لخّصلي

The oral mucosa is continuously exposed to commensal and pathogenic bacteria [1].Symptoms:

• Symptoms can develop rapidly (acute bacterial endocarditis) or gradually (subacute bacterial endocarditis)

• Prophylactic antibiotics may be recommended before certain dental or surgical procedureIt is increasingly recognized that in addition to causing specific oral diseases such as dental caries and periodontitis, oral dysbiosis is associated with inflammatory bowel diseases such as Crohn's disease and various immune disorders such as rheumatoid arthritis and diabetes mellitus [5].This finding provides the proof of concept that bacterial characteristics may contribute to the occurrence of IE in patients with S. aureus bacteremia

Bacterial endocarditis, commonly referred to as infective endocarditis, is an infection of the inner lining of the heart chambers and valves (the endocardium).Recently, it has been highlighted that stability defects in the bacterial flora (dysbiosis) undermine the interaction between commensal bacteria and host immunity and consequently causes a variety of local and systemic diseases [4].Knowledge of the interrelationship between oral commensal bacteria and oral mucosal immunity is considered essential for understanding the pathogenesis and pathophysiology of various systemic diseases.Previous researchers have analyzed neutrophils in the bone marrow and peripheral blood of germ-free (GF) mice that have never been exposed to bacteria after birth and found fewer neutrophils in comparison with normal convention mice [[8], [9], [10]].S. aureus isolates causing community-acquired, definite native-valve IE (n = 72) and bacteremia (n = 54) were collected prospectively as part of a French multicenter cohort.However, the multivariate statistical tool DAPC, applied on microarray data, segregated IE and bacteremia isolates: IE isolates were correctly reassigned as such in 80.6% of the cases (C-statistic 0.83, P < 0.001).Periodontitis is inflammation of the oral mucosa caused by microbial dysbiosis that accelerates the differentiation of CD4+ T cells into IL-17-producing proinflammatory T cells (Th17) [12].- Risk Factors: Individuals with pre-existing heart conditions (like congenital heart defects, prosthetic heart valves), those with a history of rheumatic fever, intravenous drug users, and those having certain medical procedures are at higher risk.Short-chain fatty acids produced by intestinal microflora are important for the maintenance of colonic epithelial cells and modulation of regulatory T cells [4].Neutrophils, the most abundant innate immune cells, are known to be responsible for the termination of invading bacteria at the oral mucosal barrier.In this study, we compared germ-free (GF) mice with conventional (CNV) mice to clarify the role of oral commensal bacteria in relation to oral immune cells.In parallel, the genotypic profiles of all isolates, obtained by microarray, were analyzed by discriminant analysis of principal components (DAPC)(2).Infective endocarditis (IE)(1) is a severe condition complicating 10-25% of Staphylococcus aureus bacteremia. ).2.

The oral mucosa is continuously exposed to commensal and pathogenic bacteria [1]. More than 700 different species comprise the oral commensal bacteria, which is comparable to intestinal bacteria [2]. The oral microflora is initiated by the retention of early colonizers, including Streptococcus spp. and Veillonellaspp. after birth, and evolves with the influx of various bacteria from the external environment, interacting with the immune system [3]. Oral commensal bacteria act on the immunity of the host to maintain an optimal environment for each other [4]. The role of intestinal commensal bacteria on systemic health is widely recognized. Short-chain fatty acids produced by intestinal microflora are important for the maintenance of colonic epithelial cells and modulation of regulatory T cells [4]. Recently, it has been highlighted that stability defects in the bacterial flora (dysbiosis) undermine the interaction between commensal bacteria and host immunity and consequently causes a variety of local and systemic diseases [4]. It is increasingly recognized that in addition to causing specific oral diseases such as dental caries and periodontitis, oral dysbiosis is associated with inflammatory bowel diseases such as Crohn's disease and various immune disorders such as rheumatoid arthritis and diabetes mellitus [5]. Knowledge of the interrelationship between oral commensal bacteria and oral mucosal immunity is considered essential for understanding the pathogenesis and pathophysiology of various systemic diseases.
Neutrophils, the most abundant innate immune cells, are known to be responsible for the termination of invading bacteria at the oral mucosal barrier. Furthermore, it is becoming evident that the bacterial flora and neutrophils have a symbiotic relationship, and that activation of neutrophils is governed by the microbial flora [6]. Neutrophils use intracellular and extracellular enzymes such as myeloperoxidase (MPO) and elastase as part of a bactericidal mechanism. In particular, MPO levels are often used as an indicator of neutrophil activation [7]. Previous researchers have analyzed neutrophils in the bone marrow and peripheral blood of germ-free (GF) mice that have never been exposed to bacteria after birth and found fewer neutrophils in comparison with normal convention mice [[8], [9], [10]]. These findings indicate that the presence of microorganisms in the host increases the number of neutrophils and activates the differentiation and maturation of neutrophils. However, previous reports have not clearly shown the influence of the bacterial flora on neutrophils in the oral cavity.
Healthy human oral mucosa has abundant CD4+ T cells and a small number of CD8+ T cells [11]. Periodontitis is inflammation of the oral mucosa caused by microbial dysbiosis that accelerates the differentiation of CD4⁺ T cells into IL-17-producing proinflammatory T cells (Th17) [12]. However, CD8⁺ T cells in the oral mucosa elicit regulatory functions that suppress bone destruction and repair alveolar bone [13]. In healthy human gingiva, most B cells showed a memory subset [14]. B cells in the oral mucosa possess potential for both the inhibition and progression of periodontitis [15,16]. However, it remains unclear whether oral commensal bacteria directly affect the immune differentiation of the mucosa under steady-state conditions. In this study, we compared germ-free (GF) mice with conventional (CNV) mice to clarify the role of oral commensal bacteria in relation to oral immune cells.

Infective endocarditis (IE)(1) is a severe condition complicating 10–25% of Staphylococcus aureus bacteremia. Although host-related IE risk factors have been identified, the involvement of bacterial features in IE complication is still unclear. We characterized strictly defined IE and bacteremia isolates and searched for discriminant features. S. aureus isolates causing community-acquired, definite native-valve IE (n = 72) and bacteremia (n = 54) were collected prospectively as part of a French multicenter cohort. Phenotypic traits previously reported or hypothesized to be involved in staphylococcal IE pathogenesis were tested. In parallel, the genotypic profiles of all isolates, obtained by microarray, were analyzed by discriminant analysis of principal components (DAPC)(2). No significant difference was observed between IE and bacteremia strains, regarding either phenotypic or genotypic univariate analyses. However, the multivariate statistical tool DAPC, applied on microarray data, segregated IE and bacteremia isolates: IE isolates were correctly reassigned as such in 80.6% of the cases (C-statistic 0.83, P