Oral Microbiota and Immune System Crosstalk: A Translational Research

Abstract

Background: Oral pathogens may exert the ability to trigger differently the activation of local macrophage immune responses, for instance Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans induce predominantly pro-inflammatory (M1-like phenotypes) responses, while oral commensal microbiota primarily elicits macrophage functions consistent with the anti-inflammatory (M2-like phenotypes). Methods: In healthy individuals vs. periodontal disease patients’ blood samples, the differentiation process from monocyte to M1 and M2 was conducted using two typical growth factors, the granulocyte/macrophage colony stimulating factor (GM-CSF) and the macrophage colony stimulating factor (M-CSF). Results: In contrast with the current literature our outcomes showed a noticeable increase of macrophage polarization from healthy individuals vs. periodontal patients. The biological and clinical significance of these data was discussed. Conclusions: Our translational findings showed a significant variance between control versus periodontal disease groups in M1 and M2 marker expression within the second group significantly lower skews differentiation of M2-like macrophages towards an M1-like phenotype. Macrophage polarization in periodontal tissue may be responsible for the development and progression of inflammation-induced periodontal tissue damage, including alveolar bone loss, and modulating macrophage function may be a potential strategy for periodontal disease management.

Association of IL16 polymorphisms with periodontitis in Brazilians: A case- control study

“…In fact, we did not found difference between IL-16 genotypes and IL-16 serum levels in PD studied population. Polymorphisms on genes from other cytokine, such as IL-1α, IL-1β, TNFα and IL-10, has influence in PD [35], suggesting that the presence of pro-inflammatory cytokines (and inhibition of anti-inflammatory cytokines) direct the polarization of the immune response profiles (Th1 and Th17 were predominant in PD) and, consequently, in the disorders of tissue repair in the periodontium [36]. Although it is not yet clear what effect the IL16 polymorphism has on the development of PD, it is possible that it's related to less tissue aggression and maintenance of bone homeostasis: the structural modification of IL-16 would compromise its function in chemotaxis on CD4+ cells and the production of inflammatory cytokines by these cells which would lead to a modulation of the immune response in the oral microenvironment.…”

The Human Respiratory System and its Microbiome at a Glimpse

“…and Gram-negative anaerobic species Veillonella, Prevotella, Leptotrichia and Fusobacterium. Several pathogens of the genus Streptococcus are found in the pharynx, such as S. pneumoniae , S. pyogenes (which can cause serious disorders that are not limited to the pharynx, and can also cause septic shock) and S. agalactiae ( Figure 1 ) [ 1 , 10 , 18 , 22 , 23 ].…”

Autophagy, One of the Main Steps in Periodontitis Pathogenesis and Evolution

“…Ballini et al highlighted the key role of bone host cell invasion by Porphyromonas gingivalis in the pathogenesis of bone disorders, as well as interesting scientific evidence sustaining cytokines’ important roles in the molecular mechanism of bone disease [ 42 ]. Recent experimental evidence strongly sustains the idea that the host’s inflammatory response represents the main factor affecting the stage of periodontitis [ 36 , 43 ].…”