Yes / Recent clinical trials of the hypoglycaemic sodium-glucose co-transporter-2 (SGLT2) inhibitors, which inhibit renal glucose reabsorption, have reported beneficial cardiovascular outcomes. Whether SGLT2 inhibitors directly affect cardiovascular tissues, however, remains unclear. We have previously reported that the SGLT2 inhibitor canagliflozin activates AMP-activated protein kinase (AMPK) in immortalised cell lines and murine hepatocytes. As AMPK has anti-inflammatory actions in vascular cells, we examined whether SGLT2 inhibitors attenuated inflammatory signalling in cultured human endothelial cells. Incubation with clinically-relevant concentrations of canagliflozin, but not empagliflozin or dapagliflozin activated AMPK and inhibited IL-1β-stimulated adhesion of pro-monocytic U937 cells and secretion of IL-6 and monocyte chemoattractant protein-1 (MCP-1). Inhibition of MCP-1 secretion was attenuated by expression of dominant-negative AMPK and was mimicked by the direct AMPK activator, A769662. Stimulation of cells with either canagliflozin or A769662 had no effect on IL-1β-stimulated cell surface levels of adhesion molecules or nuclear factor-κB signalling. Despite these identical effects of canagliflozin and A769662, IL-1β-stimulated IL-6/MCP-1 mRNA was inhibited by canagliflozin, but not A769662, whereas IL-1β-stimulated c-jun N-terminal kinase phosphorylation was inhibited by A769662, but not canagliflozin. These data indicate that clinically-relevant canagliflozin concentrations directly inhibit endothelial pro-inflammatory chemokine/cytokine secretion by AMPK-dependent and -independent mechanisms without affecting early IL-1β signalling. / Project Grant (PG/13/82/30483 to IPS and TMP) and PhD studentships (FS/16/55/32731 and FS/14/61/31284 to DB and AS) from the British Heart Foundation and an equipment grant (BDA11/0004309 to IPS and TMP) from Diabetes UK. OJK was supported by a Scholarship from the Iraqi Ministry of Higher Education and Scientific Research. TAA was supported by a Libyan Ministry of Education PhD Studentship.

Chemerin is a chemoattractant adipokine that regulates adipogenesis and may induce insulin resistance. Chemerin serum concentrations are elevated in obese, insulin-resistant, and inflammatory states in vivo. Here we investigate the role of omental (OM) and subcutaneous (SC) adipose tissue chemerin and CMKLR1 messenger RNA (mRNA) expression in human obesity. In addition, we test the hypothesis that changes in chemerin serum concentrations are primarily associated with reduced body fat mass in the context of 3 weight loss intervention studies. Chemerin serum concentration was measured in 740 individuals in a cross-sectional (n = 629) study including a subgroup (n = 161) for which OM and SC chemerin mRNA expression has been analyzed as well as in 3 interventions including 12 weeks of exercise (n = 60), 6 months of calorie-restricted diet (n = 19) studies, and 12 months after bariatric surgery (n = 32). Chemerin mRNA is significantly higher expressed in adipose tissue of patients with type 2 diabetes mellitus and correlates with circulating chemerin, body mass index (BMI), percentage body fat, C-reactive protein, homeostasis model assessment of insulin resistance, and glucose infusion rate in euglycemic-hyperinsulinemic clamps. CMKLR1 mRNA expression was not significantly different between the 2 fat depots. Obesity surgery–induced weight loss causes a significant reduction on both OM and SC chemerin expression. All interventions led to significantly reduced chemerin serum concentrations. Decreased chemerin serum concentrations significantly correlate with improved glucose infusion rate and reduced C-reactive protein levels independently of changes in BMI. Insulin resistance and inflammation are BMI-independent predictors of elevated chemerin serum concentrations. Reduced chemerin expression and serum concentration may contribute to improved insulin sensitivity and subclinical inflammation beyond significant weight loss.

