Infectious etiologies in acute exacerbation of COPD

Lieberman, David; Lieberman, Devora; Ben‐Yaakov, Miriam; Lazarovich, Zilia; Hoffman, S. M. J.; Ohana, Bella; Friedman, Maureen G.; Dvoskin, Bella; Leinonen, Maija; Boldur, I

doi:10.1016/s0732-8893(01)00255-3

Cited by 89 publications

(62 citation statements)

References 21 publications

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“…Mycoplasma pneumoniae (Mp), one of the human mycoplasma species, resides extracellularly in the respiratory tract mucosa, and represents one of the most common causes of communityacquired pneumonia [2]. Several studies have shown that Mp infection induces the release of proinflammatory cytokines relevant to exacerbation of chronic pulmonary diseases such as asthma and COPD [3][4]. Previous studies have demonstrated that respiratory Mp infection is characterized by lung neutrophilic inflammation along with lung lymphocyte (e.g., CD4+ T cells) infiltrate [5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

IL-23-dependent IL-17 production is essential in neutrophil recruitment and activity in mouse lung defense against respiratory Mycoplasma pneumoniae infection

Martin

Rino

et al. 2007

Microbes and Infection

250

185

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IL-23 induces IL-17 production in activated CD4+ T cells and participates in host defense against many encapsulated bacteria. However, whether IL-23/IL-17 axis contributes to a Mycoplasma pneumoniae (Mp)-induced lung inflammation (e.g., neutrophils) has not been addressed. Using an acute respiratory Mp infection murine model, we found significantly up-regulated lung IL-23p19 mRNA in the early phase of infection (4 h), and alveolar macrophages were an important cell source of Mp-induced IL-23. We further showed that Mp significantly increased IL-17 protein levels in bronchoalveolar lavage (BAL). Lung gene expression of IL-17, IL-17C and IL-17F was also markedly up-regulated by Mp in vivo. IL-17 and IL-17F were found to be derived mainly from lung CD4+ T cells, and were increased upon IL-23 stimulation in vitro. In vivo blocking of IL-23p19 alone or in combination with IL-23/IL-12p40 resulted in a significant reduction of Mp-induced IL-17 protein and IL-17/IL-17F mRNA expression, which was accompanied by a trend toward reduced lung neutrophil recruitment, BAL neutrophil activity, and Mp clearance. However, IL-23 neutralization had no effect on Mp-induced lung IL-17C mRNA expression. These results demonstrate that IL-17/IL-17F production is IL-23-dependent in an acute Mp infection, and contributes to neutrophil recruitment and activity in lung defense against the infection.

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Section: Introductionmentioning

confidence: 99%

IL-23-dependent IL-17 production is essential in neutrophil recruitment and activity in mouse lung defense against respiratory Mycoplasma pneumoniae infection

Martin

Rino

et al. 2007

Microbes and Infection

250

185

View full text Add to dashboard Cite

show abstract

“…Since late 1970's, several authors suggested a relationship between COPD and M. pneumoniae infection [Buscho et al, 1978;Gump et al, 1976;Smith et al, 1980], but it was until late 1990's and early 2000's that several studies based on serology brought attention once more on this issue. [Lieberman et al, 2001[Lieberman et al, , 2002Mogulkoc et al, 1999]. It is well known that mycoplasmas species pathogenic for humans have the ability to induce chronic disease states in which clearance of the bacteria is extremely difficult.…”

Section: Role In Copd and Asthmamentioning

confidence: 99%