Airway epithelium expresses interleukin-18

Cameron, Lisa; Taha, Rame; Tsicopoulos, Anne; Kurimoto, Masashi; Olivenstein, Ron; Wallaert, B.; Minshall, Eleanor; Hamid, Qutayba

doi:10.1034/j.1399-3003.1999.14c12.x

Cited by 123 publications

(88 citation statements)

References 30 publications

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“…IL-18 mRNA and IL-18 protein, mainly consisting of pro-IL-18, were found to be constitutively expressed within the lung. This is in agreement with earlier studies, which showed that IL-18 mRNA is expressed in lungs and other organs of normal mice (21,28,(32)(33)(34). Alveolar macrophages, the resident phagocytes within the airways, are likely important producers of IL-18 within the lung, because IL-18 is known to be mainly produced by activated macrophages (19).…”

Section: Discussionsupporting

confidence: 81%

“…Alveolar macrophages, the resident phagocytes within the airways, are likely important producers of IL-18 within the lung, because IL-18 is known to be mainly produced by activated macrophages (19). Cameron et al (32) reported that the majority of IL-18 mRNA within lung tissue of mice was localized to airway epithelium cells, although inflammatory cells, mostly lymphocytes, within the airway wall and parenchyma also expressed IL-18 mRNA. In addition, IL-18 mRNA expression was also found in granulocytes present in the lungs of LPS-treated mice.…”

Section: Discussionmentioning

confidence: 99%

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IL-18 Improves the Early Antimicrobial Host Response to Pneumococcal Pneumonia

Lauw

Branger

Florquin

et al. 2002

The Journal of Immunology

100

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To determine the role of endogenous IL-18 during pneumonia, IL-18 gene-deficient (IL-18−/−) mice and wild-type (WT) mice were intranasally inoculated with Streptococcus pneumoniae, the most common causative agent of community-acquired pneumonia. Infection with S. pneumoniae increased the expression of IL-18 mRNA and was associated with elevated concentrations of both precursor and mature IL-18 protein within the lungs. IL-18−/− mice had significantly more bacteria in their lungs and were more susceptible for progressing to systemic infection at 24 and 48 h postinoculation. Similarly, treatment of WT mice with anti-IL-18 was associated with enhanced outgrowth of pneumococci. In contrast, the clearance of pneumococci from lungs of IL-12−/− mice was unaltered when compared with WT mice. Furthermore, anti-IL-12 did not influence bacterial clearance in either IL-18−/− or WT mice. These data suggest that endogenous IL-18, but not IL-12, plays an important role in the early antibacterial host response during pneumococcal pneumonia.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

IL-18 Improves the Early Antimicrobial Host Response to Pneumococcal Pneumonia

Lauw

Branger

Florquin

et al. 2002

The Journal of Immunology

100

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“…We could not exactly verify that macrophages produce IL-12 in the serial sections of the frozen lungs because of weak IL-12 staining, but the distribution of IL-12 staining and macrophages closely overlapped beneath the bronchiolar smooth muscle coat suggesting that macrophages activated by influenza virus antigens produced mainly IL-12. While IL-18, TNF-α, and IFN-α, -β are produced not only by macrophages but also by non-immune cells such as epithelial cells, IL-12 is mainly produced by macrophages, monocytes, and dendric cells (D'Andrea et al, 1992;Cameron et al, 1999;Locksley et al, 2001;Pirhonen et al, 2001;Kashiwamura et al, 2002;Pirhonen et al, 2002;. Thus, the macrophage may be a key immune cell to induce early defense-immunity against influenza infection and IL-12 is dominantly produced in macrophages activated by influenza virus antigens.…”

Section: Discussionmentioning

confidence: 99%

Interleukin 12 is a primary cytokine responding to influenza virus infection in the respiratory tract of mice

