interleukin-8 and Cat-Diseases

The purpose of this pilot study was to detect the presence of interleukin-8 (IL-8) and the potential downstream effects of IL-8 receptor activation in 2 previously characterized feline oral squamous cell carcinoma cell lines (SCCF1 and SCCF2). Interleukin-8 messenger RNA (mRNA) was initially detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). A previously validated and commercially available enzyme-linked immunosorbent assay (ELISA) test was used to measure IL-8 production in the supernatant of the 2 cell lines. Western blot was used to detect phosphorylation of proteins (AKT, ERK1/2, JAK2, STAT3, and Src), known to be downstream of interleukin-8 receptor activation. The IL-8 receptor-specific antagonists, Reparixin and SCH527123, were used to identify effects on phosphorylation of these proteins. Interleukin-8 mRNA and protein were detected in both SCCF1 and SCCF2 by RT-PCR and ELISA, respectively. Phosphorylation of ERK1/2, STAT3, and Src was detected in both cell lines. Inhibition of the IL-8 receptor led to a decrease in phosphorylation of Src, but not ERK1/2 or STAT3. In conclusion, feline squamous cell carcinoma cell lines can produce IL-8. Phosphorylation of Src seems, at least in part, a consequence of IL-8 receptor activation. The phosphorylation of ERK1/2 and STAT3, although present, seems independent of IL-8 receptor activation. Due to its potential effects on the tumor microenvironment, in addition to its autocrine effects on Src phosphorylation, the inhibition of the IL-8 receptor may become a beneficial therapeutic tool. Evaluation of the presence of both IL-8 and Src in many cases should elucidate their importance.. Le but de cette étude pilote était de détecter la présence d’interleukine-8 (IL-8) et les effets potentiels en aval de l’activation du récepteur IL-8 dans deux lignées cellulaires de carcinome épidermoïde oral félin (SCCF1 et SCCF2) précédemment caractérisées. L’ARN messager de l’interleukine-8 (ARNm) a été initialement détecté par amplification en chaîne par la polymérase à transcription inverse quantitative (qRT-PCR). Un test immuno-enzymatique ELISA précédemment validé et disponible dans le commerce a été utilisé pour mesurer la production d’IL-8 dans le surnageant des deux lignées cellulaires. L’immunobuvardage a été utilisé pour détecter la phosphorylation des protéines (AKT, ERK1/2, JAK2, STAT3 et Src), connues pour être en aval de l’activation du récepteur de l’interleukine-8. Les antagonistes spécifiques du récepteur IL-8, Reparixin et SCH527123, ont été utilisés pour identifier les effets sur la phosphorylation de ces protéines. L’ARNm et la protéine de l’interleukine-8 ont été détectés dans SCCF1 et SCCF2 par RT-PCR et ELISA, respectivement. La phosphorylation de ERK1/2, STAT3 et Src a été détectée dans les deux lignées cellulaires. L’inhibition du récepteur IL-8 a conduit à une diminution de la phosphorylation de Src, mais pas ERK1/2 ou STAT3. En conclusion, les lignées cellulaires de carcinome épidermoïde félin sont capables de produire de l’IL-8. La phosphorylation de Src semble, au moins en partie, une conséquence de l’activation du récepteur IL-8. La phosphorylation de ERK1/2 et STAT3, bien que présente, semble indépendante de l’activation du récepteur IL-8. En raison de ses effets potentiels sur le micro-environnement tumoral, en plus de ses effets autocrines sur la phosphorylation de Src, l’inhibition du récepteur IL-8 peut devenir un outil thérapeutique bénéfique. L’évaluation de la présence à la fois d’IL-8 et de Src dans un grand nombre de cas devrait élucider leur importance.(Traduit par Docteur Serge Messier).

Topics: Animals; Carcinoma, Squamous Cell; Cat Diseases; Cats; Cell Line, Tumor; Interleukin-8; Mouth Neoplasms; Pilot Projects; RNA, Messenger; Signal Transduction; Tumor Microenvironment

In humans, plasma amino acids (AAs) levels are used as dynamic nutritional markers. Moreover, some AAs are associated with chronic inflammation. In this study, we analyzed plasma AA profiles in cats with chronic gastrointestinal (GI) diseases. Eight healthy controls (HCs) and 12 client-owned cats with chronic GI diseases including chronic enteritis (n=8) and neoplasms (n=4) were recruited. Plasma albumin, total protein, and 22 AAs (11 essential and 11 non-essential AAs) levels were estimated. There was no significant difference in plasma albumin and total protein concentrations between the cats with chronic GI diseases and HCs. The plasma concentrations of 7 essential AAs (arginine, histidine, lysine, methionine, phenylalanine, taurine, and tryptophan) and 7 non-essential AAs (asparagine, aspartic acid, glutamic acid, glycine, hydroxyproline, proline, and serine) were significantly decreased in the cats with chronic GI diseases (P<0.05). Moreover, plasma histidine and tryptophan levels were inversely correlated with severity of symptoms (histidine: r