Chemerin is a chemoattractant adipokine that regulates adipogenesis and may induce insulin resistance. Chemerin serum concentrations are elevated in obese, insulin-resistant, and inflammatory states in vivo. Here we investigate the role of omental (OM) and subcutaneous (SC) adipose tissue chemerin and CMKLR1 messenger RNA (mRNA) expression in human obesity. In addition, we test the hypothesis that changes in chemerin serum concentrations are primarily associated with reduced body fat mass in the context of 3 weight loss intervention studies. Chemerin serum concentration was measured in 740 individuals in a cross-sectional (n = 629) study including a subgroup (n = 161) for which OM and SC chemerin mRNA expression has been analyzed as well as in 3 interventions including 12 weeks of exercise (n = 60), 6 months of calorie-restricted diet (n = 19) studies, and 12 months after bariatric surgery (n = 32). Chemerin mRNA is significantly higher expressed in adipose tissue of patients with type 2 diabetes mellitus and correlates with circulating chemerin, body mass index (BMI), percentage body fat, C-reactive protein, homeostasis model assessment of insulin resistance, and glucose infusion rate in euglycemic-hyperinsulinemic clamps. CMKLR1 mRNA expression was not significantly different between the 2 fat depots. Obesity surgery–induced weight loss causes a significant reduction on both OM and SC chemerin expression. All interventions led to significantly reduced chemerin serum concentrations. Decreased chemerin serum concentrations significantly correlate with improved glucose infusion rate and reduced C-reactive protein levels independently of changes in BMI. Insulin resistance and inflammation are BMI-independent predictors of elevated chemerin serum concentrations. Reduced chemerin expression and serum concentration may contribute to improved insulin sensitivity and subclinical inflammation beyond significant weight loss.

Background: The beneficial impact of mesenchymal stem cells (MSC) on both acute and chronic liver diseases has been confirmed, although the molecular mechanisms behind it remain elusive. We aim to identify factors secreted by undifferentiated and hepatocytic differentiated MSC in vitro in order to delineate liver repair pathways potentially targeted by MSC. Methods: Secreted factors were determined by protein arrays and related pathways identified by biomathematical analyses. Results: MSC from adipose tissue and bone marrow expressed a similar pattern of surface markers. After hepatocytic differentiation, CD54 (intercellular adhesion molecule 1, ICAM-1) increased and CD166 (activated leukocyte cell adhesion molecule, ALCAM) decreased. MSC secreted different factors before and after differentiation. These comprised cytokines involved in innate immunity and growth factors regulating liver regeneration. Pathway analysis revealed cytokine-cytokine receptor interactions, chemokine signalling pathways, the complement and coagulation cascades as well as the Januskinase-signal transducers and activators of transcription (JAK-STAT) and nucleotide-binding oligomerization domain-like receptor (NOD-like receptor) signalling pathways as relevant networks. Relationships to transforming growth factor beta(TGF-beta) and hypoxia-inducible factor 1-alpha (HIF1-alpha) signalling seemed also relevant. Conclusion: MSC secreted proteins, which differed depending on cell source and degree of differentiation. The factors might address inflammatory and growth factor pathways as well as chemo-attraction and innate immunity. Since these are prone to dysregulation in most liver diseases, MSC release hepatotropic factors, potentially supporting liver regeneration.

