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Insights into the pathogenesis of the emerging pathogen Kingella kingae.

紀錄類型:	書目-語言資料,手稿 : Monograph/item
正題名/作者:	Insights into the pathogenesis of the emerging pathogen Kingella kingae./
作者:	Kehl-Fie, Thomas Everett.
面頁冊數:	1 online resource (172 pages)
附註:	Source: Dissertations Abstracts International, Volume: 70-12, Section: B.
Contained By:	Dissertations Abstracts International70-12B.
標題:	Microbiology. -
電子資源:	click for full text (PQDT)
ISBN:	9781109051537

Insights into the pathogenesis of the emerging pathogen Kingella kingae.
Kehl-Fie, Thomas Everett.

Insights into the pathogenesis of the emerging pathogen Kingella kingae. - 1 online resource (172 pages)

Source: Dissertations Abstracts International, Volume: 70-12, Section: B.

Thesis (Ph.D.)--Washington University in St. Louis, 2008.

Includes bibliographical references

Kingella kingae is a Gram-negative pathogen and a member of the Neisseriaceae. In the past, K. kingae was dismissed as an important cause of human illness due to its infrequent recovery from infected tissues. However, more recently K. kingae has become recognized as one of the leading causes of pediatric bone and joint infections. Despite the prevalence of disease caused by K. kingae, little is known regarding the pathogenesis of K. kingae disease. In studies aimed at identifying the factors that mediate K. kingae adherence, we established that K. kingae expresses type IV pili and demonstrated that these fibers are essential for adherence to both respiratory epithelial and synovial cells. Interestingly, the level of adherence to synovial cells but not to respiratory epithelial cells correlated with the level of piliation. The major pilus subunit, PilA1, was demonstrated to be encoded by a locus that also encodes a second pilin homolog called PilA2 and a pilus accessory protein called FimB. In addition to requiring PilA1, wild-type adherence was dependent on two PilC homologs. Examination of a collection of clinical isolates revealed that only piliated strains were adherent. Pili were observed to be expressed by a high percentage of isolates from the respiratory tract and blood and by a low percentage of isolates from bones and joints, suggesting that type IV pili are selected against during invasive infection. The K. kingae clinical isolates were also found to express antigenically distinct PilA1 molecules. Expression of type IV pili in K. kingae was found to be dependent upon the alternative sigma factor 654 and an atypical PilS/PilR two-component regulatory system, suggesting that regulation of K. kingae pilus expression combines aspects of Pseudomonas aeruginosa and Neisseria species regulatory mechanisms. Additional investigation revealed that K. kingae expresses a conical RTX toxin that is absent from other Kingella species and has activity against respiratory epithelial, synovial, and immune cells, providing a possible mechanism for breaching of the epithelial barrier and immune evasion. These studies provide key insights into the factors that mediate essential steps in K. kingae pathogenesis and provide a basis for future studies.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2024

Mode of access: World Wide Web

ISBN: 9781109051537Subjects--Topical Terms:

591510
Microbiology.
Subjects--Index Terms:

Kingella kingaeIndex Terms--Genre/Form:

554714
Electronic books.

Insights into the pathogenesis of the emerging pathogen Kingella kingae.
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520 $a Kingella kingae is a Gram-negative pathogen and a member of the Neisseriaceae. In the past, K. kingae was dismissed as an important cause of human illness due to its infrequent recovery from infected tissues. However, more recently K. kingae has become recognized as one of the leading causes of pediatric bone and joint infections. Despite the prevalence of disease caused by K. kingae, little is known regarding the pathogenesis of K. kingae disease. In studies aimed at identifying the factors that mediate K. kingae adherence, we established that K. kingae expresses type IV pili and demonstrated that these fibers are essential for adherence to both respiratory epithelial and synovial cells. Interestingly, the level of adherence to synovial cells but not to respiratory epithelial cells correlated with the level of piliation. The major pilus subunit, PilA1, was demonstrated to be encoded by a locus that also encodes a second pilin homolog called PilA2 and a pilus accessory protein called FimB. In addition to requiring PilA1, wild-type adherence was dependent on two PilC homologs. Examination of a collection of clinical isolates revealed that only piliated strains were adherent. Pili were observed to be expressed by a high percentage of isolates from the respiratory tract and blood and by a low percentage of isolates from bones and joints, suggesting that type IV pili are selected against during invasive infection. The K. kingae clinical isolates were also found to express antigenically distinct PilA1 molecules. Expression of type IV pili in K. kingae was found to be dependent upon the alternative sigma factor 654 and an atypical PilS/PilR two-component regulatory system, suggesting that regulation of K. kingae pilus expression combines aspects of Pseudomonas aeruginosa and Neisseria species regulatory mechanisms. Additional investigation revealed that K. kingae expresses a conical RTX toxin that is absent from other Kingella species and has activity against respiratory epithelial, synovial, and immune cells, providing a possible mechanism for breaching of the epithelial barrier and immune evasion. These studies provide key insights into the factors that mediate essential steps in K. kingae pathogenesis and provide a basis for future studies.
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