The observations made in RA may have interesting parallels with EGPA. Both RA and EGPA are autoimmune disorders and both are treated with standard immunosuppressive treatment including corticosteroids and immunosuppressants. In both diseases spontaneous and treatment-induced remission selleck compound using standard immunosuppression regimens are uncommon. Hence, in contrast to standard treatment, the case series presented herein suggest that immunomodulatory treatment of EGPA with IFN induces remission that may continue for several years. In fact, immunomodulatory therapy may be superior to standard immunosuppression

as it may induce long-term remission even after discontinuation of treatment. Little is known regarding maintenance of remission in EGPA treated with IFN. A small study with 13 patients reported a mean time to first relapse of 17 months [9]. In RA, almost half of the patients in whom maintained remission was achieved after discontinuation of therapy with DMARDs experienced check details a relapse during a 15-year follow-up period [14]. Thus, we cannot exclude that some, if not all, patients with EGPA in remission presented herein may also develop a relapse in the future. In RA, a proportion of patients with apparent clinical remission showed signs of progressive joint damage indicating subclinical disease activity [15]. This may be similar to the cases presented

above, which showed an increase in IgE serum levels and peripheral eosinophil counts whilst still being in clinical remission. In addition, there was no indication for organ

involvement including heart and lung. However, whether these biological parameters precede a relapse in EGPA remains unclear. IFN-treatment may cause significant adverse effects. All three patients experienced early side effects like arthralgia, myalgia and malaise and patient 3 also experienced depression after IFN-injections, but those side effects were transient. Patient 3 also developed hyperthyroidism, but was euthyroid under methimazole. Eventually, all patients had to discontinue IFN due to adverse events that disappeared shortly after discontinuation of treatment or did not progress ASK1 further (PNP of patient 1). Recent studies have shown that rituximab, a B-cell-depleting anti-CD20 monoclonal antibody and mepolizumab, an anti-IL-5-antibody also induce remission in EGPA [16], [17] and [18]. However, data on long-term efficacy in maintaining remission after discontinuation of treatment are not available making a reliable comparison of IFN-α to rituximab or mepolizumab impossible. We fully acknowledge the limitations of an observational study in only three patients. For instance, the patients presented were ANCA-negative. Thus, the beneficial effect of IFN may not apply to ANCA-positive cases. Previous reports [7] and [8] however have demonstrated that ANCA-positive patients equally respond to IFN-α. We also are aware that IFN may cause side effects. However, these adverse reactions were reversible.

The best known pair of coupling factors is the receptor activator of NF-κB (RANK) on osteoclast progenitors and the RANK ligand (RANKL) on osteoblasts [40]. Additionally, another pair of cell-surface molecules was more recently nominated as novel coupling factors of bone remodeling, i.e., the ephrin B2 ligand on osteoclasts and the EphB4 receptor tyrosine kinase on osteoblasts [41]. Of interest, ephrin

B2 has also been shown to be produced by periodontal ligament cells Tofacitinib research buy in a strain-dependent manner, indicating its involvement in bone remodeling upon orthodontic tooth movement [42]. Here, another mode of coupling between these cells is proposed (Fig. 4). As described in a previous section, CCN2 is produced by osteoblasts at early stages Linsitinib mw of differentiation and promotes their proliferation and osteoblastic differentiation [28]. Moreover, our recent study revealed that the same CCN2 molecule enhances osteoclastogenesis via interaction with dendritic cell-specific transmembrane protein (DC-STAMP), which is a cell-surface molecule playing a role in the cell fusion events that occur upon the maturation of osteoclasts [43]. In that report, the production of CCN2 by osteoclast progenitors was

confirmed as well. As such, this single molecule, CCN2, is indeed coupling osteoblasts and osteoclasts and modulating the action of both cells; and thus it deserves the title of single DNA ligase coupling factor of bone remodeling. Since CCN2 acts on both types of the cells positively, this factor may be coordinating efficient and balanced bone remodeling. This functional property of CCN2 is well demonstrated by the regenerative effect of CCN2 on bone defects [13]. The fact that mechanical stimuli induce CCN2 production by osteocytes also indicates the property of CCN2 as a coordinator of bone remodeling [44]. Despite that cartilage evolved from a prototypic endoskeleton that supported the body, biological missions assigned to the present permanent cartilage in the human body are quite different from those of bone. Since uncalcified cartilage does not serve as a storage depot for

