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Mechanism of action of AexU, a new type III secretion system effector from an emerging human pathogen Aeromonas hydrophila.

紀錄類型:	書目-語言資料,手稿 : Monograph/item
正題名/作者:	Mechanism of action of AexU, a new type III secretion system effector from an emerging human pathogen Aeromonas hydrophila./
作者:	Sierra, Johanna Carolina.
面頁冊數:	1 online resource (114 pages)
附註:	Source: Dissertations Abstracts International, Volume: 72-06, Section: B.
Contained By:	Dissertations Abstracts International72-06B.
標題:	Microbiology. -
電子資源:	click for full text (PQDT)
ISBN:	9781124270500

Mechanism of action of AexU, a new type III secretion system effector from an emerging human pathogen Aeromonas hydrophila.
Sierra, Johanna Carolina.

Mechanism of action of AexU, a new type III secretion system effector from an emerging human pathogen Aeromonas hydrophila. - 1 online resource (114 pages)

Source: Dissertations Abstracts International, Volume: 72-06, Section: B.

Thesis (Ph.D.)--The University of Texas Medical Branch Graduate School of Biomedical Sciences, 2010.

Includes bibliographical references

Our laboratory first reported the complete sequence of the type III secretion system (T3SS) from a diarrheal isolate SSU of A. hydrophila. We identified an effector protein (designated as AexU) of the T3SS, which exhibited ADP-ribosyltransferase (ADPRT) and GTPase-activating protein (GAP) activity. AexU was successfully expressed in the HeLa cell Tet-Off system and I provided evidence that cells expressing and producing the full length AexU showed actin reorganization followed by apoptosis. Earlier, we showed that the ΔaexU null mutant was attenuated in a mouse model, and I now demonstrated that while the parental A. hydrophila strain could be detected in the lung, liver, and spleen of infected mice, the ΔaexU mutant was rapidly cleared from these organs resulting in increased survivability of animals. The GAP activity of AexU was mainly responsible for host cell apoptosis and disruption of actin filaments. Further, AexU prevented phosphorylation of c-Jun, JNK and IκBα and inhibited IL-6 and IL-8 secretion from HeLa cells. Our data indicated that AexU operated by inhibiting NF-κB and inactivating Rho GTPases. Importantly, however, when the ΔaexU null mutant was complemented with the mutated aexU gene devoid of ADPRT and GAP activities, a higher mortality rate in mice with concomitant increase in the production of proinflammatory cytokines/chemokines was noted. These data indicated that either such a mutated AexU is a potent inducer of them or that AexU possesses yet another unknown activity that is modulated by ADPRT and GAP activities and results in this aberrant cytokine/chemokine production responsible for increased animal death.

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

Mode of access: World Wide Web

ISBN: 9781124270500Subjects--Topical Terms:

591510
Microbiology.
Subjects--Index Terms:

ADP-ribosyltransferaseIndex Terms--Genre/Form:

554714
Electronic books.

Mechanism of action of AexU, a new type III secretion system effector from an emerging human pathogen Aeromonas hydrophila.
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520 $a Our laboratory first reported the complete sequence of the type III secretion system (T3SS) from a diarrheal isolate SSU of A. hydrophila. We identified an effector protein (designated as AexU) of the T3SS, which exhibited ADP-ribosyltransferase (ADPRT) and GTPase-activating protein (GAP) activity. AexU was successfully expressed in the HeLa cell Tet-Off system and I provided evidence that cells expressing and producing the full length AexU showed actin reorganization followed by apoptosis. Earlier, we showed that the ΔaexU null mutant was attenuated in a mouse model, and I now demonstrated that while the parental A. hydrophila strain could be detected in the lung, liver, and spleen of infected mice, the ΔaexU mutant was rapidly cleared from these organs resulting in increased survivability of animals. The GAP activity of AexU was mainly responsible for host cell apoptosis and disruption of actin filaments. Further, AexU prevented phosphorylation of c-Jun, JNK and IκBα and inhibited IL-6 and IL-8 secretion from HeLa cells. Our data indicated that AexU operated by inhibiting NF-κB and inactivating Rho GTPases. Importantly, however, when the ΔaexU null mutant was complemented with the mutated aexU gene devoid of ADPRT and GAP activities, a higher mortality rate in mice with concomitant increase in the production of proinflammatory cytokines/chemokines was noted. These data indicated that either such a mutated AexU is a potent inducer of them or that AexU possesses yet another unknown activity that is modulated by ADPRT and GAP activities and results in this aberrant cytokine/chemokine production responsible for increased animal death.
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