Effects of Peroxisome Proliferator-Activated Receptor-δ Agonist on Cardiac Healing after Myocardial Infarction

Peroxisome proliferator-activated receptor-delta (PPAR-δ)-dependent signaling is associated with rapid wound healing in the skin. Here, we investigated the therapeutic effects of PPAR-δ-agonist treatment on cardiac healing in post-myocardial infarction (MI) rats. Animals were assigned to the following groups: sham-operated control group, left anterior descending coronary artery ligation (MI) group, or MI with administration of the PPAR-δ agonist GW610742 group. GW610742 (1 mg/kg) was administrated intraperitoneally after the operation and repeated every 3 days. Echocardiographic data showed no differences between the two groups in terms of cardiac function and remodeling until 4 weeks. However, the degrees of angiogenesis and fibrosis after MI were significantly higher in the GW610742-treated rats than in the untreated MI rats at 1 week following MI, which changes were not different at 2 weeks after MI. Naturally, PPAR-δ expression in infarcted myocardium was highest increased in 3 day after MI and then disappeared in 14 day after MI. GW610742 increased myofibroblast differentiation and transforming growth factor-beta 2 expression in the infarct zone at 7 days after MI. GW610742 also increased bone marrow-derived mesenchymal stem cell (MSC) recruitment in whole myocardium, and increased serum platelet-derived growth factor B, stromal-derived factor-1 alpha, and matrix metallopeptidase 9 levels at day 3 after MI. PPAR-δ agonists treatment have the temporal effect on early fibrosis of infarcted myocardium, which might not sustain the functional and structural beneficial effect.     

Discrepant Results of Experimental Human Mesenchymal Stromal Cell Therapy after Myocardial Infarction: Are Animal Models Robust Enough?

BackgroundHuman mesenchymal stromal cells (MSCs) have been reported to preserve cardiac function in myocardial infarction (MI) models. Previously, we found a beneficial effect of intramyocardial injection of unstimulated human MSCs (uMSCs) on cardiac function after permanent coronary artery ligation. In the present study we aimed to extend this research by investigating the effect of intramyocardial injection of human MSCs pre-stimulated with the pro-inflammatory cytokine interferon-gamma (iMSCs), since pro-inflammatory priming has shown additional salutary effects in multiple experimental disease models.MethodsMI was induced in NOD/Scid mice by permanent ligation of the left anterior descending coronary artery. Animals received intramyocardial injection of uMSCs, iMSCs or PBS. Sham-operated animals were used to determine baseline characteristics. Cardiac performance was assessed after 2 and 14 days using 7-Tesla magnetic resonance imaging and pressure-volume loop measurements. Histology and q-PCR were used to confirm MSC engraftment in the heart.ResultsBoth uMSC and iMSC therapy had no significant beneficial effect on cardiac function or remodelling in contrast to our previous studies.ConclusionsAnimal models for cardiac MSC therapy appear less robust than initially envisioned.     

The Adult G?ttingen Minipig as a Model for Chronic Heart Failure After Myocardial Infarction: Focus on Cardiovascular Imaging and Regenerative Therapies