Topics: Amino Acids; Animals; Cat Diseases; Cats; Chronic Disease; Female; Gastrointestinal Diseases; Histidine; Inflammation; Interleukin-8; Macrophages; Male; Tryptophan

The mechanisms involved in the establishment of the specific immune response against dermatophytes remain unknown. Polymorphonuclear neutrophils (PMNs) are recruited early during the infection process and participate in the elimination of dermatophytes. They could therefore be involved in the induction of the immune response during dermatophytoses by producing specific cytokines. The aim of this work was to assess the in vitro cytokine production by feline PMNs exposed to living arthroconidia from the dermatophyte species Microsporum canis or stimulated with either a secreted or a structural component of M. canis, the latter consisting of heat-killed arthroconidia. The levels of specific cytokines produced by PMNs were determined by capture ELISA and/or quantitative RT-PCR. Results showed that PMNs secrete TNFα, IL-1β and IL-8 following exposure to M. canis living arthroconidia and stimulation with both a secreted component and heat-killed arthroconidia. The level of IL-8 mRNA was also increased in PMNs stimulated with M. canis living arthroconidia. In conclusion, infective M. canis arthroconidia induce the production of pro-inflammatory cytokines by feline PMNs that can be activated either by secreted or structural fungal components. Our results suggest that these granulocytes are involved in the initiation of the immune response against M. canis.

Topics: Animals; Cat Diseases; Cats; Cells, Cultured; Cytokines; Dermatomycoses; Enzyme-Linked Immunosorbent Assay; Female; Interleukin-1beta; Interleukin-8; Male; Microsporum; Neutrophils; RNA, Messenger; Spores, Fungal; Tumor Necrosis Factor-alpha

Further elucidation of the consequences of Helicobacter pylori infection on gastric mucosal inflammation and gastric secretory function would be facilitated by an animal model that is susceptible to infection with H. pylori, is broadly similar in gastric physiology and pathology to people, and is amenable to repeated non-invasive evaluation. The goal of this study was to examine the interrelationship of bacterial colonization, mucosal inflammation and gastric secretory function in cats with naturally acquired H. pylori infection.. Twenty clinically healthy cats with naturally acquired H. pylori infection (cagA-, picB) and 19 Helicobacter-free cats were evaluated. Gastric colonization was determined by tissue urease activity, light microscopy, culture and PCR. The mucosal inflammatory response was evaluated by light microscopy, and by RT-PCR of the pro-inflammatory cytokines IL-1alpha, IL-1beta, IL-8 and TNF-alpha in gastric mucosa. Gastric secretory function was assessed by measuring pentagastrin-stimulated acid secretion, fasting plasma gastrin, and antral mucosal gastrin and somatostatin immunoreactivity.. H. pylori colonized the pylorus, fundus and cardia in similar density. Bacteria were observed free in the lumen of gastric glands and were also tightly adherent to epithelial cells where they were associated with microvillus effacement. Mononuclear inflammation, lymphoid follicle hyperplasia, atrophy and fibrosis were observed primarily in H. pylori-infected cats, with the pylorus most severely affected. Neutrophilic and eosinophilic infiltrates, epithelial dysplasia, and up-regulation of mucosal IL-1beta and IL-8 were observed solely in infected cats. Fasting plasma gastrin concentrations and pentagastrin-stimulated acid output were similar in both infected and uninfected cats. There was no relationship of bacterial colonization density or gastric inflammation to plasma gastrin concentrations or gastric acid output.. The pattern of colonization and the mucosal inflammatory response in cats with naturally acquired H. pylori are broadly similar to those in infected people, particularly children, and non-human primates. The upregulation of IL-8 in infected cats was independent of cagA and picB. Our findings argue against a direct acid-suppressing effect of H. pylori on the gastric secretory-axis in chronically infected cats.

Topics: Animals; Antigens, Bacterial; Bacterial Proteins; Cardia; Cat Diseases; Cats; Disease Models, Animal; Female; Gastric Acidity Determination; Gastric Fundus; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Interleukin-1; Interleukin-8; Male; Pyloric Antrum; Reverse Transcriptase Polymerase Chain Reaction; Somatostatin; Tumor Necrosis Factor-alpha