Exploring the Potential of Micro-Immunotherapy in the Treatment of Periodontitis.

Periodontitis, characterized by the progressive destruction of dental support tissues due to altered immune responses, poses a significant concern for public health. This condition involves intricate interactions between the immune response and oral microbiome, where innate and adaptive immune responses, with their diverse cell populations and inflammatory mediators, play crucial roles in this immunopathology. Indeed, cytokines, chemokines, growth factors, and immune cells perform key functions in tissue remodeling.

A Sequential Micro-Immunotherapy Medicine Increases Collagen Deposition in Human Gingival Fibroblasts and in an Engineered 3D Gingival Model under Inflammatory Conditions.

Periodontal therapies use immune mediators, but their side effects can increase with dosage. Micro-immunotherapy (MI) is a promising alternative that employs immune regulators at low and ultralow doses to minimize adverse effects. In this study, the effects of 5 capsules and the entire 10-capsule sequence of the sequential MI medicine (MIM-seq) were tested in two in vitro models of periodontitis.

BMP4 micro-immunotherapy increases collagen deposition and reduces PGE2 release in human gingival fibroblasts and increases tissue viability of engineered 3D gingiva under inflammatory conditions.

Background: We aimed to evaluate the effect of low doses (LD) bone morphogenetic protein-2 (BMP2) and BMP4 micro-immunotherapy (MI) in two in vitro models of periodontal wound healing/regeneration.

Methods: We first evaluated the effect of LD of BMP2 and BMP4 MI on a 2D cell culture using human gingival fibroblasts (hGF) under inflammatory conditions induced by IL1β. Biocompatibility, inflammatory response (Prostaglandin E2 (PGE2) release), collagen deposition and release of extracellular matrix (ECM) organization-related enzymes (matrix metalloproteinase-1 (MMP1) and metalloproteinase inhibitor 1 (TIMP1)) were evaluated after short (3 days) and long-term (24 days) treatment with BMP2 or BMP4 MI.

OmpK26, a novel porin associated with carbapenem resistance in Klebsiella pneumoniae.

Clinical isolates of Klebsiella pneumoniae resistant to carbapenems are being isolated with increasing frequency. Loss of the expression of the major nonspecific porins OmpK35/36 is a frequent feature in these isolates. In this study, we looked for porins that could compensate for the loss of the major porins in carbapenem-resistant organisms.

Role of Klebsiella pneumoniae LamB Porin in antimicrobial resistance.

To investigate the contribution of LamB in Klebsiella pneumoniae antimicrobial resistance, we determined the MICs of various antibiotics and the frequency of mutation to increased cefoxitin or meropenem resistance of the strains CSUB10S (expressing only OmpK36), CSUB10R (lacking OmpK35 and OmpK36), and their derived isogenic insertion-duplication mutants deficient in LamB. Expression of LamB was indispensable in order for CSUB10S to lose OmpK36 and become resistant to cefoxitin, while in CSUB10R, LamB deficiency promoted increased resistance to carbapenem.