calcium and phosphate, it is not necessary for cartilage to be continuously remodeled to support calcium homeostasis. Nevertheless, instead of being major skeletal components of the face, our cartilage plays a critical role by enabling flexible movement of our jaws, taking advantage of its elasticity and stiffness. The major role of articular cartilage is to soften the friction and absorb the pressure between the bones upon movement; hence, it is constantly subject to mechanical stress load and minor injury. Therefore, another mode of tissue remodeling does occur in response to these stimuli, in order to maintain the physical properties of articular cartilage. In this context, it is important to mention that CCN2 protein is induced in chondrocytes upon mechanical stress load [45].

33 The results of the present study showed a significant increase of tryptase+ MCs in SCCs compared with normal lip. These findings agree with other results in the literature.34 and 35 On the other hand, Oliveira-Neto et al.36 found a decrease of tryptase+ Ceritinib MCs in oral squamous cell carcinoma (OSCC) and leukoplakia. Studies have pointed to an increase in the number of MCs, including tryptase+ ones, in solar radiation–exposed skin.9, 37, 38, 39 and 40 This may explain the

differences in MC densities found in SCCs and ACs compared with OSCCs. Chronic exposure to radiation, particularly UV, has been described as one of the main risk factors related to AC and SCC development.35 and 40 Our results also showed a significant increase of tryptase+ MCs in SCCs compared with ACs, unlike the findings of Costa et al.,34 where similar MC densities were found in both lesions. ACs present a variety of histologic changes that primarily include varying degrees of keratosis, solar elastosis, epithelium atrophy or hyperplasia, and the absence or presence of dysplasia.1 All cases studied by Costa et al. were classified as mild epithelial dysplasia, whereas in our study only 5 cases were so classified. That may explain the different MC densities observed

in ACs between these studies. In the present study, a higher MC density was observed in the stroma compared with the tumor parenchyma. MCs may accumulate in the stroma around the tumor and take part in the inflammatory reaction that happens at the tumor edge and in the local tumor immunity.5 Nevertheless, the increase of stromal Enzalutamide concentration tryptase+ MCs has also been reported as an important factor for tumor invasion on cancers in various anatomic sites.41 and 42 Therefore, these cells may contribute to the defense against tumors as well as to their progression. Our results also pointed to a significant increase in c-Kit+ MC density in SCCs and ACs compared with control samples. These findings differ from the results of Costa et al.34 who found a similar cell density for the 3 groups. c-Kit (CD 117) is a transmembrane receptor tyrosine kinase type III that acts in cellular signal transduction in various cell types. It is usually

activated by binding to its ligand, stem cell Org 27569 factor (SCF). In this scenario, it promotes phosphorylation and activation of the intracytoplasmic signaling cascade which is essential for embryogenesis, hematopoiesis, development, proliferation, and migration. c-Kit is expressed in normal human tissue, melanocytes, breast epithelium, interstitial cells of Cajal, and MCs. SCF stimulates directional motility of both mucosal and connective tissue–type MCs. It also plays a role in MC survival and activation via up-regulation of TNF-α, chemokine production, and the induction of histamine release.43 MCs are long-lived cells that can restart the cell cycle, proliferate, and be recruited after an appropriate stimulation. This stimulus may contribute to population expansion of these cells. Kim et al.

It is hypothesised that nicotine plays

a direct role in the induction and progression of many human cancers (Heeschen et al., 2001). Nicotine induces cancer cell migration and DNA damage (Argentin and Cicchetti, 2004 and Guo et al., 2008). The interaction of nicotine with DNA and nuclear proteins is considered as the initial step in carcinogenesis. A study by Cheng et al. (2003) demonstrated that dietary constituents, such as curcumin, garlic squeeze, grapeseed extract, tea polyphenols, vitamin C and vitamin E suppress the formation of DNA-nicotine adducts. Spices are commonly used to enrich flavour and aroma in cooking learn more and to preserve food. Spices are widely used in Asia and the Middle East, not only in cooking, but also as components of a healthy diet. Their use is increasing in non-Asian countries as well. They are also traditionally thought to have beneficial effects on health and specific spices are used in traditional medicine as part of therapeutic formulations. Ethnopharmacological studies on spices revealed a wide range of biological activities, including, antioxidant, anti-inflammatory, anti-tumor, immunomodulatory and antiradical activities (Cherng et al., 2008, Ho et al., 2010, Madsen and Bertelsen, 1995 and Mueller et al., 2010). Plant phenols were found to protect DNA from oxidative damage and