Porcine models have become increasingly popular in cardiovascular research. The standard farm pig rapidly increases in body weight and size, potentially confounding serial measurements of cardiac function and morphology. We developed an adult porcine model that does not show physiologic increases in heart mass during the study period and is suitable for long-term study. We compared adult minipigs with the commonly used adolescent Yorkshire swine. Myocardial infarction was induced in adult Göttingen minipigs and adolescent Yorkshire swine by occlusion of the left anterior descending coronary artery followed by reperfusion. At 8 wk after infarction, the left ventricular ejection fraction was 34.1 ± 2.3% in minipigs and 30.7 ± 2.0% in Yorkshire swine. The left ventricular end-diastolic mass in Yorkshire pigs assessed by magnetic resonance imaging increased 17 ± 5 g, from 42.6 ± 4.3 g at week 1 after infarction to 52.8 ± 6.6 g at week 8, whereas it remained unchanged in minipigs. Cardiac anatomy and physiology in adult minipigs were evaluated invasively by angiography and noninvasively by Multidetector Computed Tomography and by Magnetic Resonance Imaging at 1.5 T and 3 T prior to myocardial infarction and during folow-up. This porcine heart failure model is reproducible, mimics the pathophysiology in patients who have experienced myocardial infarction, and is suitable for imaging studies. New heart failure therapies and devices can be tested preclinically in this adult animal model of chronic heart failure.Abbreviations: CEMRA, contrast-enhanced magnetic resonance angiography; CI, confidence interval; ECG, electrocardiogram; LAD, left anterior descending artery; LV, left ventricle; LVEF, left ventricular ejection fraction; MDCT, multidetector computed tomography; MI, myocardial infarction; MRI, magnetic resonance imagingIn the United States alone, 7.1 million people are survivors of myocardial infarction (MI) and 4.9 million people live with congestive heart failure.⁴ New medical therapies, surgical procedures and devices for heart failure all rely heavily on preclinical testing in animal models. Porcine models of MI are used because of the similarities between porcine and human hearts.^29,38 However, the commonly employed farm pigs are utilized at a young age, grow rapidly and continue to gain in mass during use, thereby complicating long-term follow-up. The utilization of farm pigs at a young age, while their hearts are still growing does not accurately reflect the remodeling that occurs in adult patients after MI and can limit accurate assessment of chronic remodeling processes. This inaccuracy can confound evaluation of devices and pharmacologic therapies.Noninvasive imaging techniques for determining anatomic and functional manifestations of congestive heart failure are accurate and reliable, and are used as surrogate markers of outcome and safety in phase I/II trials.^15,34 Cardiovascular imaging improves evaluation of the effects of new therapies and devices during preclinical assessment. Animal models of congestive heart failure should allow noninvasive imaging during a long-term follow-up period.The Göttingen minipig was developed in the early 1960s at the Institute of Animal Breeding and Genetics (University of Göttingen, Germany) to reduce space requirements and housing costs for preclinical porcine studies.⁹ They were created by crossbreeding the Minnesota minipig with Vietnamese potbelly and German Landrace pigs.¹⁹ Göttingen minipigs are white miniature pigs with good fertility and stable genetics.Göttingen minipigs have a characteristic growth curve that avoids the dramatic increase in weight in adulthood seen in farm pigs.^25,26 A newborn Göttingen minipig has a body mass of 350 to 450 g. Boars become sexually mature at 3 to 4 mo of age, weighing 6 to 8 kg, whereas sows become sexually mature at 4 to 5 mo and 7 to 9 kg. The gestational period is 112 to 114 d, and the average litter size is 5 to 6 animals. Closure of the growth plates is complete at 18 to 22 mo and 30 to 35 kg. Göttingen minipigs have a mature body weight of 35 to 45 kg,¹⁰ and they achieve 40% of the maximal body weight at approximately 10 mo (310 d) with a body weight of 21 kg. In comparison intensively fed farm pigs reach 88 kg at the same time point, with a mature weight of 220 kg, and restrictively fed farm pigs, like Yorkshire swine, typically weigh about 64 kg at 10 mo of age and 160 kg at maturity.²⁶ Characteristics of Yorkshire swine are reported in the literature.¹¹Adult Göttingen minipigs are large enough to allow testing of human equipment and devices. Until now cardiovascular parameters have only been reported in juvenile Göttingen minipigs.^9,13 Here, we demonstrate the unique value of Göttingen minipigs as a novel adult porcine heart failure model for cardiac research in the fields of regenerative medicine, electrophysiology, and noninvasive imaging.     

Deficiency of Capn4 Gene Inhibits Nuclear Factor-κB (NF-κB) Protein Signaling/Inflammation and Reduces Remodeling after Myocardial Infarction

Calpain has been implicated in acute myocardial injury after myocardial infarction (MI). However, the causal relationship between calpain and post-MI myocardial remodeling has not been fully understood. This study examined whether deletion of Capn4, essential for calpain-1 and calpain-2 activities, reduces myocardial remodeling and dysfunction following MI, and if yes, whether these effects of Capn4 deletion are associated with NF-κB signaling and inflammatory responses in the MI heart. A novel mouse model with cardiomyocyte-specific deletion of Capn4 (Capn4-ko) was employed. MI was induced by left coronary artery ligation. Deficiency of Capn4 dramatically reduced the protein levels and activities of calpain-1 and calpain-2 in the Capn4-ko heart. In vivo cardiac function was relatively improved in Capn4-ko mice at 7 and 30 days after MI when compared with their wild-type littermates. Deletion of Capn4 reduced apoptosis, limited infarct expansion, prevented left ventricle dilation, and reduced mortality in Capn4-ko mice. Furthermore, cardiomyocyte cross-sectional areas and myocardial collagen deposition were significantly attenuated in Capn4-ko mice, which were accompanied by down-regulation of hypertrophic genes and profibrotic genes. These effects of Capn4 knock-out correlated with restoration of IκB protein and inhibition of NF-κB activation, leading to suppression of proinflammatory cytokine expression and inflammatory cell infiltration in the Capn4-ko heart after MI. In conclusion, deficiency of Capn4 reduces adverse myocardial remodeling and myocardial dysfunction after MI. These effects of Capn4 deletion may be mediated through prevention of IκB degradation and NF-κB activation, resulting in inhibition of inflammatory responses.     

