Tokyo Medical and Dental University (TMDU) researchers have shown in mice that immune cells called basophils act to trigger a cascade of immune responses leading to airway degeneration resembling that in human chronic obstructive pulmonary disorder.
The airways and lungs are affected by a range of diseases, but while some have been well characterized and treated,others such as chronic obstructive pulmonary disorder (COPD) involve a variety of progressively deteriorating symptoms such as inflammation of the lungs and narrowing of the airways, but the causes of these at the cellular and molecular levels have largely remained obscure.
Picture Courtesy: Scienmage
Department of Immune Regulation,TMDU
Usage of Mouse Models :
Tokyo Medical and Dental University (TMDU) have used a variety of mouse models to explain the developmental process behind COPD.
The team showed that the immune cells basophils, previously believed to be mainly involved in fighting parasitic infections and inducing allergic responses, also induce the destruction of alveolar walls (emphysema).
Initially, mice were exposed to smoke, given the association between smoking and COPD, but this failed to mirror the progressiveness of the disease in humans even after they quit smoking. This was superseded by the approach of administering enzymes called proteases directly into the airway. Proteases break up proteins, producing more human COPD-like features.
The team started by revealing that the lung tissue destruction was caused by a molecule called MMP-12, which they found was released in excess from immune cells called interstitial macrophages when elastase was administered. They then found that these interstitial macrophages arose when the precursor immune cells called monocytes were induced by an immunity-regulating molecule called interleukin-4. Looking backward another step in this chain, the team showed that this interleukin-4 was released by the immune cells basophils.
Summary
Basophil-derived IL-4/monocyte-derived IM/MMP-12 axis plays a crucial role in emphysema formation
Lung Tissue destruction <--- MMP-12 <------ Macropages <------ Monocytes <------ Interleukin-4 <------ basophils
The airways and lungs are affected by a range of diseases, but while some have been well characterized and treated,others such as chronic obstructive pulmonary disorder (COPD) involve a variety of progressively deteriorating symptoms such as inflammation of the lungs and narrowing of the airways, but the causes of these at the cellular and molecular levels have largely remained obscure.
Picture Courtesy: Scienmage
Department of Immune Regulation,TMDU
Usage of Mouse Models :
Tokyo Medical and Dental University (TMDU) have used a variety of mouse models to explain the developmental process behind COPD.
The team showed that the immune cells basophils, previously believed to be mainly involved in fighting parasitic infections and inducing allergic responses, also induce the destruction of alveolar walls (emphysema).
Initially, mice were exposed to smoke, given the association between smoking and COPD, but this failed to mirror the progressiveness of the disease in humans even after they quit smoking. This was superseded by the approach of administering enzymes called proteases directly into the airway. Proteases break up proteins, producing more human COPD-like features.
The team started by revealing that the lung tissue destruction was caused by a molecule called MMP-12, which they found was released in excess from immune cells called interstitial macrophages when elastase was administered. They then found that these interstitial macrophages arose when the precursor immune cells called monocytes were induced by an immunity-regulating molecule called interleukin-4. Looking backward another step in this chain, the team showed that this interleukin-4 was released by the immune cells basophils.
Summary
Basophil-derived IL-4/monocyte-derived IM/MMP-12 axis plays a crucial role in emphysema formation
Lung Tissue destruction <--- MMP-12 <------ Macropages <------ Monocytes <------ Interleukin-4 <------ basophils
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