Dataset Information

Activation of the transforming growth factor beta pathway in bacterial otitis media.

ABSTRACT:

Objectives

Granulation tissue is common in otitis media (OM), yet little is known about the signaling pathways in the formation of granulation tissue in response to infections. In this study, we sought to investigate the activation of the transforming growth factor beta (TGF-beta) signaling pathway in the formation of granulation tissue in response to middle ear pathogens.

Methods

Rat OM models were made by inoculating pneumococcus type 6A or nontypeable Haemophilus influenzae into the middle ear cavity or by obstructing the eustachian tube. Various pathway activities in the middle ear mucosa were analyzed with microarrays.

Results

The TGF-beta signaling pathway was highly regulated in the middle ear cleft with bacterial OM, but not in the ears with eustachian tube obstruction. In ears with bacterial OM, the TGF-beta signaling pathway products were higher in Haemophilus-infected ears than in pneumococcus-infected ears.

Conclusions

Bacterial OM triggers granulation tissue to thrive in the middle ear cleft of rats. Nontypeable H influenzae is more potent than pneumococcus type 6A in the formation of granulation tissue. Eustachian tube obstruction alone did not contribute to granulation tissue formation in the middle ear.

SUBMITTER: Lee YW

PROVIDER: S-EPMC3081620 | biostudies-literature | 2011 Mar

REPOSITORIES: biostudies-literature

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Publications

Activation of the transforming growth factor beta pathway in bacterial otitis media.

Lee Yun-Woo YW Chung Yunju Y Juhn Steven K SK Kim Youngki Y Lin Jizhen J

The Annals of otology, rhinology, and laryngology 20110301 3

<h4>Objectives</h4>Granulation tissue is common in otitis media (OM), yet little is known about the signaling pathways in the formation of granulation tissue in response to infections. In this study, we sought to investigate the activation of the transforming growth factor beta (TGF-beta) signaling pathway in the formation of granulation tissue in response to middle ear pathogens.<h4>Methods</h4>Rat OM models were made by inoculating pneumococcus type 6A or nontypeable Haemophilus influenzae int ...[more]

PMID: 21510147

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Project description:Background and purposeHypertension is the major risk factor for stroke. Recent work unveiled that hypertension is associated with chronic neuroinflammation; microglia are the major players in neuroinflammation, and the activated microglia elevate sympathetic nerve activity and blood pressure. This study is to understand how brain homeostasis is kept from hypertensive disturbance and microglial activation at the onset of hypertension.MethodsHypertension was induced by subcutaneous delivery of angiotensin II, and blood pressure was monitored in conscious animals. Microglial activity was analyzed by flow cytometry and immunohistochemistry. Antibody, pharmacological chemical, and recombinant cytokine were administered to the brain through intracerebroventricular infusion. Microglial depletion was performed by intracerebroventricular delivering diphtheria toxin to CD11b-diphtheria toxin receptor mice. Gene expression profile in sympathetic controlling nucleus was analyzed by customized qRT-PCR array.ResultsTransforming growth factor-β (TGF-β) is constitutively expressed in the brains of normotensive mice. Removal of TGF-β or blocking its signaling before hypertension induction accelerated hypertension progression, whereas supplementation of TGF-β1 substantially suppressed neuroinflammation, kidney norepinephrine level, and blood pressure. By means of microglial depletion and adoptive transfer, we showed that the effects of TGF-β on hypertension are mediated through microglia. In contrast to the activated microglia in established hypertension, the resting microglia are immunosuppressive and important in maintaining neural homeostasis at the onset of hypertension. Further, we profiled the signature molecules of neuroinflammation and neuroplasticity associated with hypertension and TGF-β by qRT-PCR array.ConclusionsOur results identify that TGF-β-modulated microglia are critical to keeping brain homeostasis responding to hypertensive disturbance.

Dataset Information

Activation of the transforming growth factor beta pathway in bacterial otitis media.

Objectives

Methods

Results

Conclusions

Publications

Activation of the transforming growth factor beta pathway in bacterial otitis media.

Similar Datasets

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