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Altered Th1/Th2 commitment contributes to lung senescence in CXCR3-deficient mice
Junmin Huang1, Zongli Li, Xiujuan Yao
1Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders, PR China.
Experimental Gerontology
|April 16, 2013
Summary
Aging impacts lung function, with immune imbalance accelerating decline. CXCR3-deficient mice show Th2 polarization, leading to accelerated lung aging and altered physiological parameters.
Area of Science:
- Immunology
- Gerontology
- Pulmonology
Background:
- Aging is linked to immune system decline (immunosenescence) and reduced organ function, particularly in the lungs.
- The specific impact of T helper cell (Th1/Th2) balance shifts on lung aging remains unclear.
Purpose of the Study:
- To investigate how altered Th1/Th2 immune cell balance affects lung aging.
- To analyze physiological and pathological changes in the lungs of aging CXCR3-deficient mice compared to wild-type controls.
Main Methods:
- Compared 2- and 20-month-old CXCR3-deficient (CXCR3(-/-)) and wild-type (WT) C57BL/6J mice.
- Measured Th1/Th2 cell proportions, cytokine/chemokine expression, collagen levels, lung function (airway resistance, elastance, damping), and lung structure (volume, alveolar size).
Main Results:
- 20-month-old CXCR3(-/-) mice exhibited weight loss, reduced airway resistance, elastance, and damping compared to aged WT mice.
- CXCR3(-/-) mice showed increased lung volume, alveolar size, and collagen content with aging.
- Aging WT mice displayed a Th1-dominant immune profile, while CXCR3(-/-) mice showed Th2 polarization (decreased Th1, increased IL-4).
Conclusions:
- Immunosenescence is associated with lung aging.
- An altered Th1/Th2 balance, favoring Th2 predominance in CXCR3(-/-) mice, contributes to accelerated lung aging in this model.
Keywords:
B6BALFC57BL/6J inbred mouse strainCCRCXCLCXCRCXCR3C–C chemokine receptorD2DBA/2J inbred mouse strainELISAEnzyme-linked immunosorbent assayFEV(1)FRCFVCGHH & EI(a)I-TACIFNIFN-inducible T cell α chemoattractantIFN-γ-induced protein 10-kDaILIP-10ImmunosenescenceKOL(m)Lung agingLung mechanicsMIGP(airspaces)PEEPRnSaTh1/Th2 imbalanceV(L)WTairway resistancebronchoalveolar lavage fluidchemokine (C–X–C motif) ligandchemokine (C–X–C motif) receptordforced expiratory volume in one secondforced vital capacityfunctional residual capacityhematoxylin and eosin staininterferoninterleukinintersections of a test line system with interalveolar septal surfaceknockoutmean linear intercept length of alveolarmomonokine induced by IFN-γmonths oldpoints hitting airspaces in parenchymal volumepositive end-expiratory pressuressurface area of the alveolartissue dampingtissue elastanceunit lengthwhole lung volumewild-type
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