As part of the host immune response, iron is kept unavailable to bacteria by being sequestered by catecholamines (i.e., epinephrine, norepinephrine, and dopamine) or leukocyte-produced molecules like lactoferrin and transferrin ( 15, 16). In the subgingival pocket, Aa must compete for nutrients, such as iron, in order to survive. actinomycetemcomitans contributes to tissue inflammation, destruction, and bone resorption by expressing a number of virulence factors such as cytolethal disentin toxin, leukotoxin A of the RTX family of bacterial toxins, and collagenase ( 11– 14). actinomycetemcomitans has been strongly associated with periodontitis and other diseases such as rheumatoid arthritis, cardiovascular diseases, atherosclerosis, urinary tract infections, and brain abscesses ( 6– 10). Aggregatibacter actinomycetemcomitans ( Aa) is a non-motile gram-negative facultative anaerobe of the Pasteurellaceae family ( 3– 5).
Recurring inflammation of the periodontium has been associated with the initiation, exacerbation, and pathogenesis of a number of other inflammatory diseases ( 2). The disease is characterized by the progressive deepening of the sulcus and loss of attachment between the bone and gingival tissue leading to bone loss. Periodontitis consists of a chronic inflammation of the periodontium caused by the inflammatory response of the host to plaque biofilm. In the oral cavity, when host microbe homeostasis is broken, bacterial communities accumulate at the sub-gingival pocket and form biofilms that lead to oral diseases such as periodontitis ( 1). actinomycetemcomitans promotes azurophilic granule exocytosis by neutrophils as an epinephrine source to promote bacterial survival. Based on our findings, we propose that A. actinomycetemcomitans growth and induced the expression of the qseBC operon under anaerobic conditions. Finally, epinephrine-containing supernatants collected from human neutrophils promoted A. Using QseC mutants, we showed that the periplasmic domain of the QseC sensor kinase is required for the interaction between A. In addition, by selectively inhibiting granule exocytosis, we present the first evidence that epinephrine is stored in azurophilic granules. actinomycetemcomitans induced exocytosis of neutrophil granule subtypes: secretory vesicles, specific granules, gelatinase granules, and azurophilic granules. In the present study, we showed that human neutrophils synthesize, store, and release epinephrine, one of the three main types of catecholamines. actinomycetemcomitans exploits human neutrophils as a source for catecholamines. In periodontitis, large infiltration of neutrophils is found at the subgingival pocket hence, we wanted to test the hypothesis that A. It has been reported that mouse neutrophils can release catecholamines. However, the source of catecholamines has not been identified. actinomycetemcomitans, necessary for the organism to acquire iron as a nutrient to survive in the anaerobic environment. Previously, our group identified catecholamines and iron as the signals that activate the QseBC two-component system in A. Periodontitis is a chronic inflammation of the periodontium resulting from the inflammatory response of the host towards the dysbiotic microbial community present at the gingival crevice. 2Department of Oral Immunology and Infectious Diseases, School of Dentistry, University of Louisville, Louisville, KY, United StatesĪggregatibacter actinomycetemcomitans is a gram-negative facultative anaerobe and an opportunistic oral pathogen, strongly associated with periodontitis and other inflammatory diseases.1Department of Microbiology and Immunology, School of Medicine, University of Louisville, Louisville, KY, United States.
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