Adjunctive Medical Therapy with α-Blocker after Extracorporeal Shock Wave Lithotripsy of Renal and Ureteral Stones: A Meta-Analysis

Background

Although some trials assessed the efficacy and safety of the α-blocker in facilitating renal and ureteral stones expulsion after extracorporeal shock wave lithotripsy (ESWL), the role of the α-blocker in facilitating upper urinary calculi expulsion after ESWL remain controversial.

Aims

To determine the efficacy and safety of the α-blocker in facilitating renal and ureteral stones expulsion after ESWL.

Methods

A literature search was carried out using the PubMed database, EMBASE and the Cochrane Library database to identify relevant studies. Two reviewers independently extracted data and assessed methodological quality. Pooled effect estimates were obtained using a fixed- and random-effects meta-analysis.

Results

The meta-analysis included 23 RCTs, α-blocker significantly enhanced expulsion rate of upper urinary tract calculi after ESWL (P<0.00001; RR 1.21; 95% CI 1.12–1.31), significantly promoted steinstrasse expulsion (P=0.03; RR 1.25; 95% CI 1.03–1.53), significantly shortened the discharge time of upper urinary tract calculi (P=0.0001; MD -2.12; 95% CI -3.20–-1.04), significantly reduced the patient''s pain VAS score (P=0.001; RR -1.0; 95% CI -1.61–-0.39). Compared with the control group, dizziness (P=0.002; RR 5.48; 95% CI 1.91–15.77), anejaculation (P=0.02; RR 12.17; 95% CI 1.61–91.99) and headache (P=0.04; RR 4.03; 95% CI 1.04–15.72) in the α-blocker group was associated with a higher incidence.

Conclusions

Treatment with α-blocker after ESWL appears to be effective in enhancing expulsion rate of upper urinary tract calculi, shortening the discharge time of upper urinary tract calculi, reducing the patient''s pain. The side effects of α-blocker were light and few.     

Comparison of Isoflurane and α-Chloralose in an Anesthetized Swine Model of Acute Pulmonary Embolism Producing Right Ventricular Dysfunction

