07). Figure 2c demonstrates that there was no difference in the overall length of stay (Mann-Whitney U test, p = 0.072), duration of delay to surgery (Mann-Whitney U test, p = 0.35) and length of postoperative stay in hospital (Mann-Whitney

U test, p = 0.25). Figure 2 Comparison of time from admission to surgery (a), postoperative length of stay (b) and total length of stay (c) between the two groups. Box and whisker graphs represent median ± inter-quartile range. Discussion Our audit in a comparable cohort of patients over two different time periods, after a change in theatre prioritisation policy, did not demonstrate any significant differences in the outcome after appendicectomy. The intention of implementing this change was to effectively reduce waiting times to emergency surgery and hence length of hospital stay – but clearly the present study has failed selleck products to demonstrate this effect. There could be numerous reasons for this finding. Foremost, this could be due to the small sample size, which will require Selleck CCI-779 a multi-centre study.

Such a study could be hampered by non-homogeneity of the profile of emergency workload. Our hospital is one of the premier trauma units in the UK and the only site of the only Helicopter emergency medical service (HEMS) in London. Despite this, numerically at least emergency general surgery accounts for 64.2% of all the emergency surgical workload with abscesses and acute appendicitis being the two most frequent reasons for requiring theatre [11]. Of course, trauma as well as vascular operations, because of the complexity of pre-operative and operative work and multiple team involvement, take longer duration and therefore occupy a prominent part of the emergency theatre schedule. Some authors have suggested an increase in post-appendicectomy complications and longer hospital stay associated to the delay to surgery [12, 13], whilst others have failed to demonstrate this trend [14–17]; although, C1GALT1 of course most patients would

prefer immediate surgical procedure [18]. In our cohort only four patients had a complication; of those, three were operated within 10 hours from admission and only one after 18 hours. Our data doesn’t demonstrate significant changes in outcome after the appendicectomy, despite changes in theatre prioritisation. The median length of hospital stay was 76 hours, comparable to other publications [13, 14]. Delay to surgery is associated with an increased incidence of complications and length of hospital stay after appendicectomy [12, 13, 19]. Analyzing a large series of 1081 patients, Ditillo et al[12] from the Yale University, USA demonstrated that in adult patients with acute appendicitis, the risk of developing advanced pathology and postoperative complications increases with time; particularly, those risks rise proportional to delay.

A15 [55]   GTA TCC CAC CAA TGT AGC CG         tet(M) GTG GAC AAA GGT ACA ACG AG 406 X90939 pJ13 [25]   CGG TAA AGT TCG TCA CAC AC         tet(O) AAC TTA GGC ATT CTG GCT CAC 515 Y07780

pUOA1 Taylorb   TCC CAC TGT TCC ATA TCG TCA         tet(S) CAT AGA CAA GCC GTT GAC C 667 C92946 pAT451 Mulvey   ATG TTT TTG GAA CGC CAG AG         tetA(P) CTT GGA TTG CGG AAG AAG AG 676 L20800 pJIR39 Monash Universityc   ATA TGC CCA TTT AAC CAC GC         tet(Q) TTA TAC TTC CTC CGG CAT CG 904 X58717 pNFD13-2 Salyersd   ATC GGT TCG AGA ATG TCC AC         tet(X) CAA TAA TTG GTG GTG GAC CC 468 M37699 pBS5 [56]   TTC TTA CCT TGG ACA TCC CG         VX-765 nmr pse-1 CGC TTC CCG TTA ACA AGT AC 419 M69058 SU01 [28]   CTG GTT CAT TTC AGA TAG CG     gDNA   oxa1-like AGC AGC GCC AGT GCA TCA 708 AJ009819 SU05 [26]

  ATT CGA CCC CAA GTT TCC     gDNA   tem1-like TTG GGT GCA CGA GTG GGT 503 AF126482.1 SU07 [26]   TAA TTG TTG CCG GGA AGC     gDNA   a Primers selected from previously published source [26, 26]. b Provided by Dr.Taylor (University of Alberta, Edmonton, AB, Canada). c Provided by the LY2157299 price Monash University (Victoria, Australia). d Provided by Dr. Salyers (University of Illinois, Urbana, USA). For PCR amplifications, bacterial cells from a single colony were collected using a sterile toothpick and resuspended in 25 μl of sterile deionized water. Amplifications were carried out in a Dyad PCR system (Bio-Rad Laboratories, Inc., Mississauga, ON, Canada) as described by [18]. PCR mixture (total 25 μl) included 1 μl of DNA template, 1 × PCR buffer (Invitrogen), 2.5 U Platinum Taq polymerase (Invitrogen) 300 μM of dNTP (Invitrogen) and sterile deionized water.

Primers and MgCl2 concentrations for the tetracycline group were optimized as described by [25]; for the ampicillin group, pse-1 (1.0 μM), oxa1-like (1.0 μM), tem1-like (1.0 μM), and 3.0 mM MgCl2 were used. For the tetracycline group, PCR conditions were: 5 min denaturing selleck inhibitor at 94°C; 28 cycles of 94°C for 1 min, 59.5°C for 1 min and 72°C for 1.5 min; final extension 5 min at 72°C. For the ampicillin group, denaturing was 5 min at 94°C, then 25 cycles of 94°C for 30 sec, 60°C for 30 sec and 72°C for 40 sec, and final extension 5 min at 72°C. PCR products were analyzed by gel electrophoresis on a 1.5% (w/v) agarose gel in 1× TAE buffer. DNA bands were stained with ethidium bromide and visualized by UV transillumination. Reference E. coli cultures and Salmonella typhimurium control plasmids and genomic DNA (gDNA) possessing tetracycline- and ampicillin-resistance genes (Table 2) were included, as well as a 100-bp DNA ladder (Invitrogen) for assessing size of PCR products.

