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Role of T cells in LPS‐induced lung inflammation and dysfunction (695.5)
Author(s) -
Kvietys Peter,
Nader Moni
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.695.5
Subject(s) - ards , immunology , inflammation , pathogenesis , lung , medicine , t cell , systemic inflammation , pulmonary edema , hypoxemia , population , immune system , pathology , environmental health
Common pathophysiologic features of ALI/ARDS are pulmonary leukocyte infiltration, interstitial edema, and impaired gas exchange. A major component of the alveolar infiltrate is polymorphonuclear leukocytes (PMN), which are believed to be the innate immune cells responsible for the pulmonary dysfunction. In a murine LPS (i.t.) model, our experiments indicated that, at 24 hrs after LPS challenge, PMN were present in the pulmonary alveoli and there was evidence of pulmonary dysfunction, i.e., increased vascular protein leak (Evans blue) and systemic hypoxia (arterial pO2). Interestingly, the infiltrated leukocytes were not all PMN; approximately half of the leukocyte population consisted of T cells (immunohistochemistry targeting CD3+ cells). In order to determine whether CD4+ T cells were involved in the pulmonary dysfunction in our LPS model, a genetic blockade approach was used (mice deficient in CD4+ T cells). The results of these experiments indicated that the increase in vascular protein leak induced by LPS in wild type (WT) mice was completely prevented when CD4+ T cell deficient (CD4‐) mice were used. The LPS‐induced systemic hypoxemia was also substantially blunted in the CD4+ T cell deficient mice. These observations provide strong support for the hypothesis that CD4+ T cells play an important role in the pathogenesis of ALI/ARDS. Grant Funding Source : KACST‐ MED1672‐44