Pulmonary embolism (PE) is a leading cause of sudden cardiac death, and a model is needed for testing potential treatments. In developing a model, we compared the hemodynamic effects of isoflurane and α-chloralose in an acute swine model of PE because the choice of anesthesia will likely affect the cardiovascular responses of an animal to PE. At baseline, swine that received α-chloralose (n = 6) had a lower heart rate and cardiac output and higher SpO_2, end-tidal CO_2, and mean arterial pressure than did those given isoflurane (n = 9). After PE induction, swine given α-chloralose compared with isoflurane exhibited a lower heart rate (63 ± 10 compared with 116 ± 15 bpm) and peripheral arterial pressure (52 ± 12 compared with 61 ± 12 mm Hg); higher SpO₂ (98% ± 3% compared with 95% ± 1%), end-tidal CO₂ (35 ± 4 compared with 32 ± 5), and systolic blood pressure (121 ± 8 compared with 104 ± 20 mm Hg); and equivalent right ventricular:left ventricular ratios (1.32 ± 0.50 compared with 1.23 ± 0.19) and troponin I mean values (0.09 ± 0.07 ng/mL compared with 0.09 ± 0.06 ng/mL). Isoflurane was associated with widely variable fibrinogen and activated partial thromboplastin time. Intraexperiment mortality was 0 of 6 animals for α-chloralose and 2 of 9 swine for isoflurane. All swine anesthetized with α-chloralose survived with sustained pulmonary hypertension, RV-dilation-associated cardiac injury without the confounding vasodilatory or coagulatory effects of isoflurane. These data demonstrate the physiologic advantages of α-chloralose over isoflurane for anesthesia in a swine model of severe submassive PE.Abbreviations: LV, left ventricle; PAP, pulmonary arterial pressure; PE, pulmonary embolism; RV, right ventriclePulmonary embolism (PE) is one of the leading causes of noncardiac sudden death in Western nations and is the third most common cause of cardiovascular morbidity.^4,6,7,18 In survivors, severe PE damages the right heart, leading to a clinical course complicated by hypotension and circulatory shock, suggesting acute right heart failure in about 10% of patients and followed by persistent pulmonary hypertension or right ventricular dysfunction and dyspnea in at least 15% of patients.^{9,15,16,23,29} To test treatments to reduce right heart failure, a standardized model that is repeatable, accurate, and precise and that mimics the gross pathologic, cardiovascular, pulmonary, autonomic, hematologic, biochemical, and cellular characteristics of PE in humans with disease is needed.⁸Three lines of rationale favor domestic pigs as a model for PE. Several publications, using different methods of anesthesia, have found that swine manifest hemodynamic responses similar to those of humans in the presence of autologous PE, including elevated heart rate, decreased cardiac output, and reduced oxygen saturation.^2,12,30 Swine have similar platelet concentrations, and their coagulation profile on thromboelastography has been shown to be similar to humans, with the exception of higher fibrin crosslinking but less fibrin, leading to resistance to plasmin.^5,11,19,34 Market swine, which would otherwise be destined for slaughter, are relatively cost effective compared with other large animals and are of sufficient size for placement of an adult pulmonary arterial catheter for measurement of pulmonary vascular resistance in a closed-chest preparation.In view of the differences in the hemodynamic effects of different anesthetic agents, the choice of anesthesia will likely affect the cardiovascular responses of an animal to PE. However, current literature lacks a methodologic publication that compares the cardiovascular, right ventricular, pulmonary, and hematologic responses to PE in closed-chest swine models incorporating different anesthetic regimens.Figure 1 presents features of an ideal animal model for the purpose of testing treatments for PE. To develop a swine model of PE that closely resembles this physiologic ideal model, we induced PE in swine maintained in a surgical plane of anesthesia with either isoflurane or α-chloralose. Each of these agents has potential advantages and disadvantages. Isoflurane can be titrated minute by minute but causes undesirable vasodilation, whereas α-chloralose is believed to preserve cardiovascular reflexes but requires heating to dissolve and continuous infusion or repeated boluses.^26,35 We hypothesized that, compared with isoflurane, α-chloralose would meet more of the features described in Figure 1.Open in a separate windowFigure 1.Desirable features of large animal model of severe submassive PE designed for translational research.     

Cardiac-Specific Inhibition of Kinase Activity in Calcium/Calmodulin-Dependent Protein Kinase Kinase-β Leads to Accelerated Left Ventricular Remodeling and Heart Failure after Transverse Aortic Constriction in Mice

Background

The mechanism of cardiac energy production against sustained pressure overload remains to be elucidated.

Methods and Results

We generated cardiac-specific kinase-dead (kd) calcium/calmodulin-dependent protein kinase kinase-β (CaMKKβ) transgenic (α-MHC CaMKKβ^kd TG) mice using α-myosin heavy chain (α-MHC) promoter. Although CaMKKβ activity was significantly reduced, these mice had normal cardiac function and morphology at baseline. Here, we show that transverse aortic binding (TAC) in α-MHC CaMKKβ^kd TG mice led to accelerated death and left ventricular (LV) dilatation and dysfunction, which was accompanied by significant clinical signs of heart failure. CaMKKβ downstream signaling molecules, including adenosine monophosphate-activated protein kinase (AMPK), were also suppressed in α-MHC CaMKKβ^kd TG mice compared with wild-type (WT) mice. The expression levels of peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α, which is a downstream target of both of CaMKKβ and calcium/calmodulin kinases, were also significantly reduced in α-MHC CaMKKβ^kd TG mice compared with WT mice after TAC. In accordance with these findings, mitochondrial morphogenesis was damaged and creatine phosphate/β-ATP ratios assessed by magnetic resonance spectroscopy were suppressed in α-MHC CaMKKβ^kd TG mice compared with WT mice after TAC.

Conclusions

These data indicate that CaMKKβ exerts protective effects on cardiac adaptive energy pooling against pressure-overload possibly through phosphorylation of AMPK and by upregulation of PGC-1α. Thus, CaMKKβ may be a therapeutic target for the treatment of heart failure.     

