Inflammation articles within Nature Communications

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  • Article
    | Open Access

    The enzyme nicotinate phosphoribosyltransferase (NAPRT) mediates the rate-limiting step in NAD salvage pathway starting from nicotinic acid. Here the authors show that NAPRT can be detected extracellularly, binds to Toll like receptor 4, and activates NF-kB signaling and cytokine production in macrophage via NAD synthesis-independent pathways.

    • Antonella Managò
    • , Valentina Audrito
    •  & Silvia Deaglio

  • Article
    | Open Access

    An increasing number of inflammatory pathologies is associated with IL-1 production downstream of caspases 1 and 11. Here the authors show that graft-versus-host-disease (GvHD) is diminished in mice with genetic or pharmacological ablation of caspase-11, and provide mechanistic insights into the signals leading to caspase-11 activation in GvHD.

    • Yanyan Lu
    • , Ran Meng
    •  & Ben Lu

  • Article
    | Open Access

    Macrophage specific deletion of GGTase-I, a prenylation enzyme, in mice induces inflammatory response and rheumatoid arthritis. Here the authors show that GGTase-I deficiency and the resulting reduction of RAC1 prenylation increase RAC1 interaction with the adaptor protein IQGAP1, leading to GTP-loading of RAC1 and enhanced proinflammatory cytokine production.

    • Murali K. Akula
    • , Mohamed X. Ibrahim
    •  & Martin O. Bergo

  • Article
    | Open Access

    Many forms of autoimmune disorder involve abnormal T cell functions, but how this versatility is achieved is not fully clear. Here the authors show that Sharpin-deficient Treg cells induce the death of local keratinocytes via multiple programmed cell death and innate inflammation to cause skin inflammation similar to cpdm mice with genetic deletion of Sharpin.

    • Katsuhiro Sasaki
    • , Ai Himeno
    •  & Kazuhiro Iwai

  • Article
    | Open Access

    Clearance of apoptotic neutrophils by macrophages is important for the resolution of inflammation. Here, the authors show that interferon-β produced by resolution phase macrophages promotes neutrophil apoptosis and efferocytosis and induces macrophage reprogramming to a pro-resolving phenotype, thereby identifying IFN-β as a multi-pronged pro-resolution cytokine.

    • Senthil Kumaran Satyanarayanan
    • , Driss El Kebir
    •  & Amiram Ariel

  • Article
    | Open Access

    BTLA is established as a negative regulator of natural killer T (NKT) cell function, and share its ligand HVEM with CD160. Here the authors show, by analyzing NKT activation in CD160-deficient mice or with BTLA blockade, that CD160 synergizes with BTLA to negatively regulate NKT cells during hepatic injury.

    • Tae-Jin Kim
    • , Gayoung Park
    •  & Kyung-Mi Lee

  • Article
    | Open Access

    Leucine-rich repeat (LRR) domains are commonly present in immune regulatory proteins. Here the authors show that LRR exonic modularity and alternative splicing of an LRR-containing protein, NLRP3, modulate the ratio of functional/afunctional NLRP3 isoforms to instill a stochastic regulation of NLRP3-mediated inflammation and innate immunity.

    • Florian Hoss
    • , James L. Mueller
    •  & Eicke Latz

  • Article
    | Open Access

    Bone marrow-derived monocytes are recruited to the gut to replenish the local macrophage pool. Here the authors show that, while such replenishment constitutively occur under homeostasis, gut inflammation induces an immediate, Trem1-related transcription change to recruited monocyte to enable a context-dependent modulation of macrophage functions.

    • Girmay Desalegn
    •  & Oliver Pabst

  • Article
    | Open Access

    A number of therapeutic agents aimed at reducing pathology in Duchenne muscular dystrophy have been developed, but may have off-target effects when delivered systemically. Here, the authors express the therapeutic LIF transgene in leukocytes, and show this results in targeting to inflamed dystrophic muscle and reduced fibrosis by suppressing type 2 immunity.

    • Steven S. Welc
    • , Ivan Flores
    •  & James G. Tidball

  • Article
    | Open Access

    Systemic sepsis is a potentially life-threatening illness and immunocompromised individuals are especially vulnerable. Here, using a cohort of patients with intra-abdominal origin sepsis, the authors show an important role for the NLRP3 inflammasome in establishing a host response, and NLRP3 dysfunction is a common feature of sepsis mortality.

    • Juan José Martínez-García
    • , Helios Martínez-Banaclocha
    •  & Pablo Pelegrin

  • Article
    | Open Access

    Dengue virus (DENV) promotes leukocyte-platelet interactions that contribute to pathogenesis. Here, the authors report a role for C-type lectins CLEC2 and CLEC5A in platelet activation and NET formation and show that blockade of CLEC5A and TLR2 attenuates inflammation and increases survival of infected mice.

