Ann-Sophie Alm

Publications (3)5.26 Total impact

• Article: Varying susceptibility of pulmonary cytokine production to lipopolysaccharide in mice.

  Ann-Sophie Alm, Ka Li, Dong Yang, Roland Andersson, You Lu, Xiangdong Wang
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  ABSTRACT: The lipopolysaccharide (LPS)-induced acute lung injury (ALI) model has been widely applied for pathophysiological and pharmacological research. The aim of present study is to understand the variation of acute pulmonary inflammation between mouse strains. The present study investigated the susceptibility of acute production of inflammatory mediators, e.g. cytokines, chemokines and others, to LPS in C57BL/6J, Balb/cJ, DBA/1J, CD-1, NMRI, DBA/2J, A/J, and C3H/HeN mice. The susceptibility to intra-tracheal challenge with LPS varied between measured variables, durations and strains. General lung hyper-reactive susceptibility to LPS-induced pulmonary production of 6-8 inflammatory mediators followed the order NMRI, Balb/cJ, C3H/HeN, A/J, C57BL/6J, DBA/1J, DBA/2J and CD-1 mice at 4h, and A/J, C3H/HeN, CD-1, NMRI, C57BL/6J, Balb/cJ, DBA/2J and DBA/1J mice at 24h. Our data provide information for scientists to consider the proper strain of mice for the measurement of specific inflammatory mediators and to select sensitive or resistant mouse strains for understanding genetic variation in the pathogenesis and for the screening of target-oriented drug development.
  Cytokine 03/2010; 49(3):256-63. · 3.02 Impact Factor
• Article: Variation of lipopolysaccharide-induced acute lung injury in eight strains of mice.

  Ann-Sophie Alm, Ka Li, Hong Chen, Diane Wang, Roland Andersson, Xiangdong Wang
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  ABSTRACT: Clinical and experimental evidence suggests that genetic variations may play an important role in the development of acute lung injury (ALI). Lipopolysaccharide (LPS)-induced ALI models has been widely applied for pathophysiological and pharmacological research. In order to understand the variation of acute pulmonary reactions between mouse strains and find the optimal strain for target-oriented study, the present study investigated the alterations of acute lung hyperinflation, inflammation and injury in C57BL/6J, Balb/cJ, DBA/1J, CD-1, NMRI, DBA/2J, A/J and C3H/HeN mice after the intra-tracheal challenge with LPS. We found that LPS-induced ALI varied between measured variables, durations and strains. General score of LPS-induced acute lung hyperinflation, inflammation and edema followed the order CD-1, A/J, Balb/c, DBA/2J, C57BL/6J, DBA/1J, NMRI, C3H/HeN mice at 4h, and CD-1, C57BL/6J, Balb/c, C3H/HeN, NMRI, A/J, DBA/2J, DBA/1 mice at 24h. Thus, these data provide useful information to select sensitive or resistant strain mouse for understanding genetic variation of pathogenesis and screening of target-oriented drugs.
  Respiratory Physiology & Neurobiology 02/2010; 171(2):157-64. · 2.24 Impact Factor
• Article: Significance of lung hyperinflation in chronic obstructive pulmonary disease

  Ann-Sophie Alm, Annika Ingvarsson, Xiangdong Wang
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  ABSTRACT: Lung hyperinflation is a critical characteristic of pathophysiological changes in chronic obstructive pulmonary disease (COPD), and is associated with the severity and prognosis of the disease. In an attempt to understand the importance of lung hyperinflation in the pathogenesis of chronic lung disease, we will discuss in this review the understanding of the disease, measurements of lung hyperinflation in COPD, clinical findings of lung hyperinflation in emphysema, potential mechanisms of lung hyperinflation, its potential reversibility and comparison of lung hyperinflation between asthma and COPD. Multiple factors may contribute to the development of lung hyperinflation, including compromised alveolar walls, increased intra-airway pressure, inflammation, goblet cell hyperplasia and metaplasia and tissue remodeling. The development of new technology to measure lung hyperinflation will be helpful in the diagnosis and monitoring of the disease. Improvement in lung hyperinflation should become one of the most important criteria to evaluate the therapeutic effects of drugs.
  07/2009; 3(1):44-54.