Characterization of a glycoside hydrolase family 42 ��-galactosidase from Deinococcus geothermalis

A putative recombinant β-galactosidase from Deinococcus geothermalis was purified as a single 79 kDa band of 42 U activity/mg using His-Trap affinity chromatography. The molecular mass of the native enzyme was a 158 kDa dimer. The catalytic residues E151 and E325 of β-galactosidase from D. geothermalis were conserved in all aligned GH family 42 β-galactosidases, indicating that this enzyme is also a GH family 42 β-galactosidase. Maximal activity of the enzyme was at pH 6.5 and 60°C. It has a unique hydrolytic activity for p-nitrophenyl(pNP)-β-D-galactopyranoside (k (cat)/K (m) = 69 s(-1) mM(-1)), pNP-β-D-fucopyranoside (13), oNP-β-D-galactopyranoside (9.5), oNP-β-D-fucopyranoside (2.6), lactose (0.97), and pNP-α-L-arabinopyranoside (0.78), whereas no activity, or less than 2% of the pNP-β-D-galactopyranoside activity, for other pNP- and oNP-glycosides.     

Characterization of a chalcone synthase (CHS) flower-specific promoter from Lilium orential ��Sorbonne��

The first enzyme in the flavonoid pathway, chalcone synthase, is encoded by a gene (CHS) whose expression is normally under developmental control. In our previous studies, an 896-bp promoter region of a flower-specific CHS gene was isolated from Lilium orential ‘Sorbonne’, and designated as PLoCHS. Here, the PLoCHS promoter was fused to the β-glucuronidase (GUS) gene to characterize its spatial and temporal expression in Petunia hybrida ‘Dreams Midnight’ using an Agrobacterium-mediated leaf disc transformation method. Our results demonstrated that GUS expression was present in flowers, but reduced or absent in the other tissues (leaf and stem) examined. In petals, GUS activity reached its peak at flower developmental stage 4, and decreased at later stages. Deletion analysis indicated that even a 307-bp fragment of the PLoCHS promoter could still direct flower-specific expression. Further deletion of the region from −261 to −72 bp resulted in weak expression in different organs, including flowers, leaves and stems. This evidence combined with prediction of cis-acting elements in the PLoCHS promoter suggests that the TACPyAT box located in this promoter plays a key role in the regulation of organ-specific expression.     

The Vaginal Microbiota: What Have We Learned after a Decade of Molecular Characterization?

We conducted a systematic review of the Medline database (U.S. National Library of Medicine, National Institutes of Health, Bethesda, MD, U.S.A) to determine if consistent molecular vaginal microbiota (VMB) composition patterns can be discerned after a decade of molecular testing, and to evaluate demographic, behavioral and clinical determinants of VMB compositions. Studies were eligible when published between 1 January 2008 and 15 November 2013, and if at least one molecular technique (sequencing, PCR, DNA fingerprinting, or DNA hybridization) was used to characterize the VMB. Sixty three eligible studies were identified. These studies have now conclusively shown that lactobacilli-dominated VMB are associated with a healthy vaginal micro-environment and that bacterial vaginosis (BV) is best described as a polybacterial dysbiosis. The extent of dysbiosis correlates well with Nugent score and vaginal pH but not with the other Amsel criteria. Lactobacillus crispatus is more beneficial than L. iners. Longitudinal studies have shown that a L. crispatus-dominated VMB is more likely to shift to a L. iners-dominated or mixed lactobacilli VMB than to full dysbiosis. Data on VMB determinants are scarce and inconsistent, but dysbiosis is consistently associated with HIV, human papillomavirus (HPV), and Trichomonas vaginalis infection. In contrast, vaginal colonization with Candida spp. is more common in women with a lactobacilli-dominated VMB than in women with dysbiosis. Cervicovaginal mucosal immune responses to molecular VMB compositions have not yet been properly characterized. Molecular techniques have now become more affordable, and we make a case for incorporating them into larger epidemiological studies to address knowledge gaps in etiology and pathogenesis of dysbiosis, associations of different dysbiotic states with clinical outcomes, and to evaluate interventions aimed at restoring and maintaining a lactobacilli-dominated VMB.     