    • Pei-Shan Sung
    • , Tur-Fu Huang
    •  & Shie-Liang Hsieh

  • Article
    | Open Access

    The capsular polysaccharide A (PSA) of Bacteroides fragilis is known to have immunomodulatory capability during sterile inflammatory disorders. Here Ramakrishna and colleagues show that PSA administration in a murine model of herpes simplex encephalitis induces IL-10 producing B and T cell populations that confer protection against lethal challenge and brain pathology.

    • Chandran Ramakrishna
    • , Maciej Kujawski
    •  & Edouard M. Cantin

  • Article
    | Open Access

    Endothelial cell regeneration is essential for blood vessels to recover from inflammation-induced injury. Here Liu et al. show that the transcription factor Sox17 is required for endothelial regeneration following endotoxemia, and that delivery of a transgene expressing Sox17 to lung endothelial cells enhances recovery after injury.

    • Menglin Liu
    • , Lianghui Zhang
    •  & Asrar B. Malik

  • Article
    | Open Access

    In inflammasomes, caspase-1 activation leads to pyroptosis mediated by gasdermin D, but cells lacking gasdermin-D still initiate caspase-dependent cell death. Here, Tsuchiya et al. show that these cells undergo Bid- and caspase-3-dependent apoptosis.

    • Kohsuke Tsuchiya
    • , Shinsuke Nakajima
    •  & Takashi Suda

  • Article
    | Open Access

    Maintaining the intestinal barrier function requires a balance of multiple signalling pathways. Here the authors show that A20, an anti-inflammatory and anti-apoptotic protein, and Atg1611, an autophagy regulator, cross-regulate their respective protein levels and function to serve compensatory and redundant roles in fine-tuning gut barrier homeostasis.

    • Karolina Slowicka
    • , Inmaculada Serramito-Gómez
    •  & Geert van Loo

  • Article
    | Open Access

    The inflammasomes are important mediators of protective immunity by promoting inflammatory cytokine production and cell death. Here the authors show that a lncRNA, Neat1, is mobilized by inflammasome-activating signals to promote the assembly of several inflammasome complexes and cytokine maturation to regulate inflammation.

    • Pengfei Zhang
    • , Limian Cao
    •  & Mian Wu

  • Article
    | Open Access

    Stimulation of peripheral nerve activity may be used to treat metabolic and inflammatory disorders, but current approaches need implanted devices. Here, the authors present a non-invasive approach, and show that ultrasound-mediated stimulation can be targeted to specific sub-organ locations in preclinical models and alter the response of metabolic and inflammatory neural pathways.

    • Victoria Cotero
    • , Ying Fan
    •  & Christopher Puleo

  • Article
    | Open Access

    Modulation of the cholinergic pathway and spleen function can reduce inflammation with invasive implants. Here, the authors show that non-invasive ultrasound stimulation of the spleen reduces disease severity in a mouse model of inflammatory arthritis, partly via altering B and T cell function.

    • Daniel P. Zachs
    • , Sarah J. Offutt
    •  & Hubert H. Lim

  • Article
    | Open Access

    Allograft can induces local chronic inflammation, but how this feeds back to regulating late immunity is still not clear. Here the authors show, by charactering B cell transcriptome landscape dynamic in human allografts and in mouse kidneys transitioning from acute to chronic injury, that late B cell activation is associated with renal dysfunction and inflammation.

    • Pietro E. Cippà
    • , Jing Liu
    •  & Andrew P. McMahon

  • Article
    | Open Access

    Neutrophils and macrophages are both involved in the initiation of inflammation, but whether and how they may participate in inflammation resolution is unclear. Here the authors show that neutrophils may mediate the conversion of macrophage into a pro-resolution phenotype via reactive oxygen species production to promote liver repair.

    • Wenting Yang
    • , Yuandong Tao
    •  & Li Tang

  • 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

    Fibroblasts can be directly reprogrammed to cardiomyocytes, but reprogramming is less efficient for adult compared to embryonic fibroblasts. Here, the authors find that inhibition of inflammation and Cox-2-prostaglandin-cAMP-IL-1β signaling enhances reprogramming efficiency of adult, but not embryonic fibroblasts.

    • Naoto Muraoka
    • , Kaori Nara
    •  & Masaki Ieda

  • Article
    | Open Access

    Type-2 innate lymphoid cells (ILC2s) are an immune population secreting Th2 cytokines playing a role in the regulation of adipose metabolic homeostasis. Here the authors show that engagement of GITR, a member of the TNF superfamily, in activated ILC2s is protective against insulin resistance in both a preventive and a therapeutic manner in the context of obesity.