Hama

Kurokawa²,

Imakita³

et al. 2009

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. Abbreviations: BALF = bronchoalveolar lavage fluid; IFN = interferon; IL = interleukin; i.n. = intranasal; MAb(s) = monoclonal antibody(ies); p.i. = post infection; TNF = tumor necrosis factor Interleukin 12 is a primary cytokine responding to influenza virus infection in the respiratory tract of mice Summary. -We have reported previously that an increase in interleukin 12 (IL-12) production in the lungs of mice infected with Influenza A virus or an intranasal (i.n.) administration of IL-12 to the infected mice alleviated pneumonia (Tsurita et al., J. Pharmacol. Exp. Therapeut. 298, 362-368, 2001). In this study, we found that in the bronchoalveolar lavage fluids (BALF) obtained from mice infected i.n. with Influenza A virus IL-12 was elevated on day 1 post infection (p.i.) and was followed by tumor necrosis factor α (TNF-α), IL-18, and interferons α, β, and γ (IFN-α, -β, and -γ) on day 2 p.i. Histochemical analyses of the infected lungs on day 1 p.i. showed the presence of IL-12 and IL-12 mRNA in mononuclear and macrophage-like cells and colocalization of macrophages with viral antigen, while other cytokines were absent. Thus, IL-12 was produced by macrophages infiltrating the infected epithelium as the first response cytokine and its production at the site of infection may direct an early immune defense to alleviate the severity of infection.

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“…Recent studies have demonstrated enhanced expression of IL-12 (20 -22) and IL-12R (23,24) in sarcoid lungs. IL-18 expression was reported to be increased in the airway epithelial cells of sarcoid cases (25). However, the cooperative roles of IL-12 and IL-18 in sarcoidosis have not been fully resolved in Th1 response.…”

mentioning

confidence: 99%

IL-12 and IL-18 Are Increased and Stimulate IFN-γ Production in Sarcoid Lungs

Shigehara

Shijubo²,

Ohmichi

et al. 2001

The Journal of Immunology

168

101

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Sarcoidosis is a systemic chronic granulomatous disease of unknown cause. Recent investigations revealed that the cytokine profile in inflamed lesions of sarcoidosis is Th1 dominant. To obtain better immunopathologic understanding of sarcoidosis, we examined the expression of IL-12 and IL-18 and their roles in IFN-γ production in pulmonary sarcoidosis. Sarcoid cases had significantly elevated levels of IL-12 (p40 and p70) and IL-18 in bronchoalveolar lavage (BAL) fluids compared with healthy subjects. IL-12 p70 and IL-18 were immunohistochemically expressed in the epithelioid cells and giant cells of sarcoid granulomas. Significant induction of IFN-γ, IL-12 p70, and IL-18 was observed from sarcoid BAL fluid cells with LPS stimulation, whereas LPS tended to induce only IL-12 p70 in BAL fluid cells from healthy subjects. Sarcoid cases had significantly greater IFN-γ induction with LPS stimulation than healthy subjects did. IL-18 mRNA expression was observed in freshly isolated sarcoid BAL fluid cells as well as in LPS-stimulated sarcoid BAL fluid cells, but IFN-γ and IL-12 mRNA expression was observed only in LPS-stimulated BAL fluid cells. Treatment with anti-IL-12- and anti-IL-18-neutralizing Abs significantly inhibited IFN-γ production from LPS-stimulated BAL fluid cells of sarcoid cases. Coadministration of rIL-12 or rIL-18 induced greater IFN-γ production in sarcoid BAL fluid cells than in normal BAL fluid cells. We concluded that bioactive IL-12 and IL-18 were produced in sarcoid BAL fluid cells and synergistically induced IFN-γ production, indicating important cytokines in the Th1 response of sarcoidosis.

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Airway epithelium expresses interleukin-18

Cited by 123 publications

References 30 publications

IL-18 Improves the Early Antimicrobial Host Response to Pneumococcal Pneumonia

IL-18 Improves the Early Antimicrobial Host Response to Pneumococcal Pneumonia

Interleukin 12 is a primary cytokine responding to influenza virus infection in the respiratory tract of mice

IL-12 and IL-18 Are Increased and Stimulate IFN-γ Production in Sarcoid Lungs

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