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UnknownSecreted protein Del-1 regulates myelopoiesis in the hematopoietic stem cell niche.
Hematopoietic stem cells (HSCs) remain mostly quiescent under steady-state conditions but switch to a proliferative state following hematopoietic stress, e.g., bone marrow (BM) injury, transplantation, or systemic infection and inflammation. The homeostatic balance between quiescence, self-renewal, ...
S-EPMC5617665 | biostudies-literature
UnknownNeutrophil homeostasis and periodontal health in children and adults.
This review summarizes the current state of knowledge on neutrophil basic biology and discusses how the breakdown of neutrophil homeostasis affects periodontal health. The homeostasis of neutrophils is tightly regulated through coordinated bone marrow production, release into the circulation, transm...
S-EPMC3929973 | biostudies-literature
UnknownComplement and periodontitis.
Although the complement system is centrally involved in host defense, its overactivation or deregulation (e.g., due to inherent host genetic defects or due to pathogen subversion) may excessively amplify inflammation and contribute to immunopathology. Periodontitis is an oral infection-driven chroni...
S-EPMC2955993 | biostudies-literature
UnknownRole of complement in host-microbe homeostasis of the periodontium.
Complement plays a key role in immunity and inflammation through direct effects on immune cells or via crosstalk and regulation of other host signaling pathways. Deregulation of these finely balanced complement activities can link infection to inflammatory tissue damage. Periodontitis is a polymicro...
S-EPMC3706506 | biostudies-literature
UnknownOptimization of the ligature-induced periodontitis model in mice.
Periodontitis is a prevalent oral inflammatory disease that leads to alveolar bone loss and may exert an adverse impact on systemic health. Experimental animal models are critical tools to investigate mechanisms of periodontal pathogenesis and test new therapeutic approaches. The ligature-induced pe...
S-EPMC3707981 | biostudies-literature
UnknownInhibition of Porphyromonas gingivalis-induced periodontal bone loss by CXCR4 antagonist treatment.
Microbial pathogens have evolved mechanisms to proactively manipulate innate immunity, thereby improving their fitness in mammalian hosts. We have previously shown that Porphyromonas gingivalis exploits CXC-chemokine receptor-4 (CXCR4) to instigate a subversive crosstalk with Toll-like receptor 2 th...
S-EPMC3494490 | biostudies-literature
UnknownComplement-targeted therapeutics in periodontitis.
Periodontitis is a prevalent oral chronic inflammatory disease which, in severe forms, may exert a major impact on systemic health. Clinical and histological observations, as well as experimental animal studies, suggest involvement of the complement system in periodontitis. However, the precise role...
S-EPMC3466049 | biostudies-literature
UnknownMicrobial manipulation of receptor crosstalk in innate immunity.
In the arms race of host-microbe co-evolution, successful microbial pathogens have evolved ingenious ways to evade host immune responses. In this Review, we focus on 'crosstalk manipulation' - the microbial strategies that instigate, subvert or disrupt the molecular signalling crosstalk between rece...
S-EPMC3077082 | biostudies-literature
UnknownPorphyromonas gingivalis: Immune subversion activities and role in periodontal dysbiosis.

Purpose of review

This review summarizes mechanisms by which Porphyromonas gingivalis interacts with community members and the host so that it can persist in the periodontium under inflammatory conditions that drive periodontal disease.

Recent findings

Recent advances indicate ...
S-EPMC7747940 | biostudies-literature
UnknownGenetic and intervention studies implicating complement C3 as a major target for the treatment of periodontitis.
Chronic periodontitis is induced by a dysbiotic microbiota and leads to inflammatory destruction of tooth-supporting connective tissue and bone. The third component of complement, C3, is a point of convergence of distinct complement activation mechanisms, but its involvement in periodontitis was not...
S-EPMC4078411 | biostudies-literature
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