Experimental pulmonary fibrosis induced by trisodium citrate and acid-citrate-dextrose

Mitsuhashi, Takehiro; Shimazaki, Masayoshi; Chanoki, Yorihiko; Kuwahara, Hideki; Sakai, Takeo; Masuda, Hiroshi

doi:10.1016/0014-4800(85)90032-2

Cited by 19 publications

(7 citation statements)

References 13 publications

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“…In this study we adopted Mitsuhashi´s definition of fibrosis 23 , namely, a lung disorder associated to the progressive loss of pulmonary volume and of the functionality of the alveolus-capillary junction. Morphologically, fibrosis is characterized by an abnormal increase or an altered disposition of the connective tissue (collagens I, III).…”

Section: Histopathological Studiesmentioning

confidence: 99%

Fibrotic sequelae in pulmonary paracoccidioidomycosis: histopathological aspects in BALB/c mice infected with viable and non-viable Paracoccidioides brasiliensis propagules

Cock¹,

Cano

Velez

et al. 2000

Rev. Inst. Med. trop. S. Paulo

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Patients with paracoccidioidomycosis often present pulmonary fibrosis and exhibit important respiratory limitations. Based on an already established animal model, the contribution of viable and non-viable P. brasiliensis propagules to the development of fibrosis was investigated. BALB/c male mice, 4-6 weeks old were inoculated intranasally either with 4x10(6) viable conidia (Group I), or 6. 5x10(6) fragmented yeast cells (Group II). Control animals received PBS. Six mice per period were sacrificed at 24, 48, 72h (initial) and 1, 2, 4, 8, 12 and 16 weeks post-challenge (late). Paraffin embedded lungs were sectioned and stained with H&E, trichromic (Masson), reticulin and Grocot&tacute;s. During the initial period PMNs influx was important in both groups and acute inflammation involving 34% to 45% of the lungs was noticed. Later on, mononuclear cells predominated. In group I, the inflammation progressed and granulomas were formed and by the 12th week they fussed and became loose. Thick collagen I fibers were observed in 66.6% and 83.3% of the animals at 8 and 12 weeks, respectively. Collagen III, thick fibers became apparent in some animals at 4 weeks and by 12 weeks, 83% of them exhibited alterations in the organization and thickness of these elements. In group II mice, this pattern was different with stepwise decrease in the number of inflammatory foci and lack of granulomas. Although initially most animals in this group had minor alterations in thin collagen I fibers, they disappeared by the 4th week. Results indicate that tissue response to fragmented yeast cells was transitory while viable conidia evoked a progressive inflammatory reaction leading to granuloma formation and to excess production and/or disarrangement of collagens I and III; the latter led to fibrosis.

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Section: Histopathological Studiesmentioning

confidence: 99%

Fibrotic sequelae in pulmonary paracoccidioidomycosis: histopathological aspects in BALB/c mice infected with viable and non-viable Paracoccidioides brasiliensis propagules

Cock¹,

Cano

Velez

et al. 2000

Rev. Inst. Med. trop. S. Paulo

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“…Interestingly, SCA increased cell proliferation, which was further enhanced by addition of citrate, which has been shown to induce fibroblast proliferation [10] ( fig. 2 ).…”

Section: Sca Induces Fibroblast Proliferation In Vitro and Regulates mentioning

confidence: 99%

Molecular Basis for the Regenerative Properties of a Secretion of the Mollusk <i>Cryptomphalus aspersa</i>

Brieva¹,

Philips

Tejedor

et al. 2007

Skin Pharmacol Physiol

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A screen for natural products bearing pharmacological properties has yielded a secretion of the mollusk Cryptomphalus aspersa (SCA), which possesses skin-regenerative properties. In this report, we outline some of the cellular and molecular effects underlying this observation. First, we found that SCA contained antioxidant SOD and GST activities. In addition, SCA stimulated fibroblast proliferation and rearrangement of the actin cytoskeleton. Additional mechanisms involved in the regenerative effect of SCA included the stimulation of extracellular matrix assembly and the regulation of metalloproteinase activities. Together, these effects provide an array of molecular mechanisms underlying SCA-induced cellular regeneration and postulate its use in regeneration of wounded tissue.

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“…Pulmonary fibrosis (PF) has been induced by direct instillation of acid into the airways of animals in experimental models of PF [16][17][18]. In a pilot study, abnormal acid GER was documented in 16 out of 17 patients with IPF [19].…”

mentioning

confidence: 99%

High prevalence of abnormal acid gastro-oesophageal reflux in idiopathic pulmonary fibrosis

Han¹

2006

European Respiratory Journal

579

406

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The aim of this prospective study was to determine the prevalence and characteristics of acid gastro-oesophageal reflux (GER) in patients with idiopathic pulmonary fibrosis (IPF).Sixty-five consecutive patients with well-defined IPF were subjected to 24-h pH monitoring and oesophageal manometry. A total of 133 consecutive patients with intractable asthma and symptoms of GER were used as comparisons.The prevalence of abnormal acid GER in IPF patients was 87%, with 76% and 63% demonstrating abnormal distal and proximal oesophageal acid exposures, respectively. Abnormal acid GER was significantly more common in IPF patients than asthma patients. Only 47% of IPF patients experienced classic GER symptoms. Despite treatment with standard doses of proton pump inhibitors (PPIs), 12 out of 19 patients receiving PPIs during the 24-h pH monitoring had abnormal oesophageal acid exposures by pH probe. There was no correlation between IPF severity and acid GER severity.In conclusion, abnormal acid gastro-oesophageal reflux is highly prevalent, but often clinically occult in patients with idiopathic pulmonary fibrosis. Standard doses of proton pump inhibitors may not suppress the acid gastro-oesophageal reflux in this population. Therefore, further studies are needed to determine if acid abnormal gastro-oesophageal reflux represents an important risk factor for idiopathic pulmonary fibrosis development or progression, and if optimal suppression of acid gastro-oesophageal reflux slows the progression of idiopathic pulmonary fibrosis and/or decreases episodic exacerbations of idiopathic pulmonary fibrosis.

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Experimental pulmonary fibrosis induced by trisodium citrate and acid-citrate-dextrose

Cited by 19 publications

References 13 publications

Fibrotic sequelae in pulmonary paracoccidioidomycosis: histopathological aspects in BALB/c mice infected with viable and non-viable Paracoccidioides brasiliensis propagules

Fibrotic sequelae in pulmonary paracoccidioidomycosis: histopathological aspects in BALB/c mice infected with viable and non-viable Paracoccidioides brasiliensis propagules

Molecular Basis for the Regenerative Properties of a Secretion of the Mollusk <i>Cryptomphalus aspersa</i>

High prevalence of abnormal acid gastro-oesophageal reflux in idiopathic pulmonary fibrosis

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