a study on the extracts of sumach showed that this spice protected DNA from H2O2-induced oxidative stress (Fabiani et al., 2008). However, there are no reports available on the DNA protecting effect of other spices. Hence, in this study, we analysed the DNA protecting activity and inhibition of cancer cell click here migration of ethanolic extracts of a number of common spices that are popular in Asian and, increasingly, in Western cooking, using 3T3-L1 mouse

fibroblasts and MCF-7 human breast cancer cells. Hydrogen peroxide (H2O2) was used to induce DNA damage; H2O2 produces reactive hydroxyl radicals by the Fenton reaction. The hydroxyl radicals bind to DNA at metal binding sites and induce strand Parvulin breaks. Our aim was to investigate whether the selected spices protect cells from hydroxyl radical-induced and nicotine-induced toxicity. Cumin (Cuminum cyminum), fennel (Foeniculum vulgare), star anise (Illicium verum), pepper (Piper nigrum), long pepper (Piper longum), ginger (Zingiber officinale), clove (Eugenia carophyllata), cardamom (Elettaria cardamomum) and caraway (Carum carvi) were purchased from a local market. The dried spices (100 g each) were ground into fine powder using a kitchen blender. The powder (100 g) was extracted with 95% of ethanol for 16 h. Ethanol was removed using a rotary vacuum evaporator and the extracts were stored at −20 °C. The total phenolic content was assayed with Folin–Ciocalteu reagent using gallic acid as the standard (Taga, Miller, & Pratt, 1984). Spice extracts (100 μl, 10 mg/ml) were added to 2 ml of 2% Na2CO3.

Species rich in phenolic compounds, ascorbic acid and carotenes are usually associated with prominent biological properties such as increased protection against cellular oxidation, antimicrobial

and anticarcinogenic activities ( Katalinić et al., 2010, Link et al., 2010, Proteggente et al., 2002 and Sun et al., 2002). The beneficial effects of fruit and vegetable consumption in the prevention of chronic-degenerating diseases have been challenged ( Boffetta et al., 2010). However, the majority of studies suggest that increased consumption of fruit, vegetables and grains contributes to prevent chronic-degenerating diseases, such as cancer, cardiovascular diseases, diabetes and neurodegenerative diseases ( Bazzano et al., 2002, Liu et al., 2004 and Schroeter et al., 2005). In this study, fruit from six araçá genotypes (accessions) were characterised Rapamycin by quantification of individual phenolic

compounds, l-ascorbic acid, total phenolic, total anthocyanin, and total carotene content. Acetone and aqueous fruit extracts were analysed in terms of radical scavenging power, antioxidant protection of Saccharomyces cerevisiae, antimicrobial effect against Salmonella enteritidis and antiproliferative effect on human cancer cells, MCF-7 (breast) and Caco-2 (colon). Red (accessions find more AR9, AR19 and AR29) and yellow (accessions AR27, AR46 and AR72) araçá (P. cattleianum Sabine) were collected from a research orchard (germplasm collection of Embrapa Clima Temperado, Pelotas, RS, Brazil) when fruit was ripe. One kilogram of fruit Ponatinib from three plants (clones) of each accession was harvested. Fruit were washed, seeds removed, and fruit flesh was frozen

in liquid nitrogen and stored at −80 °C until further analyses. All analyses were performed in triplicate. Soluble solids content was determined by refractometry, and the results expressed as % (w/w). Total acidity (TA) and pH were measured directly from the extracted fruit juice. TA was determined by titration and results were expressed as milligrams of citric acid per 100 grams of fresh fruit pulp (mg 100 g-1 ffp). Phenolic compounds were extracted following the method described by Souza et al. (2008). Frozen pulp (10 g) was ground in a mortar and pestle, extracted with 20 mL deionized water (DW) and placed on an orbital shaker set at 200 rpm for 1 h at room temperature (20 ± 3 °C) in the dark. Extracts were then centrifuged at 12000g for 15 min at 4 °C and the supernatant was concentrated in a freeze-drier and the final volume adjusted to 10 mL with DW. The same extraction was performed using acetone instead of water. In this case the extract was concentrated in a rotary evaporator at 40 °C under reduced pressure and the residue was redissolved in 10 mL of DW. Total phenolic content was determined using the method described by Dewanto, Wu, Adom, and Liu (2002).

