Effects of Clarithromycin on Cultured Human Nasal Epithelial Cells and Fibroblasts

Miyanohara, Toshio; Ushikai, Masato; Matsune, Shoji; Ueno, Kazuyoshi; Katahira, Shoko; Kurono, Yuichi

doi:10.1097/00005537-200001000-00023

Cited by 71 publications

(47 citation statements)

References 39 publications

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“…This suggests the inhibition of IL-8, NF-B, and DNA-binding activities by erythromycin. Similar findings have been reported for airway epithelial cell, fibroblast, monocyte, and leukemia cell lines (2,55,102,140,191).…”

Section: Effects On Cell Signalingsupporting

confidence: 89%

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Mechanisms of Action and Clinical Application of Macrolides as Immunomodulatory Medications

2010

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SUMMARY Macrolides have diverse biological activities and an ability to modulate inflammation and immunity in eukaryotes without affecting homeostatic immunity. These properties have led to their long-term use in treating neutrophil-dominated inflammation in diffuse panbronchiolitis, bronchiectasis, rhinosinusitis, and cystic fibrosis. These immunomodulatory activities appear to be polymodal, but evidence suggests that many of these effects are due to inhibition of extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation and nuclear factor kappa B (NF-κB) activation. Macrolides accumulate within cells, suggesting that they may associate with receptors or carriers responsible for the regulation of cell cycle and immunity. A concern is that long-term use of macrolides increases the emergence of antimicrobial resistance. Nonantimicrobial macrolides are now in development as potential immunomodulatory therapies.

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Section: Effects On Cell Signalingsupporting

confidence: 89%

“…Macrolides also inhibit mRNA expression of mediators and cytokines such as IL-1, endothelin-1, iNOS, and MUC5AC (191,216,284,291). The mechanism for this is likely to involve suppression of NF-B and AP-1 (2, 11, 55, 140).…”

Section: Effects On Cell Signalingmentioning

confidence: 99%

Mechanisms of Action and Clinical Application of Macrolides as Immunomodulatory Medications

2010

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“…CM, for example, has been found to suppress the production of IL-1b, IL-6, IL-8, and granulocyte-macrophage colony stimulating factor [18][19][20][21], as well as to reduce ICAM-1 gene expression on nasal fibroblasts [18]. As ICAM-1 is the receptor for the major RVs, and since IL1b, IL-6, and IL-8 play significant roles in the pathophysiology of RV infection [22], CM may be able to modulate inflammatory processes during RV infection.…”

Section: Discussionmentioning

confidence: 99%

“…However, CM pretreatment was found to suppress IL-1b induced nuclear factor (NF)-kB activity in bronchial epithelial cells, but had no effect on NF-kB activity in the absence of IL-1b stimulation [13]. Since the ability of macrolides to inhibit the secretion of pro-inflammatory cytokine is mediated by inhibition of NF-kB [27], CM may have no effect on the constitutive expression of ICAM-1 and pro-inflammatory cytokines, which may not be associated with NF-kB activation [18]. However, further experiments are required to clarify this discrepancy.…”

Section: Discussionmentioning

confidence: 99%

Effect of clarithromycin on rhinovirus-16 infection in A549 cells

Jang

Kwon²,

Bj³

2006

Eur Respir J

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Clarithromycin (CM) has been found to inhibit the production of the intercellular adhesion molecule (ICAM)-1 and the secretion of interleukin (IL)-6 and IL-8, which may have beneficial effects on the pathophysiological changes related to rhinovirus (RV) infection. The effect of CM on RV infection in A549 cells was therefore investigated.Cells were pre-treated with 1, 10 or 100 mM CM, either starting 3 days before infection and continuing thereafter, or by addition at the time of infection. RV titre, as measured by culture on Medical Research Council 5 cells, was reduced by CM, with the degree of reduction being greater when CM was added 3 days before infection than when it was added at the time of infection.CM treatment inhibited the RV-induced increase in ICAM-1 mRNA and protein, as well as the RVinduced secretion of IL-1b, IL-6, and IL-8. These effects were greater in cells treated with 10 mM than in those treated with 100 mM CM, and the maximum effect was observed 3 days after viral infection. In contrast, secretion of IL-8 was not inhibited significantly when CM was added at the time of viral infection.The findings of this study suggest that, in A549 cells, clarithromycin inhibits the induction of intercellular adhesion molecule-1 expression, cytokine elaboration, and viral infection.

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“…The emigrated neutrophils then secrete IL-1β, which amplifies the expression of E-selectin and ICAM-1, resulting in further neutrophil infiltration 24 . Miyanohara et al 25 revealed that clarithromycin suppressed IL-1β gene expression in human nasal epithelial cells in vitro.…”

Section: A Peric D Vojvodic N Baletic a Peric O Miljanovicmentioning

confidence: 99%

Influence of Allergy on the Immunomodulatory and Clinical Effects of Long-Term Low-Dose Macrolide Treatment of Nasal Polyposis

Perić¹,

Vojvodić²,

Baletić³

et al. 2010

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Aims. Cytokine levels in nasal secretions reflect the inflammatory status of the nasal and paranasal sinus mucosa and the development of mucosal disease. The results of previous investigations suggest that macrolide antibiotics can be effective in treatment of chronic rhinosinusitis and nasal polyposis. The aim of this prospective study was to compare the immunomodulatory and clinical effects of long-term low-dose macrolide treatment of nonatopic and atopic patients with nasal polyposis.Methods. Forty (n = 40) patients with nasal polyposis, 22 allergic and 18 nonallergic were administered clarithromycin (CAM) 500 mg/day single oral dose for eight weeks. We measured the levels of proinflammatory Th1 cytokines TNF-α and IL-1β, Th2 cytokines IL-4, IL-5 and IL-6, and chemokine IL-8 in the nasal fluid samples, before and after treatment, using flow cytometric method. We also scored each of the 40 patients before and after therapy according to nasal symptom score and endoscopic score.Results. Following treatment, we found significantly reduced levels of IL-8 (p<0.01) and TNF-α (p<0.01) in nasal secretions in nonallergic patients. In subjects with nasal polyposis and allergy, we found decreased levels of IL-8 (p<0.01), IL-6 (p<0.05) and IL-1β (p<0.01). Macrolide therapy decreased the size of polyps in 45.45% of nonatopic and in 50% of atopic patients. After macrolide treatment, we found 67.83% patients in nonallergic group and 55.55% patients in allergic group with improved nasal symptoms.Conclusions. Long-term low-dose treatment with CAM was effective in the management of nasal polyposis. Our results showed that macrolide treatment of nasal polyposis have different immunomodulatory and similar clinical effects in allergic and nonallergic patients.

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Effects of Clarithromycin on Cultured Human Nasal Epithelial Cells and Fibroblasts

Cited by 71 publications

References 39 publications

Mechanisms of Action and Clinical Application of Macrolides as Immunomodulatory Medications

Mechanisms of Action and Clinical Application of Macrolides as Immunomodulatory Medications

Effect of clarithromycin on rhinovirus-16 infection in A549 cells

Influence of Allergy on the Immunomodulatory and Clinical Effects of Long-Term Low-Dose Macrolide Treatment of Nasal Polyposis

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