Le dysfonctionnement endothélial et le dérèglement du système immunitaire sont les deux principaux mécanismes physiopathologiques responsables de la fibrose de la peau et des organes internes dans la sclérodermie systémique (ScS). La pneumopathie interstitielle diffuse (PID) est devenue la principale cause de mortalité de la maladie. L'inflammation pulmonaire est la conséquence de l'activation du système immunitaire, qui stimule la NO synthase inductible (NOS-2) et augmente la production alvéolaire de monoxyde d'azote (NO). L'augmentation de la concentration alvéolaire de NO (CANO) est significativement corrélée à la sévérité de la PID chez les patients atteints de ScS. L'augmentation de la CANO est liée à l'effet inducteur du sérum des malades sur la prolifération des fibroblastes pulmonaires et leur différentiation en myofibroblastes, faisant ainsi le lien biologique entre l'inflammation alvéolaire et la fibrose pulmonaire dans la ScS. Nous avons ensuite testé la valeur prédictive de la CANO dans la détérioration de la PID. Les patients ayant une CANO supérieure à 5,3 ppb présentent un risque élevé (> 6 fois) de voir survenir l'aggravation de la fibrose pulmonaire ou le décès (évènement combiné) par rapport à ceux qui ont une CANO inférieure ou égale à 5,3 ppb. Une valeur de CANO supérieure ou égale à 8,5 ppb permet de détecter les patients avec un risque de 90% de survenue d'évènement combiné dans les trois ans. Ces patients pourraient alors bénéficier d'un traitement approprié précoce. Nous avons évalué l'inflammation pulmonaire dans deux modèles murins de fibrose pulmonaire induite par l'acide hypochloreux et la bléomycine, par la mesure non-invasive du NO expiré (FENO). Le pic d'augmentation de FENO se situe 4 semaines après le début des injections, et précède la fibrose pulmonaire, qui ne devient significative qu'à partir de 6 semaines d'intoxication. L'augmentation de la FENO est liée à l'augmentation de l'expression de la NOS-2 aussi bien aux niveaux des bronches qu'aux niveaux des alvéoles. Enfin, la forte production de NO constatée provoque un effet délétère direct sur le tissu pulmonaire attesté par la présence de 3-nitrotyrosines, marqueurs du stress nitrosatif.Mots-clés: sclérodermie systémique, pneumopathie interstitielle diffuse, monoxyde d'azote, physiopathologie. / Summary not transmitted

Mieloma Múltiplo é a segunda doença com maior prevalência nas doenças malignidades hematológica, incurável com média de sobrevivência de 3-5 anos. MM é uma malignidade das células do plasma caracterizada pela destruição e reabsorção óssea e supressão da formação do osso. A quimiocina SDF-1 (CXCL12) e seu receptor CXCR4 têm um importante papel direcional na migração, homing das células do plasma em mieloma múltiplo e mobilização das células de MM para fora da medula óssea. A talidomida tem sido usada com êxito no tratamento de pacientes com mieloma múltiplo. Neste estudo verificamos o efeito da talidomida na expressão da quimiocina SDF-1 e seu receptor CXCR4 em pacientes com mieloma múltiplo e em linhagem de células de mieloma múltiplo humano (RPMI-8226) tratados e sem tratamento de talidomida. Nossos resultamos mostraram uma expressão heterogênea na expressão da quimiocina SDF-1 e seu receptor CXCR4 nos pacientes com mieloma múltiplo estudado (n= 79). Entretanto, pacientes com mieloma múltiplo tratados com talidomida mostraram uma baixa expressão da quimiocina SDF-1 e seu receptor CXC4 quando comparados com pacientes recém diagnosticados para mieloma múltiplo e pacientes com mieloma múltiplo tratados com outros medicamentos. Nossos resultados sugerem que o tratamento com talidomida induz uma baixa regulação na expressão no ligante SDF-1 e seu receptor CXCR4 em pacientes com mieloma múltiplo / Multiple Myeloma (MM) is a second most prevalent hematological malignancy and remains incurable with a median survival of 3-5 years. MM is a plasma cell malignancy characterized by devastating bone destruction due to the enhanced bone resorption and suppressed bone formation. The chemokine stromal-derived factor-1 (SDF-1) and its receptor CXCR4 play an important role in directional migration, homing of plasma cells in multiple myeloma (MM) and mobilization of MM cells out of the bone marrow. The drug thalidomide has been successfully used in the treatment of patients with MM. In this study, we assessed the effect of thalidomide on SDF-1 and CXCR4 expression in MM patients and human myeloma-derived cell line, RPMI 8226 treated with or without thalidomide. A heterogeneous expression pattern of chemokines SDF-1 and CXCR4 receptor were observed for all MM patients studied. However, patients treated with thalidomide showed a significantly decrease in expression of SDF-1 and CXCR4 as compared to newly diagnosed MM patients and MM patients treated with other drugs. RPMI 8226 cell line treated with 10, 20 and 100µM thalidomide also demonstrated decrease in SDF-1 and CXCR4 expression as compared with cell control (RPMI-8226 without thalidomide). Ours results indicate that thalidomide therapy induces down-regulation of CXCR4 and its ligand SDF-1 in multiple myeloma