Common chemical hazards include metal particulates and gases. However, the fume and noxious gases formed during the Selleckchem MK-8776 welding process are considered to be the most harmful exposure in comparison with the other byproducts of welding. Significant levels of different toxic gases (i.e., carbon

monoxide, ozone, nitrogen oxides) and metal fumes (i.e. aluminum, barium, cadmium, chromium, copper, iron, magnesium, nickel and tin) may be formed during common arc welding processes.3 Many pulmonary problems, usually attributed to these toxic fumes and gases, have been described in the literature until now. Lung cancer, occupational asthma, rhinitis, cough, dyspnea, obstructive and restrictive lung disease, pneumoconiosis, lung function impairment and pneumonia are among the most frequent respiratory problems due to welding process.4 In addition, welding workers suffer from non-pulmonary health problems such as eye irritation, photokeratitis,

cataract, skin irritation, erythema, pterygium, non-melanocytic skin cancer, malignant melanoma, reduced sperm count, motility and infertility.1 There are a lot of pulmonary and systemic diseases reasons of hemoptysis,5 however, to our knowledge, welding has not been listed as an etiology in any study. Alveolar hemorrhage due to welding fumes has never been defined before. We attributed alveolar hemorrhage to welding fumes in our patient in three ways: 1) We exclude all possible reasons of the pulmonary hemorrhage Tenofovir price (i.e. Behcet’s Syndrome and other vasculitides, GSK-3 activation tuberculosis, benign and malign tumors, acute and chronic bronchitis, hemorrhagic diatheses, systemic diseases) clinically, radiologically and with serological markers; 2) The patient was working as welder for a long time and he has been suffering diseases such as

chronic headache and chronic conjunctivitis demonstrating chronic welding fumes exposure; 3) Patient’s alveolar hemorrhage was reduced after avoidance welding fumes in a few days without any specific treatment, and no relapse was observed in 2-year follow-up period. The pathogenesis of hazardous effects of welding fumes has not been studied extensively before. However, many pulmonary effects of welding fumes has been connected to carcinogenic, fibrinojenic and irritative effects of metal constituents such as barium, cadmium, chromium, zinc and nickel, etc. of welding fumes. In animal studies,6 and 7 it has been shown that welding fumes especially manuel metal arc welding using a stainless steel electrode cause an elevated toxic lung response by means of enhanced macrophage production of highly reactive oxygen radicals and inflammatory cytokines. We think that welding fumes may produce an inflammatory and irritative response resulting with bronchial epithelial damage finally causing hemoptysis and even alveolar hemorrhage as in our patient. This case shows that welding fumes can hazard alveolar epithelium and vasculature and lead to massive hemorrhage.

Ideally, a clear understanding of the quantitative linkages between exposure, dose, and biomarker levels will exist for any biomarker that is used in an epidemiological study. Considering Selleckchem KU-57788 the invasive nature of target tissue sampling, most biomarker-based epidemiological

studies utilize samples of blood, urine, hair, or other easily-accessible matrices. Elucidating quantitative relationships between biomarker measurements from these matrices and exposure/dose levels requires an understanding of chemical absorption, distribution, metabolism, and elimination (ADME); these processes are frequently described using pharmacokinetic (PK) models, or physiologically-based pharmacokinetic (PBPK) models. Prior to the use of biomarkers in an epidemiological study, a solid understanding of chemical ADME should exist, as well as the intrinsic (e.g., genetics, life-stage, pregnancy, gender) and extrinsic (e.g., diet, medication, medical conditions) factors that are likely to affect ADME. Furthermore, for short-lived biomarkers, it is important to know specific timing details (e.g., time of day, time since last meal for those chemicals associated with dietary exposure, time since last urine void) in relation to sample collection. Ideally, the

relationships between this website biomarker concentration and exposure/dose levels, and the effects of intrinsic, extrinsic, and timing factors on these relationships, will be thoroughly evaluated before the biomarker is used in an epidemiological study. Critical information that is needed to properly interpret the biomarker (with respect to exposure/dose) should then be collected and carefully evaluated as part of the study. The costs and benefits of each biomarker of exposure should be carefully examined and interpreted as part of any epidemiological evaluation. Immune system It is important to note that matrix selection is an integral component of exposure and/or epidemiology research, and multiple

