Calcium signaling for host cell death: In response to microbial pathogens, some plants kill off their own cells to limit further spread of infection. The Toll/Interleukin-1 receptor/Resistance class of nucleotide-binding leucine-rich repeat receptors (known as TNLs) function in plants as immune receptors. These TNLs work together with a dedicated set of helper proteins. Jacob et al. reveal the structure of one of these helpers known as NRG1 (N REQUIREMENT GENE 1). The structure resembles a known animal cation channel. The authors demonstrate that helper NLRs directly control calcium ion influx to initiate host cell death, providing a mechanism for TNL outputs. Science , abg7917, this issue p. 420

Chemical signalling in the plant microbiome can have drastic effects on microbial community structure, and on host growth and development. Previously, we demonstrated that the auxin metabolic signal interference performed by the bacterial genus Variovorax via an auxin degradation locus was essential for maintaining stereotypic root development in an ecologically relevant bacterial synthetic community. Here, we dissect the Variovorax auxin degradation locus to define the genes iadDE as necessary and sufficient for indole-3-acetic acid (IAA) degradation and signal interference. We determine the crystal structures and binding properties of the operon’s MarR-family repressor with IAA and other auxins. Auxin degradation operons were identified across the bacterial tree of life and we define two distinct types on the basis of gene content and metabolic products: iac-like and iad-like. The structures of MarRs from representatives of each auxin degradation operon type establish that each has distinct IAA-binding pockets. Comparison of representative IAA-degrading strains from diverse bacterial genera colonizing Arabidopsis plants show that while all degrade IAA, only strains containing iad-like auxin-degrading operons interfere with auxin signalling in a complex synthetic community context. This suggests that iad-like operon-containing bacterial strains, including Variovorax species, play a key ecological role in modulating auxins in the plant microbiome.

Inflammasome initiates inflammation via the maturation of interleukin-1 beta (IL-1β). Periodontitis is a prevalent, male-biased disease characterized by inflammation-driven bone loss, yet the mechanism(s) of this sex bias is unknown. This study explored whether enhanced inflammasome represents a causal mechanism for this bias. Analyses of three separate human studies (>6,200 samples) show that males have significantly higher IL-1β in the gingival crevicular fluid than females during health and periodontitis. This pattern is experimentally reproduced with different versions of the ligature-induced periodontitis mouse model where males show greater IL-1β secretion than females. The inflammasome drives bone resorption in males but not females as revealed by analyses of inflammasome gene-deletion mice. Pharmacologic treatment with a caspase-1/4 inhibitor reduces inflammatory cell infiltration, dampens osteoclastogenesis signaling (via the receptor activator of nuclear factor-kappa B pathway), and prevents bone resorption in males but not females during experimental periodontitis. While ovariectomized females show no change in their nonresponsiveness to caspase-1/4 inhibition, orchiectomized males no longer respond to the inhibition, suggesting the importance of an intact male reproductive system in the mediation of this inhibition. Thus, our study identifies inflammasome activation as causal for male-biased experimental periodontitis and supports sex-stratified studies to foster future advancement of inflammasome therapeutics in periodontics.

Periodontitis is a chronic inflammatory disease associated with persistent oral microbial dysbiosis. The human β-glucuronidase (GUS) degrades constituents of the periodontium and is used as a biomarker for periodontitis severity. However, the human microbiome also encodes GUS enzymes, and the role of these factors in periodontal disease is poorly understood. Here, we define the 53 unique GUSs in the human oral microbiome and examine diverse GUS orthologs from periodontitis-associated pathogens. Oral bacterial GUS enzymes are more efficient polysaccharide degraders and processers of biomarker substrates than the human enzyme, particularly at pHs associated with disease progression. Using a microbial GUS-selective inhibitor, we show that GUS activity is reduced in clinical samples obtained from individuals with untreated periodontitis and that the degree of inhibition correlates with disease severity. Together, these results establish oral GUS activity as a biomarker that captures both host and microbial contributions to periodontitis, facilitating more efficient clinical monitoring and treatment paradigms for this common inflammatory disease.

Background: Permanently replacing missing teeth in the younger population is a clinical challenge. However, dental autotransplantation offers a viable treatment option in this demographic. To be performed predictably, it requires proper diagnoses, planning, and adherence to established guidelines in a multidisciplinary approach. Such guidelines should use evidence-based dentistry to anticipate and limit complications. The aim of this study is to evaluate the current literature on dental autotransplantation, discuss an evidence-based protocol, highlight steps for minimizing complications, and present a case report on two autotransplantations conducted at the Graduate Periodontology clinic at the University of North Carolina at Chapel Hill, Adams School of Dentistry, in the context of representative cases. Methods: A literature search using PubMed was conducted with the goal of constructing a comparative table on both survival and success rates of autotransplantation, providing a comparison of protocols and clinical studies and informing this narrative review. This review is illustrated by cases with the intention to highlight critical steps, limitations, and strengths of this mode of treatment. Results and Conclusions: Given the information presented, it is concluded that autotransplantation is a valuable treatment option provided established guidelines are followed. It is particularly useful for the younger population where implants or other options are not appropriate or feasible. This study also highlights some of the gaps in knowledge in autotransplantation which present opportunity for further studies to be developed.