Tag: Tissue

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Effect of compound Maqin decoction on TGF-?1/Smad proteins and IL-10 and IL-17 content in lung tissue of asthmatic rats.

Effect of compound Maqin decoction on TGF-?1/Smad proteins and IL-10 and IL-17 content in lung tissue of asthmatic rats.

Genet Mol Res. 2016 Sep 2;15(3):

Authors: Xie YH, Li XP, Xu ZX, Qian P, Li XL, Wang YQ

Abstract
In this research, compound Maqin decoction (CMD) has been shown to positively affect in airway inflammation of asthma models. We evaluated the effects of CMD on the expression of transforming growth factor (TGF)-?1/Smad proteins, interleukin (IL)-17, and IL-10 in lung tissue of asthmatic rats. Asthma was induced in a rat model using ovalbumin. After a 4-week treatment with CMD, rats were killed to evaluate the expression of TGF-?1 and Smad proteins in lung tissue. IL-10 and IL-17 levels in lung tissue homogenates were determined by ELISA. The expression of TGF-?1 and Smad3 protein increased, whereas expression of Smad7 protein decreased upon high-dose or low-dose treatment with CMD or by intervention with dexamethasone, compared to the control. There was a significant difference between treatment with a high dose CMD and the control treatment, but no significant difference was found between high-dose CMD treatment and dexamethasone intervention. The expression of TGF-?1 and Smad7 protein increased, whereas the expression of Smad3 protein decreased in the model group compared to other groups. In the CMD high-dose group, low-dose group, and dexamethasone intervention group, the IL-17 concentrations in lung tissue homogenates were decreased, while IL-10 levels were increased. Again, there was a significant difference between CMD high-dose and control treatment, but not between CMD high-dose treatment and dexamethasone intervention. Thus, positive effects of CMD against asthmatic airway remodeling may be due to its regulatory effect on TGF-?1, Smad3, and Smad7 protein levels and on cytokines such as IL-10 and IL-17.

PMID: 27706676 [PubMed – in process]

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Bronchial lesions of mouse model of asthma are preceded by immune complex vasculitis and induced bronchial associated lymphoid tissue (iBALT).

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Bronchial lesions of mouse model of asthma are preceded by immune complex vasculitis and induced bronchial associated lymphoid tissue (iBALT).

Lab Invest. 2015 Jun 1;

Authors: Guest IC, Sell S

Abstract
We systematically examined by immune histology the lungs of some widely used mouse models of asthma. These models include sensitization by multiple intraperitoneal injections of soluble ovalbumin (OVA) or of OVA with alum, followed by three intranasal or aerosol challenges 3 days apart. Within 24?h after a single challenge there is fibrinoid necrosis of arterial walls with deposition of immunoglobulin (Ig) and OVA and infiltration of eosinophilic polymorphonuclear cells that lasts for about 3 days followed by peribronchial B-cell infiltration and slight reversible goblet cell hypertrophy (GCHT). After two challenges, severe eosinophilic vasculitis is present at 6?h, increases by 72?h, and then declines; B-cell proliferation and significant GCHT and hyperplasia (GCHTH) and bronchial smooth muscle hypertrophy recur more prominently. After three challenges, there is significantly increased induced bronchus-associated lymphoid tissue (iBALT) formation, GCHTH, and smooth muscle hypertrophy. Elevated levels of Th2 cytokines, IL-4, IL-5, and IL-13, are present in bronchial lavage fluids. Sensitized mice have precipitating antibody and positive Arthus skin reactions but also develop significant levels of IgE antibody to OVA but only 1 week after challenge. We conclude that the asthma like lung lesions induced in these models is preceded by immune complex-mediated eosinophilic vasculitis and iBALT formation. There are elevations of Th2 cytokines that most likely produce bronchial lesions that resemble human asthma. However, it is unlikely that mast cell-activated atopic mechanisms are responsible as we found only a few presumed mast cells by toluidine blue and metachromatic staining limited to the most proximal part of the main stem bronchus, and none in the remaining main stem bronchus or in the lung periphery.Laboratory Investigation advance online publication, 1 June 2015; doi:10.1038/labinvest.2015.72.