factors must be considered including measurement capability, contamination issues, and target analyte association with exposure or health outcome. BEES-C addresses each of these issues separately. Bisphenol A (BPA) is measured in urine in the free form (parent), as sulfate- or glucoronide-bound conjugates, or as a combination (total BPA) of the free and conjugated forms (Harthé et al., 2012, LaKind et al., 2012a, Völkel et al., 2008 and Ye et al., 2005). Several recent studies have examined endocrine-related health outcomes associated with BPA exposure. The most biologically-relevant biomarker is the free (parent) BPA, because only parent BPA is considered active in terms of estrogenicity (EPA (US Environmental Protection Agency), 2013 and WHO (World Health Organization), 2011).

On these trials (n = 25), participants saw a printed word appearing in the center of the screen: 15 of these words had been used previously in the experiment (e.g., they were names of characters shown in earlier pictures) and 10 were new. The design of the experiment included one three-level factor (Prime condition: agent primes, patient primes, neutral primes). Two mirror-reversed versions of each target picture were created, one in which the agent appeared on the left hand-side and one in which the agent appeared on the right hand-side of the screen. Crossing this factor with the priming selleck antibody manipulation produced six different lists of stimuli, with each

target picture being presented in a different Prime condition and with a different spatial layout of characters on each list. All analyses collapsed

across the two mirror-reversed versions of each item. Within lists, there were 10 target pictures Cell Cycle inhibitor in each Prime condition, and no two prime-target pairs from the same condition were presented in succession. The prime-target pairs were separated by 4–5 intervening unrelated trials (filler trials and word trials). Participants were seated at an Eye-link 1000 eye-tracker (500 Hz sampling rate). Instructions appeared on the screen and were paraphrased by the experimenter. Participants were told that they would see a series of pictures and of single words. Each trial began with a fixation point at the top of the screen: participants had to look at the fixation point and press a key to continue. On picture trials, they then saw a picture of an event and their task was to describe the event

with one sentence, mentioning all characters shown in the event. On a subset of picture trials, participants first saw the word LISTEN printed in the center of the screen and then a pictured event accompanied by a recorded 3-oxoacyl-(acyl-carrier-protein) reductase sentence: here, their task was to listen to the sentence and then repeat it out loud. On word trials, participants saw a printed word in the center of the screen instead of a picture: they were instructed to read this word out loud and decide whether they had produced it before in the experiment by saying “yes” or “no. Sentences produced on target trials were scored as actives, full passives, or sentences with other constructions. The latter category included truncated passives, get-passives, intransitive sentences, sentences beginning with a “There is/are…” construction, and sentences with indefinite pronouns (e.g., someone). Two items were excluded from the analyses as they elicited a very small number of transitive responses and one item was excluded for technical reasons. In the remaining dataset, trials were excluded if the first fixation in that trial was not on the fixation point at the top of the screen (80 trials) or if onsets were longer than 5 s and longer than 3 standard deviations from the grand mean (11 sentences). The final dataset consisted of 648 sentences (.71 actives, .29 full passives).

Ginsenoside-Rh2 treatment modulates the protein level of p21 and cyclin D, which results in a marked reduction in proliferation on MCF-7 human breast cancer cells [16]. Ginsenoside-Rh2 also induces apoptosis through the activation of p53 and the increase of the proapoptotic regulator, Bax, in colorectal cancer cells [37]. In addition, Ginsenoside-Rh2 markedly inhibits the viability of breast cancer cells (MCF-7 and MDA-MB-231) with G1 phase cell cycle arrest, which is caused by p15 Ink4B and p27 Kip1-dependent inhibition of

cyclin-dependent kinases [10]. Although many selleck chemicals studies describing the anticancer effect of ginsenoside-Rh2 have been conducted, much of its mechanism relating to anticancer activities remains unclear. AMPK is a pleiotropic kinase that selleckchem signals for both survival and apoptosis of cells. It plays a key role as a regulator of cellular energy homeostasis [39]. The kinase is activated in response to ATP depletions, such as those of glucose starvation, hypoxia, ischemia, and heat shock. Moreover, a proapoptotic function of AMPK was also reported, where the connection of AMPK with several tumor suppressors suggests that AMPK is a mediator of apoptosis. The LKB1 tumor suppressor that mutated in Peutz–Jeghers syndrome directly phosphorylates and activates AMPK [40] and [41]. The TSC2 tumor suppressor is directly phosphorylated by AMPK, and the AMPK-mediated phosphorylation of

