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Early-Life Exposure to Clostridium leptum Causes Pulmonary Immunosuppression.

Huang F, Qiao HM, Yin JN, Gao Y, Ju YH, Li YN - PLoS ONE (2015)

Bottom Line: Low Clostridium leptum levels are a risk factor for the development of asthma.Early-life C. leptum exposure induced an immunosuppressive environment in the lung concurrent with increased Treg cells, resulting in the inhibition of Th1, Th2, Th9, and Th17 cell responses.These findings demonstrate a mechanism whereby C. leptum exposure modulates adaptive immunity and leads to failure to develop asthma upon OVA sensitization later in life.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopedics, China-Japan Union Hospital of Jilin University, Changchun, Jilin, PR China.

ABSTRACT

Introduction: Low Clostridium leptum levels are a risk factor for the development of asthma. C. leptum deficiency exacerbates asthma; however, the impact of early-life C. leptum exposure on cesarean-delivered mice remains unclear. This study is to determine the effects of early-life C. leptum exposure on asthma development in infant mice.

Methods: We exposed infant mice to C. leptum (fed-CL) and then induced asthma using the allergen ovalbumin (OVA).

Results: Fed-CL increased regulatory T (Treg) cells in cesarean-delivered mice compared with vaginally delivered mice. Compared with OVA-exposed mice, mice exposed to C. leptum + OVA did not develop the typical asthma phenotype, which includes airway hyper-responsiveness, cell infiltration, and T helper cell subset (Th1, Th2, Th9, Th17) inflammation. Early-life C. leptum exposure induced an immunosuppressive environment in the lung concurrent with increased Treg cells, resulting in the inhibition of Th1, Th2, Th9, and Th17 cell responses.

Conclusion: These findings demonstrate a mechanism whereby C. leptum exposure modulates adaptive immunity and leads to failure to develop asthma upon OVA sensitization later in life.

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Related in: MedlinePlus

Schematic of a mouse model of early-life C. leptum ± OVA asthma.All analyses were carried out 48 h after the final protocol day. HE, hematoxylin–eosin; AL(OH)3, aluminum hydroxide.
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pone.0141717.g002: Schematic of a mouse model of early-life C. leptum ± OVA asthma.All analyses were carried out 48 h after the final protocol day. HE, hematoxylin–eosin; AL(OH)3, aluminum hydroxide.

Mentions: Eight-day-old CD pups were fed with C. leptum as described above before we established an OVA model of asthma. The asthma model was established when the mice were 52 days old, and lung tissue samples were collected when the mice were 54 days old (Fig 2).


Early-Life Exposure to Clostridium leptum Causes Pulmonary Immunosuppression.

Huang F, Qiao HM, Yin JN, Gao Y, Ju YH, Li YN - PLoS ONE (2015)

Schematic of a mouse model of early-life C. leptum ± OVA asthma.All analyses were carried out 48 h after the final protocol day. HE, hematoxylin–eosin; AL(OH)3, aluminum hydroxide.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4643994&req=5

pone.0141717.g002: Schematic of a mouse model of early-life C. leptum ± OVA asthma.All analyses were carried out 48 h after the final protocol day. HE, hematoxylin–eosin; AL(OH)3, aluminum hydroxide.
Mentions: Eight-day-old CD pups were fed with C. leptum as described above before we established an OVA model of asthma. The asthma model was established when the mice were 52 days old, and lung tissue samples were collected when the mice were 54 days old (Fig 2).

Bottom Line: Low Clostridium leptum levels are a risk factor for the development of asthma.Early-life C. leptum exposure induced an immunosuppressive environment in the lung concurrent with increased Treg cells, resulting in the inhibition of Th1, Th2, Th9, and Th17 cell responses.These findings demonstrate a mechanism whereby C. leptum exposure modulates adaptive immunity and leads to failure to develop asthma upon OVA sensitization later in life.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopedics, China-Japan Union Hospital of Jilin University, Changchun, Jilin, PR China.

ABSTRACT

Introduction: Low Clostridium leptum levels are a risk factor for the development of asthma. C. leptum deficiency exacerbates asthma; however, the impact of early-life C. leptum exposure on cesarean-delivered mice remains unclear. This study is to determine the effects of early-life C. leptum exposure on asthma development in infant mice.

Methods: We exposed infant mice to C. leptum (fed-CL) and then induced asthma using the allergen ovalbumin (OVA).

Results: Fed-CL increased regulatory T (Treg) cells in cesarean-delivered mice compared with vaginally delivered mice. Compared with OVA-exposed mice, mice exposed to C. leptum + OVA did not develop the typical asthma phenotype, which includes airway hyper-responsiveness, cell infiltration, and T helper cell subset (Th1, Th2, Th9, Th17) inflammation. Early-life C. leptum exposure induced an immunosuppressive environment in the lung concurrent with increased Treg cells, resulting in the inhibition of Th1, Th2, Th9, and Th17 cell responses.

Conclusion: These findings demonstrate a mechanism whereby C. leptum exposure modulates adaptive immunity and leads to failure to develop asthma upon OVA sensitization later in life.

Show MeSH
Related in: MedlinePlus