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Role of interleukin-10 in idiopathic pulmonary fibrosis

¹ , Nikis 33, Syntagma, Athens and ² Medical school, University of Thessaly, Larissa, Greece

To the Editors:

We have read with great interest the article of Bergeron et al. 1, concerning the cytokine profile in tissues of patients with idiopathic pulmonary fibrosis (IPF). We strongly agree that finding out the roles of cytokines in IPF might be the key in understanding the pathogenesis of the disease, as well as inventing new therapy strategies for this foetal and unresolved disorder. We think that outlining the cytokine profile in the tissues of those patients is very important, even though, as the authors also mention, the number of patients included in their study (five) was unfortunately small.

We conducted a study in the University Hospital in Thessaly (central Greece), involving 20 patients with IPF and 11 patients with pulmonary fibrosis of a known cause, as well as 40 healthy volunteers, in whom we measured the serum levels of several cytokines, such as interleukin (IL)-2, IL-4, IL-8, IL-10 and interferon gamma. Interestingly, we found several differences between the serum levels of the two different patient groups, as well as those in patients and healthy volunteers. One striking result was that IL-10 was detected in increased levels in sera of patients with IPF, in comparison to healthy volunteers (p<0.05), and was not detected at all in patients with pulmonary fibrosis of a secondary cause. We have suggested the use of IL-10 in the differential diagnosis of patients with IPF, while Bergeron et al. 1, suggest it might be a possible therapeutic target for IPF.

We agree with the observation of Bergeron et al. 1, and think that IL-10 might be an important cytokine in IPF. Although the above observations have been made in both studies in a "given moment", the elevation in the amounts of IL-10 in both the tissues and serum of patients with IP, is an observation, which, we think, should not be ignored. Nevertheless, we assume that those "given moments" happened to be the same in both studies, since the serum and tissue samples have been obviously collected during the onset of the disease, before any treatment was administered. However, this was not very clear in the paper of Bergeron et al. 1, and we would like to know if it really happened as we assume.

The existing literature of observations concerning the IL-10 profile in pulmonary fibrosis is scarce. Most papers suggest that IL-10 has an antifibrotic effect, and derives from the alveolar macrophages 2, as well as from the pulmonary fibroblasts 3. Its action is basically opposed to that of TNF-, which is a rather inflammatory cytokine 2. It is considered, as well as IL-4, a major IL in the T-helper cell type 2 immune response 4. Interestingly, IL-10 levels have been found to be high in rat tissues with pulmonary fibrosis, while in rats with IL-10 deficiency, the inflammatory response has been found to be more intense than in the wild animals 5. In in vitro studies, the addition of IL-10 in fibroblasts has lessened the expression of type 1 collagen, the production of which is stimulated by transforming growth factor-ß 6. Those observations support the findings of Bergeron et al. 1, as well those from our own studies, that IL-10 might be an important target for future therapies, as well as a diagnostic tool.

We think that investigating the interleukin-10 pathways and possible therapeutic uses might be important in discovering more about idiopathic pulmonary fibrosis and providing patients with a more effective treatment. Moreover, serum and tissue cytokine profiles might be important in this direction.

References

1. Bergeron A, Soler P, Kambouchner M, et al. Cytokine profiles in idiopathic pulmonary fibrosis suggest an important role for TGF-ß and IL-10. Eur Respir J 2003;22:69–76.[Abstract/Free Full Text]
2. Martinez JA, King TE, Brown K, et al. Increased expression of the interleukin-10 gene by alveolar macrophages in interstitial lung disease. Am J Physiol 1997;273:676–683.
3. Vancheri C, Mastruzzo C, Tomaselli V, et al. Normal human lung fibroblasts differently modulate interleukin-10 and interleukin-12 production by monocytes: implications for an altered immune response in pulmonary chronic inflammation. Am J Respir Cell Mol Biol 2001;25:592–599.[Abstract/Free Full Text]
4. Zhou Y, Giscombe R, Huang D, Levfert AK. Novel genetic association of Wegener's granulomatosis with the interleukin 10 gene. J Rheumatol 2002;29:317–320.[Abstract/Free Full Text]
5. Huaux F, Louahed J, Hudspith B, et al. Role of interleukin-10 in the lung response to silica in mice. Am J Resp Cell Mol Biol 1998;18:51–59.[Abstract/Free Full Text]
6. Arai T, Abe K, Matsuoka H, et al. Introduction of the interleukin- gene into mice inhibited bleomycin- lung injury in vivo. Am J Physiol Lung Cell Mol Physiol 2000;278:914–922.

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