that urolithin A and a synthetic analogue enhance gut barrier function via Nrf2-dependent pathways and mitigate inflammation and colitis in mice, highlighting a potential application for inflammatory bowel diseases.

    • Rajbir Singh
    • , Sandeep Chandrashekharappa
    •  & Venkatakrishna R. Jala

  • Article
    | Open Access

    Inducible nitric oxide (NO) synthase (iNOS) is essential in the response to mycobacterial infection, yet NOS signalling can occur through NO-dependent or NO-independent pathways. Here the authors show macrophage Gch1 and tetrahydrobiopterin mediate NO-independent control of Mycobacterial infection.

    • Eileen McNeill
    • , Elena Stylianou
    •  & Keith M. Channon

  • Article
    | Open Access

    M1 and M2 cells are representative of proinflammatory versus resolving macrophages, respectively. Here the authors characterize the lipid mediator response to bacterial infection by these cells and show that differing panels of leukotrienes and specialized pro-resolving mediators contribute to control of the dichotomy.

    • Oliver Werz
    • , Jana Gerstmeier
    •  & Charles N. Serhan

  • Article
    | Open Access

    Excessive inflammation can be tissue destructive and contributes to auotinflammatory diseases and sepsis pathology. Here the authors show that the lncRNA Mirt2 is an endogenous negative feedback regulator of LPS-induced inflammation by limiting ubiquitination of TRAF6 and NF-κB activation.

    • Meng Du
    • , Lin Yuan
    •  & Kai Huang

  • Article
    | Open Access

    Macrophage metabolism controls differentiation and subsequent adaptive immune responses. Here the authors show that mitochondrial membrane protein Fam73b regulates TLR-mediated mitochondrial switching of fusion to fission to induce IL-12 production via accumulation of Parkin and stabilization of IRF1 in macrophages, resulting in control of anti-tumor immunity in mice.

    • Zhengjun Gao
    • , Yiyuan Li
    •  & Jin Jin

  • Article
    | Open Access

    ROCK is associated with T cell movement in lymph nodes. Here the authors use an LPS lung damage model and two-photon imaging to show that CD8+ T cells in lung tissue engage in ROCK-dependent fast linear migration alternating with bursts of slower confined migration that together optimize contact with target cells.

    • Paulus Mrass
    • , Sreenivasa Rao Oruganti
    •  & Judy L. Cannon

  • Article
    | Open Access

    MicroRNAs (miR) are important regulators of gene transcription, with miR-155 and miR-146a both implicated in macrophage activation. Here the authors show that NF-κB signalling, miR-155 and miR-146a form a complex network of cross-regulations to control gene transcription in macrophages for modulating inflammatory responses.

    • Mati Mann
    • , Arnav Mehta
    •  & David Baltimore

  • Article
    | Open Access

    Excessive inflammasome activation leads to inflammatory diseases, but how inflammasomes are regulated by PYD-only adaptors is unclear. Here the authors show that the PYD-only protein POP2 inhibits both inflammasome priming and assembly by interfering, respectively, with IκBα activation and NLRP3-ASC interaction.

    • Rojo A. Ratsimandresy
    • , Lan H. Chu
    •  & Christian Stehlik

  • Article
    | Open Access

    Thrombospondin-1 (TSP-1) activates latent TGF-β in the extracellular matrix. Here the authors show that inappropriate activation of latent TGF-β in murine, bovine and human lung by monocyte-produced TSP-1 causes pulmonary hypertension, and that interference with the activation process prevents disease development.

    • Rahul Kumar
    • , Claudia Mickael
    •  & Brian B. Graham

  • Article
    | Open Access

    Neutrophil adhesion is tightly regulated to enforce protective immunity, but it is unclear how mechanochemical processes such as catch bonds and slip bonds modulate neutrophilsin vivo. Here the authors show that a point mutation in the adhesion molecule L-selectin alters mechanochemical regulation to affect neutrophil functions in mice.

    • Zhenghui Liu
    • , Tadayuki Yago
    •  & Rodger P. McEver

  • Article
    | Open Access

    Non-resolving bacterial pneumonia results in lung tissue damage owing to overactive inflammation. Here the authors show that the mitochondrial DAMP cardiolipin contributes to persistent inflammation by SUMOylating PPARγ, which promotes binding of the corepressor NCOR/HDAC3 complex to the IL-10 promoter.

    • Krishnendu Chakraborty
    • , Mahesh Raundhal
    •  & Prabir Ray

  • Article
    | Open Access

    Acute kidney injury can progress to chronic kidney disease. Here Dehnadiet al. develop a post-ischaemic chronic kidney disease model in cynomolgus monkeys and show that prophylactic inhibition of CD11b/CD18 leukocyte receptor via a monoclonal antibody inhibits progression of kidney disease and fibrosis.

    • Abbas Dehnadi
    • , A. Benedict Cosimi
    •  & M. Amin Arnaout

  • Article
    | Open Access

    The role of NLRP12 in immunity to bacterial infection is controversial as varied and contrasting results have been published using C57BL/6 mice. Here the authors shed light on this issue, showing that unlike C57BL/6N mice, C57BL/6J mice have a missense point mutation in NLRP12 that is associated with defective neutrophil recruitment.

    • Tyler K. Ulland
    • , Nidhi Jain
    •  & Fayyaz S. Sutterwala

  • Article
    | Open Access

    Fat-associated lymphoid clusters (FALC) in the serous cavities house rapid IgM-producing B1 cells, but how the clusters are activated to respond to infection is unclear. Here the authors show that in response to lung inflammation or pleural nematode infection adipose stromal cell-derived IL-33 activates ILC2s to produce IL-5, thus driving the B1 response in the FALCs.

    • Lucy H. Jackson-Jones
    • , Sheelagh M. Duncan
    •  & Cécile Bénézech

  • Article
    | Open Access

    Hypoxia induced during inflammation promotes the resolution phase. Here the authors show that the hypoxia results from the respiratory burst in myeloid cells, and induces local EPO production and signaling, which enhances macrophage phagocytosis of debris and migration to draining lymph nodes to promote resolution.

    • Bangwei Luo
    • , Jinsong Wang
    •  & Zhiren Zhang

  • Article
    | Open Access

    Endothelial cell activation by inflammation requires extracellular ATP release. Here the authors show that TNF-α induces Src-family kinase-dependent ATP release by Pannexin1 channels in endothelial cells, and that Pannexin1 is required for leukocyte adhesion and emigration into the inflamed tissue.

    • Alexander W. Lohman
    • , Igor L. Leskov
    •  & Brant E. Isakson

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