Tanto a invasão local como o comprometimento de linfonodos cervicais tem grande impacto na sobrevida de pacientes portadores de carcinomas epidermóides de cabeça e pescoço. Em nosso trabalho nós primeiramente determinamos a expressão dos receptores de quimiocinas de CXCR1 a CXCR5, além de CCR7 e CX3CR1 pelo método do ensaio de proteção à ribonuclease (RPA) em 98 fragmentos de tumores primários, 91 fragmentos de mucosas adjacentes e 26 linfonodos comprometidos e correlacionamos estes dados com parâmetros anátomo-patológicos e sobrevida. CXCL12 ligante do receptor CXCR4 e CCL19 e CCL21 ambos ligantes de CCR7 foram determinados em 38 fragmentos de tumores, 33 mucosas adjacentes e 25 linfonodos comprometidos pela técnica de real-time PCR. Os tumores primários apresentam expressão aumentada do mRNA de CXCR1 (P=0.013), CXCR3 (P=0.008) e CXCR4 (P=0.025). Não observamos correlações entre status linfonodal ou tamanho de tumor. Os linfonodos comprometidos expressam mais mRNA dos receptores de quimiocinas CXCR4, CXCR5, CCR7 e CX3CR1 (todos com P<0.0001) em comparação aos tumores comprometidos. Observamos um aumento de sobrevida (P=0.048) e uma tendência a aumento de sobrevida livre de doença (P=0.074) nos pacientes negativos para a expressão de CX3CR1 (n=17) em comparação aos pacientes positivos (n=21) somente no subgrupo de pacientes portadores de carcinomas da cavidade oral. O mesmo foi observado com os pacientes CCR7 negativos também no subgrupo de pacientes portadores de carcinomas da cavidade oral, tanto em sobrevida global (P=0.024) como para sobrevida livre de doença (P=0.049). Em relação aos ligantes de quimiocinas observamos um aumento do mRNA de CCL21 em linfonodos comprometidos em relação aos tumores primários (P=0.059). Concluímos que a interação quimiotática entre CCR7 e de seu ligante CCL21, poderia ser um mecanismo de atração de células tumorais para os linfonodos em tumores de cavidade oral, além disso a negatividade da expressão do mRNA de CCR7 e CX3CR1 são candidatos marcadores de uma melhor sobrevida em carcinomas epidermóides de cavidade oral. / Local invasion and lymph nodal spread impact in the outcome of Head and Neck squamous cell carcinoma (HNSCC) patients (pts). We determined CXCR1-5, CCR7 and CX3CR1 mRNA expression by means of RNAse protection assay in 98 HNSCC primary tumors and 91 adjacent mucosa and 26 metastatic lymph nodes, correlating this data with outcome. CXCL12 and CCL19/CCL21, ligands for CXCR4 and CCR7, were determined in 38 tumor fragments, 33 adjacent mucosas and 25 de metastatic lymph nodes, by means of Quantitative Real-Time PCR. Tumors presented higher CXCR1 (P=0.013), CXCR3 (P=0.008) and CXCR4 mRNA (P=0.025) expression as compared to mucosa. No correlations are observed neither lymph nodal status nor tumor size impacted on chemokine receptor expression. Metastatic lymph nodes expressed more CXCR4, CXCR5, CCR7 and CX3CR1 (P<0.0001) as compared to matched tumors. We found a longer overall survival (OS) (P=0.048) and a trend toward longer disease free survival (DFS) (P=0.074) in CX3CR1 negative (n=17) as compared to positive pts (n=21) only in oral subgroup. The same occurred for CCR7 negative oral SCC, in terms of OS (P=0.024) and DFS (P=0.049). We conclude that, of the chemokine receptors here studied, CCR7 and CX3CR1 mRNA expression seems to better reflect outcome in oral subsite only. In addition, CCL21, a CCR7 ligand mRNAs is more expressed in metastatic lymph nodes than tumors (P=0.059). Further studies are warranted to confirm these results.