TSC2 has an important role in cell survival [42] and [43]. The present study focuses on identifying the mechanism that underlies the anticancer activity of ginsenoside-Rh2. In this study, we show that in HepG2 cells treated with ginsenoside-Rh2, AMPK activity is increased in a time- and dose-dependent manner (Fig. 3 and Fig. 4). To confirm the role of AMPK in ginsenoside-Rh2-induced apoptosis, HepG2 cells were treated with ginsenoside-Rh2,

and were then assessed for the degree of apoptosis according to the degree of variation in AMPK activity. In this study, we have shown that AMPK activity is caused by ginsenoside-Rh2-mediated ROS generation (Fig. 5), and that it contributes to cancer cell growth and survival under treatment with ginsenoside-Rh2 Interleukin-2 receptor (Fig. 4). These observations indicate that AMPK can function as an antiapoptotic molecule. It is well documented that MAPK pathways modulate gene expression, mitosis, proliferation, metabolism, and apoptosis. Previous studies have demonstrated that MAPK signaling is involved in ginsenoside-mediated anticarcinogenesis. Ginsenoside Rg3 and Rh2 inhibit the proliferation of prostate cancer cells by modulating MAPK [17]. Ginsenoside Rb1 inhibits histamine release and IL-4 production induced by substance P, a neurotransmitter, via the ERK pathway [44]. A ginseng saponin metabolite, compound K, suppresses phorbol ester-induced matrix metalloproteinase-9 expression through the inhibition of MAPK signaling in human astroglioma cells [45].

, 2011).The injection of BMDMC even in normal lungs led to neutrophil increase in lung tissue, with no functional effects. This increment may be attributed to: presence of neutrophils in the pool of BMDMC and/or recruitment of these Protein Tyrosine Kinase inhibitor cells by chemoattractive stimuli (Araújo et al., 2010, Prota et al., 2010, Abreu et al., 2011a and Maron-Gutierrez

et al., 2011). Several studies have reported that circulating precursor cells are reduced (Bonsignore et al., 2006 and Huertas et al., 2010), and that VEGF-dependent precursor cell mobilization is impaired (Hattori et al., 2001) in human COPD. In this line, the administration of exogenous BMDMC in the current study might have contributed to the reduction of airway epithelial cell damage, tissue remodeling and inflammatory processes by increasing the available pool of circulating precursor cells. We demonstrated that early BMDMC administration led to less hyperinflation and collapsed areas as well as inflammatory cell infiltration

in the lung parenchyma, reduced small airways collagen deposition, and elastic fiber preservation. This is in agreement with a recent report that mechanical force-induced failure of the locally weakened collagen is correlated to structural changes in the lung undergoing heterogeneous consequences of elastase injury (Hamakawa et al., 2010). Ultrastructural analysis selleck inhibitor using electron microscopy revealed higher preservation of endothelial cells, type II pneumocyte and basement membrane, associated with reduction of collagen fiber deposition and elastic fiber breakdown. Besides, several typical features of regenerative processes, such as enlarged type II pneumocytes with augmented lamellar bodies, as well as the presence of multinucleated and undifferentiated cells in lung parenchyma were observed in the E-CELL group, suggesting that BMDMC may modulate elastase injury and play an important role in the repair of damaged areas. However, the exact mechanisms responsible for cell restoration remain unclear. It has been suggested that these multinucleated

Montelukast Sodium cells could be the result of a fusion between macrophages and BMDMCs, or between macrophages and injured epithelial cells (Krause, 2008). Additionally, it has been described that macrophages behave in vitro as stem cell attractors. Once at the site of injury, the ability of precursor cells to reconstitute the damaged tissues depends on the signals generated in situ by the macrophages ( Lolmede et al., 2009). Besides their proven plasticity, most beneficial effects of stem cells have been attributed to paracrine effects, that is, a capacity of modulating cytokines and growth factor synthesis without being present at the injury site (Abreu et al., 2011b and Doorn et al., 2011). Paracrine effects have been demonstrated in several models of lung diseases, including emphysema (Shigemura et al., 2006, Zhen et al., 2010, Huh et al.