Lindsay Lohan rushed to hospital with lung infection: Actress’ father says … – New York Daily News


New York Daily News

Lindsay Lohan rushed to hospital with lung infection: Actress' father says
New York Daily News
“She's fine, but she had a bad case of asthma as a kid, so she has to take these things seriously,” Michael Lohan told the Daily News. “When she was a kid, we almost lost her a couple of times because of the asthma.” He said the lung infection has been

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Recurring viral infection triggers asthma attack – Deccan Herald


gulfnews.com

Recurring viral infection triggers asthma attack
Deccan Herald
In a new finding, a husband-wife researcher duo of Indian origin claimed that repeated attacks by common virus known as respiratory syncytial virus (RSV), could cripple a portion of a child's own immune system triggering asthma attacks in adulthood.
Viral infections may cause asthmagulfnews.com

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Chlamydia muridarum Lung Infection in Infants Alters Hematopoietic Cells to Promote Allergic Airway Disease in Mice.

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Chlamydia muridarum Lung Infection in Infants Alters Hematopoietic Cells to Promote Allergic Airway Disease in Mice.

PLoS One. 2012;7(8):e42588

Authors: Starkey MR, Kim RY, Beckett EL, Schilter HC, Shim D, Essilfie AT, Nguyen DH, Beagley KW, Mattes J, Mackay CR, Horvat JC, Hansbro PM

Abstract
BACKGROUND: Viral and bacterial respiratory tract infections in early-life are linked to the development of allergic airway inflammation and asthma. However, the mechanisms involved are not well understood. We have previously shown that neonatal and infant, but not adult, chlamydial lung infections in mice permanently alter inflammatory phenotype and physiology to increase the severity of allergic airway disease by increasing lung interleukin (IL)-13 expression, mucus hyper-secretion and airway hyper-responsiveness. This occurred through different mechanisms with infection at different ages. Neonatal infection suppressed inflammatory responses but enhanced systemic dendritic cell:T-cell IL-13 release and induced permanent alterations in lung structure (i.e., increased the size of alveoli). Infant infection enhanced inflammatory responses but had no effect on lung structure. Here we investigated the role of hematopoietic cells in these processes using bone marrow chimera studies.
METHODOLOGY/PRINCIPAL FINDINGS: Neonatal (<24-hours-old), infant (3-weeks-old) and adult (6-weeks-old) mice were infected with C. muridarum. Nine weeks after infection bone marrow was collected and transferred into recipient age-matched irradiated naïve mice. Allergic airway disease was induced (8 weeks after adoptive transfer) by sensitization and challenge with ovalbumin. Reconstitution of irradiated naïve mice with bone marrow from mice infected as neonates resulted in the suppression of the hallmark features of allergic airway disease including mucus hyper-secretion and airway hyper-responsiveness, which was associated with decreased IL-13 levels in the lung. In stark contrast, reconstitution with bone marrow from mice infected as infants increased the severity of allergic airway disease by increasing T helper type-2 cell cytokine release (IL-5 and IL-13), mucus hyper-secretion, airway hyper-responsiveness and IL-13 levels in the lung. Reconstitution with bone marrow from infected adult mice had no effects.
CONCLUSIONS: These results suggest that an infant chlamydial lung infection results in long lasting alterations in hematopoietic cells that increases the severity of allergic airway disease in later-life.

PMID: 22870337 [PubMed – in process]

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TLR2, but Not TLR4, Is Required for Effective Host Defence against Chlamydia Respiratory Tract Infection in Early Life.

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TLR2, but Not TLR4, Is Required for Effective Host Defence against Chlamydia Respiratory Tract Infection in Early Life.

PLoS One. 2012;7(6):e39460

Authors: Beckett EL, Phipps S, Starkey MR, Horvat JC, Beagley KW, Foster PS, Hansbro PM

Abstract
Chlamydia pneumoniae commonly causes respiratory tract infections in children, and epidemiological investigations strongly link infection to the pathogenesis of asthma. The immune system in early life is immature and may not respond appropriately to pathogens. Toll-like receptor (TLR)2 and 4 are regarded as the primary pattern recognition receptors that sense bacteria, however their contribution to innate and adaptive immunity in early life remains poorly defined. We investigated the role of TLR2 and 4 in the induction of immune responses to Chlamydia muridarum respiratory infection, in neonatal wild-type (Wt) or TLR2-deficient ((-/-)), 4(-/-) or 2/4(-/-) BALB/c mice. Wt mice had moderate disease and infection. TLR2(-/-) mice had more severe disease and more intense and prolonged infection compared to other groups. TLR4(-/-) mice were asymptomatic. TLR2/4(-/-) mice had severe early disease and persistent infection, which resolved thereafter consistent with the absence of symptoms in TLR4(-/-) mice. Wt mice mounted robust innate and adaptive responses with an influx of natural killer (NK) cells, neutrophils, myeloid (mDCs) and plasmacytoid (pDCs) dendritic cells, and activated CD4(+) and CD8(+) T-cells into the lungs. Wt mice also had effective production of interferon (IFN)�³ in the lymph nodes and lung, and proliferation of lymph node T-cells. TLR2(-/-) mice had more intense and persistent innate (particularly neutrophil) and adaptive cell responses and IL-17 expression in the lung, however IFN�³ responses and T-cell proliferation were reduced. TLR2/4(-/-) mice had reduced innate and adaptive responses. Most importantly, neutrophil phagocytosis was impaired in the absence of TLR2. Thus, TLR2 expression, particularly on neutrophils, is required for effective control of Chlamydia respiratory infection in early life. Loss of control of infection leads to enhanced but ineffective TLR4-mediated inflammatory responses that prolong disease symptoms. This indicates that TLR2 agonists may be beneficial in the treatment of early life Chlamydia infections and associated diseases.

PMID: 22724018 [PubMed – in process]

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Biota Reports Positive Phase IIb Data For Asthmatic Patients With HRV Infection – NASDAQ

Biota Reports Positive Phase IIb Data For Asthmatic Patients With HRV Infection
NASDAQ
The Phase II multicenter, randomized, double-blind, placebo controlled study in asthmatic adults with symptomatic, naturally acquired human rhinovirus infection was conducted over two consecutive seasons in 48 centers in the US Subjects received either
Biota Announces Positive Phase IIb Data for Asthmatic Patients With Human MarketWatch (press release)

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Familial asthma risk and infant respiratory infection etiology and severity – HealthCanal.com

Familial asthma risk and infant respiratory infection etiology and severity
HealthCanal.com
Both RSV and HRV lower respiratory tract infections (LRTIs) during infancy and early childhood are associated with an increased risk of asthma later in childhood. However, the risk for developing asthma is higher among children who had an HRV LRTI

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Gastric bacterium infection can protect against allergy-induced asthma – TruthDive


MedIndia

Gastric bacterium infection can protect against allergy-induced asthma
TruthDive
Washington, July 02 (ANI): Researchers have indicated that infection with the gastric bacterium Helicobacter pylori provides reliable protection against allergy-induced asthma. The results confirmed the hypothesis recently put forward that the dramatic
Gastric bacterium Helicobacter pylori protects against asthmaEurekAlert (press release)
Gastric bacterium Helicobacter pylori allegedly guards against asthmaHealthJockey.com

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