Local invasion and lymph nodal spread impact in the outcome of Head and Neck squamous cell carcinoma (HNSCC) patients (pts). We determined CXCR1-5, CCR7 and CX3CR1 mRNA expression by means of RNAse protection assay in 98 HNSCC primary tumors and 91 adjacent mucosa and 26 metastatic lymph nodes, correlating this data with outcome. CXCL12 and CCL19/CCL21, ligands for CXCR4 and CCR7, were determined in 38 tumor fragments, 33 adjacent mucosas and 25 de metastatic lymph nodes, by means of Quantitative Real-Time PCR. Tumors presented higher CXCR1 (P=0.013), CXCR3 (P=0.008) and CXCR4 mRNA (P=0.025) expression as compared to mucosa. No correlations are observed neither lymph nodal status nor tumor size impacted on chemokine receptor expression. Metastatic lymph nodes expressed more CXCR4, CXCR5, CCR7 and CX3CR1 (P<0.0001) as compared to matched tumors. We found a longer overall survival (OS) (P=0.048) and a trend toward longer disease free survival (DFS) (P=0.074) in CX3CR1 negative (n=17) as compared to positive pts (n=21) only in oral subgroup. The same occurred for CCR7 negative oral SCC, in terms of OS (P=0.024) and DFS (P=0.049). We conclude that, of the chemokine receptors here studied, CCR7 and CX3CR1 mRNA expression seems to better reflect outcome in oral subsite only. In addition, CCL21, a CCR7 ligand mRNAs is more expressed in metastatic lymph nodes than tumors (P=0.059). Further studies are warranted to confirm these results. / Bone tissue alterations and vascular calcification (VC) are commonly found in patients with chronic renal failure (CKD). The importance of phosphorus (P) and parathyroid hormone (PTH) is not clear, yet. An in vitro study showed that inorganic phosphate was able to transform vascular smooth muscle cells (VSMC) into calcifying cells confirmed for up-expression of Runx2 in these cells. Besides, it has been demonstrated the in vivo expression of Runx2 in intimal and medial VSMC in calcified arteries of CKD patients. We evaluated the effect of phosphorus (P) and parathyroid hormone (PTH) on bone remodeling and on the expression of bone proteins (Runx2, Osteoprotegerin, type I Collagen, Osteocalcin, Osteopontin and NF?B) in aortic valve and heart in experimental uremia. Wistar rats were submitted to parathyroidectomy, nephrectomy (Nx) and continuous infusion of 1-34 rat PTH in physiologic or 5 times the normal values. The diet was identical, however the P content was low (LP: 0,2%) or high (HP: 1,2%). We performed biochemical, histomorphometric, imuno-histochemistry and RT-PCR analysis. Rats submitted to Nx developed renal failure. The P overload contributed to loss bone volume independent of uremia. Besides Nx animals that received high PTH doses bone loss was slight probably because of the anabolic effect of PTH, which was attenuated by the phosphorus overload toxic. VC was only observed in Nx animals that received high PTH doses independently of P overload. However, the P overload with physiologic PTH doses induced phenotypic changes in VSMC that was confirmed for the up-expression of Runx2 on aorta of these animals. The high concentrations of P and PTH promoted histological changes on expression of osteoprotegerin and type I Collagen in calcified arteries and heart. This study does not established ideal levels of PTH sufficient for the maintenance of the bone integrity and also to prevent VC when animal are submitted to different P overload.

Bei der Kreuzpräsentation durch dendritische Zellen (DC) werden extrazelluläre Antigene in den MHC I-Präsentationsweg eingeschleust und CD8+ T-Zellen präsentiert. Bisher werden die kreuzpräsentierenden DC der Maus durch die Expression der Moleküle CD8 in der Milz und CD103 in der Peripherie abgegrenzt; der kreuzpräsentierende Subtyp primärer humaner DC war vor Beginn dieser Arbeit nicht bekannt. Innerhalb dieser Arbeit konnte erstmals eine durchflusszytometrische Färbung von XCR1 auf der Oberfläche von Zellen etabliert werden, wodurch demonstriert wurde, dass XCR1 auf 83 % der CD8+ und 4 % der CD8-CD4- DC der Milz exprimiert wird. Der Phänotyp der XCR1+ DC der Milz unterschied sich deutlich von dem der XCR1- DC. In Milzen von Batf3- und Irf 8-defizienten Mäusen konnten keine XCR1+ DC detektiert werden. Zudem wurde nach Applikation des Wachstumsfaktors Flt3 Ligand in C57BL/6 Mäusen der Anteil der XCR1+ DC signifikant erhöht. Diese Ergebnisse verdeutlichen, dass die Entwicklung der XCR1+ DC von diesen Faktoren abhängig ist. Funktionell waren die XCR1+ DC wesentlich effektiver in der Kreuzpräsentation von löslichen und zellassoziierten Antigenen. Damit kann XCR1 als Oberflächenmarker verwendet werden, um murine kreuzpräsentierende DC zu kennzeichnen. Um herauszufinden, ob XCR1+ DC auch im Menschen existieren, wurde die Expression von XCR1 auf Zellen des humanen peripheren Blutes anhand von qPCR und Durchflusszytometrie untersucht. Ausschließlich CD141+ DC exprimierten XCR1-mRNA und -Protein. Durch die Etablierung