PMID: 26006019 [PubMed – as supplied by publisher]

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Chlamydophila pneumonia inhibits the corticosteroid-induced suppressions of metalloproteinase-9 and tissue inhibitor metalloproteinase-1 secretion by human peripheral blood mononuclear cells.

Chlamydophila pneumonia inhibits the corticosteroid-induced suppressions of metalloproteinase-9 and tissue inhibitor metalloproteinase-1 secretion by human peripheral blood mononuclear cells.

J Med Microbiol. 2012 Jan 26;

Authors: Park CS, Lee YS, Kwon HS, Lee TH, Kim TB, Moon KA, Yoo B, Moon HB, Cho YS

Abstract
Chlamydophila pneumoniae infection has been suggested to be associated with severe asthma characterized by persistent airway limitation, which may be related to airway remodeling. We investigated whether C. pneumoniae infection affected the secretion of metalloproteinase-9 (MMP9) and tissue inhibitor metalloproteinase-1 (TIMP1), and altered the responsiveness of inflammatory cells to corticosteroids. Human peripheral blood mononuclear cells (PBMC) were cultured in vitro in the presence or absence of C. pneumoniae. Secretion of both MMP9 and TIMP1 was strongly suppressed by dexamethasone treatment in uninfected cells. MMP9 secretion was also significantly inhibited by dexamethasone in C. pneumoniae-infected cells, but TIMP1 secretion was not; hence the MMP9 to TIMP1 ratio decreased. Interestingly, expression of human glucocorticoid receptor (GR)?, which is believed to confer resistance to corticosteroids, was enhanced by dexamethasone treatment in C. pneumoniae-infected PBMC. We conclude that C. pneumoniae infection may promote airway remodeling by decreasing the ratio of MMP9 to TIMP1 secreted by inflammatory cells, and by altering cellular responsiveness to corticosteroids.

PMID: 22282461 [PubMed – as supplied by publisher]

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Breakthrough asthma operation burns away lung tissue with radio waves – Daily Mail


Daily Mail

Breakthrough asthma operation burns away lung tissue with radio waves
Daily Mail
By Daily Mail Reporter Millions of asthma sufferers could breathe easier thanks to a breakthrough operation performed on the NHS for the first time. Doctors at Wythenshawe hospital in Manchester performed a technique called bronchial thermoplasty on a …

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Insights gained from growing cold-causing virus on sinus tissue – EurekAlert (press release)

Insights gained from growing cold-causing virus on sinus tissue
EurekAlert (press release)
"We now have evidence that there may be new approaches to treating or preventing HRV-C infections," says senior author James Gern, professor of medicine at the UW-Madison School of Medicine and Public Health and an asthma expert at American Family …

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‘Taste Buds’ In Lung Tissue Could Help Ease Asthma Attacks – RTT News


Daily Mail

'Taste Buds' In Lung Tissue Could Help Ease Asthma Attacks
RTT News
According to lead researcher, Dr. Stephen Ligget, bitter substances worked better at easing asthma-like symptoms than any other medication in their trials. …
Discovery could lead to new asthma treatmentsLos Angeles Times
Lungs Have Bitter Taste Receptors That May Help Treat AsthmaTIME
Taste Receptors On Lungs May Help Fight AsthmaGant Daily
LiveScience.com –Science News –Times of India
all 474 news articles »

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NIH-Funded Researchers Make Progress Toward Regenerating Tissue to Replace Joints

A team of NIH-funded researchers has successfully regenerated rabbit
joints using a cutting edge process to form the joint inside the body,
or in vivo. Regenerative in vivo procedures are performed by stimulating
previously irreparable organs or tissues to heal themselves. In this
study, bioscaffolds, or three-dimensional structures made of biocompatible
and biodegradable materials in the shape of the tissue, were infused
with a protein to promote growth of the rabbit joint.

View full post on National Institutes of Health (NIH) News Releases