Epstein-Barr-virus-induced interstitial lung disease

Marzouk, Kamel; Corate, Lalaine; Saleh, Samer; Sharma, Om P.

doi:10.1097/01.mcp.0000176678.38539.9a

Cited by 33 publications

(20 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The most compelling evidence for a viral co-factor in IPF comes from studies concerning the association between the gamma-herpesvirus, EBV [3]–[9], [14], while data from human studies are limited and have produced conflicting results [5]–[9]. For instance, latent EBV infection is most often found in B cells [21]; however, in patients with IPF, EBV was found in lung tissue, including epithelial cells [22], [23]. Our results are not in disagreement with the aforementioned studies, as we did not evaluate the incidence of EBV in our samples.…”

Section: Discussionmentioning

confidence: 99%

Detection of Herpes Simplex Virus Type-1 in Patients with Fibrotic Lung Diseases

et al. 2011

View full text Add to dashboard Cite

The current study intends to investigate i) the incidence of herpes viruses including Herpes Simplex Virus type-1 (HSV-1), Cytomegalovirus (CMV) and Human Herpes Virus -6, -7, -8 (HHV6, HHV7, HHV8) in two biological samples, bronchoalveolar lavage fluid (BALF) and lung tissue biopsy, in different forms of pulmonary fibrosis, and ii) the induction of molecular pathways involved in fibrosis by herpesvirus infection in primary cell cultures. PCR was employed for the detection of CMV, HHV6-8 and HSV-1 DNA in lung specimens (4 controls and 11 IPF specimens) and BALF pellet [6 controls and 20 fibrotic Idiopathic Intestitial Pneumonias (f-IIPs) samples: 13 idiopathic pulmonary fibrosis (IPF) and 7 nonspecific idiopathic interstitial pneumonia (NSIP)] samples. Among all herpesviruses tested, HSV-1 was detected in 1/11 (9%) specimens from IPF lung tissue and in 2/20 (10%) samples of f-IIPs BALF whereas the control group was negative. Primary cell cultures from BALF of patients with IPF and healthy controls were infected in vitro with wild-type HSV-1 virus and Real Time PCR was employed for the detection of gene transcription of specific axes implicated in lung fibrosis. Primary cell cultures were permissive to HSV-1, resulting in an upregulation of the fibrotic growth factors TGFβ1 and FGF, the angiogenetic markers SDF1a, SDF1b, VEGF, FGF and the regulators of tissue wound healing MMP9 and CCR7. Downregulation was noted for the CXCR4 and MMP2 genes, while a different response has been detected in healthy donors regarding the expression of the aforementioned markers. These results implicate for the first time the HSV-1 with Fibrotic Idiopathic Interstitial Pneumonias since the virus presented similar incidence in two different biological samples.

show abstract

Section: Discussionmentioning

confidence: 99%

Detection of Herpes Simplex Virus Type-1 in Patients with Fibrotic Lung Diseases

et al. 2011

View full text Add to dashboard Cite

show abstract

“…Differential diagnosis in this setting can be even more troublesome in the case of patients with preexisting ILD [40]. Pathogens to consider as potential ILD mimickers are Pneumocystis jiroveci, fungal [40] and viral infections such as Epstein-Barr [146] and cytomegalovirus [147]. The main differential diagnosis based on radiological aspects is presented in Table 2.…”

Section: Differential Diagnosismentioning

confidence: 99%

The Multifaceted Aspects of Interstitial Lung Disease in Rheumatoid Arthritis

Cavagna

Monti

Grosso

et al. 2013

BioMed Research International

View full text Add to dashboard Cite

Interstitial lung disease (ILD) is a relevant extra-articular manifestation of rheumatoid arthritis (RA) that may occur either in early stages or as a complication of long-standing disease. RA related ILD (RA-ILD) significantly influences the quoad vitam prognosis of these patients. Several histopathological patterns of RA-ILD have been described: usual interstitial pneumonia (UIP) is the most frequent one, followed by nonspecific interstitial pneumonia (NSIP); other patterns are less commonly observed. Several factors have been associated with an increased risk of developing RA-ILD. The genetic background plays a fundamental but not sufficient role; smoking is an independent predictor of ILD, and a correlation with the presence of rheumatoid factor and anti-cyclic citrullinated peptide antibodies has also been reported. Moreover, both exnovo occurrence and progression of ILD have been related to drug therapies that are commonly prescribed in RA, such as methotrexate, leflunomide, anti-TNF alpha agents, and rituximab. A greater understanding of the disease process is necessary in order to improve the therapeutic approach to ILD and RA itself and to reduce the burden of this severe extra-articular manifestation.

show abstract

“…Fibrotic changes can also appear as sequelae to insults by a diverse group of infectious, environmental, and therapeutic exposures (20,38,40,43). Some familial and sporadic forms are associated with genetic polymorphisms (58).…”

mentioning

confidence: 99%

PPAR-γ agonists inhibit profibrotic phenotypes in human lung fibroblasts and bleomycin-induced pulmonary fibrosis

Milam

Keshamouni

Phan³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

187

171

View full text Add to dashboard Cite

Pulmonary fibrosis is characterized by alterations in fibroblast phenotypes resulting in excessive extracellular matrix accumulation and anatomic remodeling. Current therapies for this condition are largely ineffective. Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) is a member of the nuclear hormone receptor superfamily, the activation of which produces a number of biological effects, including alterations in metabolic and inflammatory responses. The role of PPAR-gamma as a potential therapeutic target for fibrotic lung diseases remains undefined. In the present study, we show expression of PPAR-gamma in fibroblasts obtained from normal human lungs and lungs of patients with idiopathic interstitial pneumonias. Treatment of lung fibroblasts and myofibroblasts with PPAR-gamma agonists results in inhibition of proliferative responses and induces cell cycle arrest. In addition, PPAR-gamma agonists, including a constitutively active PPAR-gamma construct (VP16-PPAR-gamma), inhibit the ability of transforming growth factor-beta1 to induce myofibroblast differentiation and collagen secretion. PPAR-gamma agonists also inhibit fibrosis in a murine model, even when administration is delayed until after the initial inflammation has largely resolved. These observations indicate that PPAR-gamma is an important regulator of fibroblast/myofibroblast activation and suggest a role for PPAR-gamma ligands as novel therapeutic agents for fibrotic lung diseases.

show abstract

Epstein-Barr-virus-induced interstitial lung disease

Cited by 33 publications

References 19 publications

Detection of Herpes Simplex Virus Type-1 in Patients with Fibrotic Lung Diseases

Detection of Herpes Simplex Virus Type-1 in Patients with Fibrotic Lung Diseases

The Multifaceted Aspects of Interstitial Lung Disease in Rheumatoid Arthritis

PPAR-γ agonists inhibit profibrotic phenotypes in human lung fibroblasts and bleomycin-induced pulmonary fibrosis

Contact Info

Product

Resources

About