NBS1 is required for macrophage homeostasis and functional activity in mice

Pereira-Lopes, Selma; Tur, Juan; Calatayud-Subias, Juan A.; Lloberas, Jorge; Stracker, Travis H.

doi:10.1182/blood-2015-04-637371

Cited by 40 publications

(40 citation statements)

References 56 publications

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“…It has recently been reported that stimulated neutrophils generate a burst of ROS that induce DNA damage signaling in activated neutrophils and macrophages, suppressing cytokine production and inducing apoptosis. If the DNA damage reparative systems are effective cells will survive, otherwise they will become apoptotic and die [35][36][37].…”

Section: Cellular Apoptosis Induction and Regulation Pathwaysmentioning

confidence: 99%

Role of Neutrophils Apoptosis in Osteomyelitis Pathogenesis

Asensi¹,

Collazos²,

Valle-Garay³

2017

Clin Microbiol

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EditorialOsteomyelitis is a bone infection characterized by progressive inflammatory destruction of the infected bone and new apposition of bone at the site of infection. In adults, osteomyelitis is usually a complication of open wounds due to fractures, surgery, or both, with or without the presence of foreign bodies such as prosthetic devices. In fact, it is estimated that about 0.4 to 7% of trauma and orthopaedic interventions are complicated by osteomyelitis [1][2][3][4][5][6].Bone infections can also be the result of bacteraemia, mostly in children and in elderly patients, in whom the infection involves mainly the axial skeleton. The microorganism most frequently isolated in both post-traumatic and haematogenous cases is Staphylococcus aureus.Osteomyelitis constitutes a difficult-to-treat infection, with high rates of recurrence of about 20-30% despite appropriate medical and surgical therapies, causing significant morbidity and mortality [7][8][9][10][11][12][13].Much attention has been dedicated to improving the medical and surgical treatments of osteomyelitis, but little progress has been made toward understanding its pathogenesis. It is clear that it is multifactorial and influenced mainly by local factors related to the bone lesion and microorganisms inoculated into the bone, but inherited factors and cell immunity dysfunctions could play some role as well [14][15][16][17][18][19][20][21][22][23][24][25][26].

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Section: Cellular Apoptosis Induction and Regulation Pathwaysmentioning

confidence: 99%

Role of Neutrophils Apoptosis in Osteomyelitis Pathogenesis

Asensi¹,

Collazos²,

Valle-Garay³

2017

Clin Microbiol

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“…2,3 DNA damage responses also regulate celltype-specific programs, including cell survival and differentiation. [4][5][6] In their study, Harbort et al show that DNA damage signaling is activated by ROS in neutrophils and represses proinflammatory functions. In response to invading pathogens, neutrophils secrete proinflammatory cytokines, which recruit additional neutrophils and other immune cells.…”

mentioning

confidence: 99%

“…4,5 figure). This suggests that the increased inflammation in CGD is, in part, a consequence of the defect in ROS-mediated ATM activation and the associated repression of proinflammatory cytokines.…”

mentioning

confidence: 99%

“…[4][5][6] Characterization of these pathways will establish the important contributions of DNA damage signaling to normal development and disease states.…”

mentioning

confidence: 99%

“…9 Conversely, using a photochemically induced model of thrombosis, impaired necrotic platelet formation, occurring as a result of cyclophilin D deficiency, resulted in accelerated thrombotic occlusion. 5 Finally, recent studies have even questioned the physiologic role of platelets in supporting local thrombin generation. Fibrin formation and prothrombinase activity are minimally associated with platelets in a laser-induced nonocclusive thrombus.…”

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confidence: 99%

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DNA damage signals inhibit neutrophil function

Bednarski¹

2015

Blood

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Extracellular Proteins Isolated from L. acidophilus as an Osteomicrobiological Therapeutic Agent to Reduce Pathogenic Biofilm Formation, Regulate Chronic Inflammation, and Augment Bone Formation In Vitro

Pugazhendhi,

Seal,

Hughes

et al. 2023

Adv Healthcare Materials

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Periprosthetic joint infection (PJI) is a challenging complication that can occur following joint replacement surgery. Efficacious strategies to prevent and treat PJI and its recurrence remain elusive. Commensal bacteria within the gut convey beneficial effects through a defense strategy named “colonization resistance” thereby preventing pathogenic infection along the intestinal surface. This blueprint may be applicable to PJI. The aim is to investigate Lactobacillus acidophilus spp. and their isolated extracellular‐derived proteins (LaEPs) on PJI‐relevant Staphylococcus aureus, methicillin‐resistant S. aureus, and Escherichia coli planktonic growth and biofilm formation in vitro. The effect of LaEPs on cultured macrophages and osteogenic, and adipogenic human bone marrow‐derived mesenchymal stem cell differentiation is analyzed. Data show electrostatically‐induced probiotic‐pathogen species co‐aggregation and pathogenic growth inhibition together with LaEP‐induced biofilm prevention. LaEPs prime macrophages for enhanced microbial phagocytosis via cathepsin K, reduce lipopolysaccharide‐induced DNA damage and receptor activator nuclear factor‐kappa B ligand expression, and promote a reparative M2 macrophage morphology under chronic inflammatory conditions. LaEPs also significantly augment bone deposition while abating adipogenesis thus holding promise as a potential multimodal therapeutic strategy. Proteomic analyses highlight high abundance of lysyl endopeptidase, and urocanate reductase. Further, in vivo analyses are warranted to elucidate their role in the prevention and treatment of PJIs.

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NBS1 is required for macrophage homeostasis and functional activity in mice

Cited by 40 publications

References 56 publications

Role of Neutrophils Apoptosis in Osteomyelitis Pathogenesis

Role of Neutrophils Apoptosis in Osteomyelitis Pathogenesis

DNA damage signals inhibit neutrophil function

Extracellular Proteins Isolated from L. acidophilus as an Osteomicrobiological Therapeutic Agent to Reduce Pathogenic Biofilm Formation, Regulate Chronic Inflammation, and Augment Bone Formation In Vitro

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