    • Lauriane Galle-Treger
    • , Ishwarya Sankaranarayanan
    •  & Omid Akbari

  • 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

    A chromatin remodelling factor Satb1 is essential for T cell lineage development in the thymus. Here the authors show that while Satb1 is dispensable for the differentiation of Th17 cells and their response to gut commensals, it plays a critical role in pathogenic Th17 effector function in EAE by directly activating Bhlhe40 and modulating PD-1.

    • Keiko Yasuda
    • , Yohko Kitagawa
    •  & Keiji Hirota

  • Article
    | Open Access

    Group 2 innate lymphoid cells (ILC2) are important mediators for allergy, but how ILC2 are regulated under chronic inflammation is still unclear. Here the authors show that Runx transcription factors, which normally suppresses ILC2 activation at steady state, help promote ILC2 activation and type 2 cytokine production in lung allergy mouse models.

    • Chizuko Miyamoto
    • , Satoshi Kojo
    •  & Takashi Ebihara

  • Article
    | Open Access

    Host metabolic reprogramming plays a role in functional responses against pathogens. Here, the authors characterise malonylated proteins in macrophages and show that malonylation of the glycolytic enzyme GAPDH impacts cytokine production by modulating both its enzymatic activity and RNA-binding capacity.

    • Silvia Galván-Peña
    • , Richard G. Carroll
    •  & Luke A. O’Neill

  • Article
    | Open Access

    B cells produce antibodies to mediate various immune functions, but are also reported to negatively regulate immune responses. Here, the authors show that a subset of mature B cells expressing low levels of IgD, present in both mice and human, may pursue this regulatory function indirectly by inducing the proliferation of regulatory T cells via GITRL.

    • Avijit Ray
    • , Mohamed I. Khalil
    •  & Bonnie N. Dittel

  • 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

    The role of innate T cell subsets in the pathogenesis of spondyloarthritis (SpA) is not well understood. Here, the authors examine the role of invariant natural killer T (iNKT) and γδ-T cells in SpA and show that disease-derived iNKT and γδ-T cells have unique and Th17-skewed phenotype and gene expression profiles within inflamed joints.

    • Koen Venken
    • , Peggy Jacques
    •  & Dirk Elewaut

  • 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

    Faecal microbiota transplantation (FMT) is becoming a therapeutic option in several gastrointestinal disorders. Here, Burrello et al. study the immunological mechanisms by which FMT reduces colonic inflammation and initiates the restoration of intestinal homeostasis in a mouse model of colitis.

    • Claudia Burrello
    • , Federica Garavaglia
    •  & Federica Facciotti

  • Article
    | Open Access

    B cells contribute to rheumatoid arthritis pathogenesis and bone erosion, but the underlying mechanisms are still unclear. Here the authors show, using mouse models and patient tissues, that B cells directly inhibit osteoblast differentiation by producing CCL3 and TNF, thereby providing a potentially new direction for arthritis therapy.

    • Wen Sun
    • , Nida Meednu
    •  & Lianping Xing

  • Article
    | Open Access

    Neutrophils normally fulfil their metabolic demands by glycolysis and have limited mitochondrial activity. Here the authors show that tumours promote neutrophils adapted to oxidative mitochondria metabolism that function in the glucose-restrained tumour microenvironment to promote tumour growth by maintaining local immune suppression.

    • Christopher M. Rice
    • , Luke C. Davies
    •  & Daniel W. McVicar

  • Article
    | Open Access

    Abdominal aortic aneurysms (AAA) are characterized by extensive extracellular matrix degradation. Here Hadi et al. identify a netrin-1/neogenin-based crosstalk between macrophages and vascular smooth muscle cells (VSMCs), leading to the secretion of the matrix metalloproteinase MMP-3 by VSMCs and subsequent matrix degradation in AAA lesions.

    • Tarik Hadi
    • , Ludovic Boytard
    •  & Bhama Ramkhelawon

  • Article
    | Open Access

    Nuclear factor-kappa B (NF-κB) signaling is regulated by ubiquitin to maintain immune homeostasis. Here the authors show that a peptidylprolyl isomerase, CYPJ, blocks TAB2/3 or LUBAC ubiquitin chain sensing and suppress NF-κB activation, with CYPJ-deficiency leading to susceptibility to inflammatory stimuli.

    • Chunjie Sheng
    • , Chen Yao
    •  & Shuai Chen

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