Lung Remodeling in a Mouse Model of Asthma Involves a Balance between TGF-β1 and BMP-7

A key event in chronic allergic asthma is the TGF-β-induced activation of fibroblasts into α-SMA-positive myofibroblasts which synthesize type-I collagen. In the present study we investigated the effect of the anti-fibrotic molecule BMP-7 in asthma. Balb/c mice were immunized i.p. with ovalbumin in alum and challenged every 2 days with ovalbumin aerosol (two or six challenges for acute and chronic protocols, respectively). The lung was evaluated for: α-SMA and type-I collagen by immunohistochemistry; BMP-7 and TGF- β1 gene expression by qRT-PCR; type-I collagen and Smads 2 and 3 by immunoblotting; mucus by PSA staining. Type-I collagen around bronchi, α-SMA, mucus secretion, TGF- β1 and BMP-7 gene expression were all increased in asthma. The TGF- β1/BMP-7 ratio was higher in the chronic group and correlated with higher levels of collagen. Fibroblasts isolated from asthmatic and healthy lungs produced type-I collagen upon stimulation with TGF- β1 via phosphorylation of Smad-2, Smad-3. Pre-treatment of the fibroblasts with BMP-7 reduced collagen production and Smads phosphorylation. Intranasal treatment of asthmatic mice with recombinant BMP-7 during the immunization protocol reduced lung inflammation and type I collagen deposition. These results suggest a protective role for BMP-7 in lung allergic inflammation, opposing the pro-fibrotic effects of TGF- β1.     

Ventricular arrhythmias after reperfusion: is there a correlation with infarct size?

The aim of this investigation was to examine whether any correlation exists between enzymatically estimated infarct size and arrhythmias arising in response to coronary reperfusion. Four hour occlusion of the left anterior coronary artery followed by reperfusion was carried out in conscious dogs. Serum creatine phosphokinase (CPK) analysis and planimetric determination of infarct size were performed. The Holter monitoring technique was used to analyze the arrhythmias. A good correlation was observed between the number of premature ventricular complexes (PVC) occurring during 4-h coronary artery occlusion and peak serum CPK values (CPKmax; r = 0.74). While PVC in the early 2-h reperfusion phase and on days 1 and 2 of the late reperfusion phase did not show a correlation with CPKmax nor with occlusion arrhythmias, arrhythmic activity on day 3 of the late reperfusion phase correlated well with CPKmax (r = 0.71) and occlusion arrhythmias (r = 0.75). Whereas it cannot be ruled out that arrhythmias on days 1 and 2 are related to coronary reperfusion as well as to the established infarction, we speculated that arrhythmias on day 3 are delayed arrhythmias in response to the occlusion procedure and not a consequence of reperfusion. Providing that arrhythmias occurring in the early reperfusion phase are almost exclusively induced by the arrhythmogenic phenomenon of reperfusion, we conclude that in contrast to occlusion arrhythmias, reperfusion arrhythmias are not markers of infarct size. Thus, a higher number of arrhythmias after reperfusion is not necessarily associated with a larger infarct size.     

Frequency of Antibiotic Resistance in a Swine Facility 2.5 Years After a Ban on Antibiotics

The addition of antibiotics to livestock feed has contributed to the selection of antibiotic-resistant bacteria in concentrated animal feeding operations and agricultural ecosystems. The objective of this study was to assess the occurrence of resistance to chlortetracycline and tylosin among bacterial populations at the Swine Complex of McGill University (Province of Quebec, Canada) in the absence of antibiotic administration to pigs for 2.5 years prior to the beginning of this study. Feces from ten pigs born from the same sow and provided feed without antibiotic were sampled during suckling (n = 6 for enumerations, n = 10 for PCR), weanling (n = 10 both for PCR and enumerations), growing (n = 10 both for PCR and enumerations), and finishing (n = 10 both for PCR and enumerations). The percentage of chlortetracycline-resistant anaerobic bacterial populations (Tet^R) was higher than that of tylosin-resistant anaerobic bacterial populations (Tyl^R) at weanling, growing, and finishing. Prior to the transportation of animals to the slaughterhouse, resistant populations varied between 6.5 and 9.4 Log colony-forming units g humid feces⁻¹. In all pigs, tet(L), tet(O), and erm(B) were detected at suckling and weanling, whereas only tet(O) was detected at growing and finishing. The abundance of tet(O) was similar between males and females at weanling and growing and reached 5.1 × 10⁵ and 5.6 × 10⁵ copies of tet(O)/ng of total DNA in males and females, respectively, at finishing. Results showed high abundances and proportions of Tet^R and Tyl^R anaerobic bacterial populations, as well as the occurrence of tet and erm resistance genes within these populations despite the absence of antibiotic administration to pigs at this swine production facility since January 2007, i.e., 2.5 years prior to the beginning of this study. This work showed that the occurrence of bacterial resistance to chlortetracycline and tylosin is high at the Swine Complex of McGill University.