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Objective: Patients with systemic lupus erythematosus (SLE) often develop multi-organ damages including heart and kidney complications. We sought to better define the underlying mechanisms with a focus on the chemokine receptor CX3CR1. Methods: We generated Cx3cr1-deficient MRL/lpr lupus-prone mice through backcrossing. We then employed heterozygous intercross to generate MRL/lpr littermates that were either sufficient or deficient of CX3CR1. The mice were also treated with either Lactobacillus spp. or a high-fat diet (HFD) followed by assessments of the kidney and heart, respectively. Results: Cx3cr1–/– MRL/lpr mice exhibited a distinct phenotype of exacerbated glomerulonephritis compared to Cx3cr1+/+ littermates, which was associated with a decrease of spleen tolerogenic marginal zone macrophages and an increase of double-negative T cells. Interestingly, upon correction of the gut microbiota with Lactobacillus administration, the phenotype of exacerbated glomerulonephritis was reversed, suggesting that CX3CR1 controls glomerulonephritis in MRL/lpr mice through a gut microbiota-dependent mechanism. Upon treatment with HFD, Cx3cr1–/– MRL/lpr mice developed significantly more atherosclerotic plaques that were promoted by Ly6C+ monocytes. Activated monocytes expressed ICOS-L that interacted with ICOS-expressing follicular T-helper cells, which in turn facilitated a germinal center reaction to produce more autoantibodies. Through a positive feedback mechanism, the increased circulatory autoantibodies further promoted the activation of Ly6C+ monocytes and their display of ICOS-L. Conclusions: We uncovered novel, Cx3cr1 deficiency-mediated pathogenic mechanisms contributing to SLE-associated glomerulonephritis and cardiovascular disease. [ABSTRACT FROM AUTHOR]

Purpose: Understanding anatomical variations of the facial artery and its branches is important for dental and medical practitioners. Methods: Routine cadaveric dissection of the head and neck was performed to demonstrate the origin and branches of the facial artery. Results: Facial artery emerged from a common linguofacial trunk off the external carotid artery. On the face, the facial artery first gave off a pre-masseteric branch. Immediately after, an aberrant artery emerged from the facial artery that coursed along the ramus of the mandible, which upon further dissection and examination was found to anastomose with inferior alveolar artery within the ramus of the mandible. Conclusions: We report a unique anastomosis between facial and inferior alveolar arteries, vessels that have not been previously shown to communicate. This case report may provide useful information for oral and maxillofacial surgeons as well as dentists performing inferior alveolar nerve blocks. [ABSTRACT FROM AUTHOR]