einer effektiven Sortierungsstrategie zur Isolierung aller DC-Subtypen konnte erstmals gezeigt werden, dass die CD141+ DC den einzigen effektiven kreuzpräsentierenden DC-Subtyp des Blutes darstellen. XCR1 ist somit auch im humanen System spezifisch auf kreuzpräsentierenden DC exprimiert. Zusammengefasst zeigen die Ergebnisse, dass es sich bei den XCR1+ DC der Maus und des Menschen um funktionelle Homologe handelt. / Cross-presentation by dendritic cells (DC) is a process, in which extracellular antigen is shunted into the MHC I presentation pathway and presented to CD8+ T cells. So far, murine cross-presenting DC were defined by the expression of the molecules CD8 in the spleen and CD103 in the periphery. However, cross-presenting DC have not been characterized in humans. In this work, a flow cytometric staining of XCR1 was established for the first time which allowed the detection of XCR1 on 83 % of CD8+ DC and 4 % of CD8-CD4- DC of the spleen. The phenotype of splenic XCR1+ DC differed markedly from XCR1- DC. Both, Batf3- and Irf 8-deficient mouse strains showed an absence of splenic XCR1+ DC. Furthermore, the frequency of XCR1+ DC was significantly increased in spleens of C57BL/6 mice treated with Flt3 ligand. These results demonstrate that the development of XCR1+ DC is dependent of these factors. To test the ability to cross-present antigen, all splenic conventional DC were sorted according to their expression of CD8 and XCR1. XCR1+ DC were most efficient in cross-presenting soluble and cell-associated antigen to CD8+ T cells. Therefore, XCR1 is the first surface marker that can be used to delineate murine cross-presenting DC and the development of this distinct DC population is strongly dependent on Batf3, IRF-8 and Flt3 ligand. To explore if XCR1+ DC also exist in men, cell populations of human peripheral blood were analysed for their XCR1-expression using qPCR and flow cytometric staining. Only CD141+ DC express XCR1 mRNA and protein. An efficient sorting strategy for the isolation of all DC subsets was established to compare their ability to cross-present soluble and cell-associated antigen. CD141+ DC were the only effective cross-presenting DC subtype. Therefore, XCR1 is also in the human a receptor expressed specifically on cross-presenting DC. In summary, the data show that the XCR1+ DC of mouse and men are functional homologues.

Prostatacancer är en av världens vanligaste cancerformer. Varje år diagnostiseras ungefär 1,3 miljoner män världen över med prostatacancer och trots det vet man inte de bakomliggande orsakerna. Det finns flera studier som visar att det finns en koppling mellan infektion och olika typer av cancer och Cutibacterium acnes återfinns i hög utsträckning i prostatacancervävnad. Det har därför föreslagits att det finns ett samband mellan infektion av C. acnes och prostatacancer. Närvaro av tumörassocierade makrofager har visats sig vara gynnande för olika typer av cancer och från dessa makrofager frisätts kemokiner, bland annat CCL22. CCL22 kan vara inblandad i en lokal hämning av immunförsvaret som ofta förknippas med tillväxt av cancer. I detta arbete odlas makrofager från blodgivare med C. acnes för att ta reda på om makrofagerna ökar sitt uttryck av CCL22 mRNA. Genom att analysera resultaten från en kvantitativ realtids-PCR indikeras det att makrofager som behandlats med C. acnes signifikant ökar sitt uttryck av CCL22 mRNA. Sammanfattningsvis bedöms resultaten från detta arbete styrka uppfattningen att det kan finnas en koppling mellan C. acnes och orsakerna bakom prostatacancer men mer arbete återstår för att kunna klargöra dess relevans. / Prostate cancer is one of world´s most common forms of cancer. Every year about 1.3 million men around the world are diagnosed with prostate cancer and even so we cannot fully explain the etiology. There have been several studies indicating that there is a correlation between infection and different forms of cancer. Cutibacterium acnes (C.acnes) can be found to a large extent in prostate cancer tissue and a correlation between infection of C. acnes and prostate cancer has therefore been suggested. The presence of tumor-associated macrophages has been shown to favor various types of cancer. Several chemokines including CCL22 are released from these macrophages. CCL22 may be involved in a local inhibition of the immune system that is often associated with cancer growth. In this work, macrophages from a blood donor are grown with C. acnes to find out if the macrophages increase their expression of CCL22 mRNA after this exposure. By analyzing the results of a quantitative real-time PCR for CCL22 mRNA, it was demonstrated that macrophages treated with C. acnes significantly increase their expression of CCL22 mRNA. In conclusion, the results of this work indicate that there could be a link between C. acnes and the causes of prostate cancer, but more work remains to be able to clarify its relevance.