Inflammatory Compounds: Neuropeptide Substance Pand Cytokines

Periodontitis may be a risk factor for atherosclerosis and coronary heart disease. The influence of periodontal pathogens in cardiovascular diseases needs further investigation. Therefore, the aims of this clinical study are: to test the presence of periodontal bacteria DNA in aortic valves and to assess the concomitant presence of the same periodontal bacteria DNA in whole blood samples in patients affected by aortic valve stenosis and chronic periodontitis. Nineteen consecutive patients (12 males and 7 females, age: 49–85 years) were enrolled in this study after having been subjected to a complete periodontal evaluation to confirm the diagnosis of chronic periodontitis. All patients were scheduled for aortic valve replacement surgery. After clinical and microbial periodontal examination, the aortic valve tissue specimens were obtained by excision during valve replacement surgery and the patients were subjected to the whole blood sampling before the surgery. The polymerase chain reaction technology was used to detect the putative periodontal pathogens Tannerella forshytia, Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Prevotella intermedia, Fusobacterium nucleatum, Campylobacter rectus, Eikenella corrodens and Treponema denticola. Neither the 19 aortic valve specimens nor the blood samples were positive for the genoma of the selected periodontal pathogens. The selected periodontal pathogens did not colonize the aortic valve of patients affected by stenosis and bacterial genoma was not present in whole blood samples. A high blood pressure at the aortic valve may prevent the adhesion and proliferation of bacterial colonies.

Section: Dna Extraction and Per Assaymentioning

confidence: 99%

Examination of Periodontal Pathogens in Stenotic Valve Specimens and in Whole Blood Samples in Patients Affected by Aortic Valve Stenosis and Chronic Periodontitis

Raffaelli

Santangelo

Falchetti³

et al. 2010

“…As the infection progresses, the inflammatory response becomes mast-cell-and T cell-dependent. Moreover, in T. spiralis infection a wide range of inflammatory cytokines such as IL-I, IL-4, IL-6, IL-8, IFN-y and TNF-a and chemokines are produced (3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13).…”

mentioning

confidence: 99%

Microarray Analysis of NF-κB Signaling Pathways in PBMC of Mice Infected by Trichinella Spiralis

Symeonidou

Pappa

Kourelis

et al. 2010

The NF-kappaΒ pathway gene expression profiles were compared between 10, 20 and 39 days after Trichinella spiralis experimental infection in BALB/c mice. Out of 128 genes, 19 (14.8%) genes were present in non-infected and post-infected mice. The expression of 7 (36.8%) genes was downregulated 10 and 20 days post-infection while 3 (15.8%) genes were upregulated 39 days post-infection. The present study lists the candidate genes of the NF-kappaB signaling pathway that were commonly and differentially expressed between the specific points of T. spiralis infection, thus suggesting that these genes need to be further investigated to reveal the mechanism of the T. spiralis modulation of the NF-kappaB signaling pathways.

“…Several studies indicate that IL-31 sustains the survival of hematopoietic stem cells and recruits the Jakl, Jak2, STAT-I, STAT-3 and STAT5 signaling pathways, as well as the PI3-kinase (33)(34)(35)(36)(37)(38).…”

Section: ML Castellani Et Almentioning

confidence: 99%

IL-31 a TH2 Cytokine Involved in Immunity and Inflammation

Castellani

Felaco

Galzio

et al. 2010

Self Cite

Cytokines are immunal regulatory proteins, however they also play a relevant role in inflammatory diseases. IL-31 is a newly discovered cytokine expressed primarily in TH2 cells, introduced by activated CD4+ T cells. IL-31 is capable of inducing chemokines and other cytokines in several inflammatory diseases via its surface receptor. This cytokine is also produced by mast cells and mast cell line, suggesting a role in allergic diseases. In this editorial we revisit the biological role of IL-31 in immunity and inflammation.