These techniques vary in their efficacy with regard to fascial closure rates, associated morbidity and mortality rates. A number of systematic reviews have concluded

that the artificial burr and NPWT have the highest fascial closure and lowest mortality rates [3, 4]. Because of its relative ease of application, and preservation of fascial tissue, NPWT is becoming a dominant choice for TAC in the open abdomen patient [1]. TAC can be appropriate in the treatment of OA derived from a wide range of traumatic, post-operative and septic MK-2206 order clinical scenarios. Together these form a complex and diverse group of wounds. Much of the published literature describing outcomes in OA is difficult to interpret

due to grouping together of these heterogeneous clinical scenarios with widely varying aetiologies, prognoses and even treatment goals. This leads to Small molecule library mouse highly variable reported outcomes and complication rates. The rate of fascial closure in open abdomen patients treated with NPWT has been reported as low as 22% [5] (in pancreatitis) and as high as 92% [6] (in trauma). In order to understand how outcomes and potentially treatment protocols vary in different types of open abdomen patients, researchers must first publish results from homogenous and well-defined subgroups. The World Society of Abdominal Compartment Isotretinoin Syndrome (WSACS) has proposed a simple clinical classification for describing the open abdomen (Bjorck et al.) [7] in order

to facilitate comparison of study outcomes and clinical approach (see Table 1). The aim of the current study was to use the Bjorck classification to report outcomes of a well-defined group of patients, (with grade 1 or 2 open abdomens derived from traumatic injury) following treatment with a recently introduced NPWT system for TAC in the open abdomen. A systematic review of the literature, identifying studies with comparable homogenous study populations, was carried out as a means of comparing results from this study with results from the literature. Table 1 Open abdomen classification Grade 1A Clean OA without adherence between bowel and abdominal wall or fixity of the abdominal wall (lateralization of the abdominal wall). Grade 1B Contaminated OA without adherence/fixity Grade 2A Clean OA developing adherence/fixity Grade 2B Contaminated OA developing adherence/fixity Grade 3 OA complicated by fistula formation Grade 4 Frozen OA with adherent bowel, unable to close surgically, with or without fistula Adapted from Bjorck et al. [7]. Methods Temporary abdominal closure A prospective, open labelled, non-comparative study was carried out in two centres in South Africa between August 2010 and December 2011.

Vasculitis or congestion of mesenteric

veins may be caused by right sided heart failure [13, 14]. The differential diagnosis between POT and SOT is difficult and has seldom been made during the operation. Helpful is US or CT scan. Usually US findings are evaluated as normal [7]. Some times US may show a complex mass or a mixture of solid material and hypoechoic zones. US is a diagnostic procedure useful to exclude other acute abdominal conditions. CT scan is an GDC-0973 order effective procedure in diagnosis of acute abdominal torsion [15–17]. Preoperative US or CT scan are mandatory and the preoperative diagnosis can be accurately accomplished by these procedures. With increased use of US and CT scan, preoperative diagnosis of POT may increased in frequency [18] and in selected cases can avoid surgery and lead to conservative treatment [19–21]. In practice, US and CT scan are often avoided only for economical reasons. CT scan of our patient showed an inhomogeneous selleck products irregular edge profile mass of 38×30×25 cm of omental appearance localized

at the right side. Concentric distribution of fibrous and fatty folds converging radially toward the torsion with oedema of the fat tissue, of the mesentery and little fluid collection between the right muscle wall and the lower liver surface were shown. The same pattern of concentric linear streaks in the omental fat with high-attenuated vascular structure of omentum running perpendicular to the axial plane at the centre of a concentrically layered streaks was observed by selleck chemical Sakamoto et al. [22]. In their report, CT scan showed also a closed vascular pedicle. Balthazar et al. [15] showed effective also the MRI specially when OT is complicated by bleeding or development of an abscess [15]. Conversely, the radiography studies are ineffective in differential diagnosis between infarction of great omentum

and infarction caused by torsion [9]. OT is usually diagnosed during explorative laparotomy that represents diagnostic and therapeutic procedure. Thus, laparoscopy is the first choice procedure for diagnosis and treatment of acute omental torsion [23]. This procedure permits definitive diagnosis, when US and imaging (CT and MRI) findings are unclear [24]. In all cases laparoscopy permits a correct diagnosis of omental infarction and surgical excision [25]. The minimally invasive access to the abdominal cavity without surgical incision evocates less pain than traditional procedure and permits a praecox discharge of the patient in the first postoperative day [26]. Furthermore, in cases of POT with extensive mass of omentum, the laparoscopic technique alone might require to long surgery time; in such cases the therapeutic management of choice is diagnostic laparoscopy proceeding to laparotomy [18], which can permit the omental excision with small abdominal incision. Conclusions POT is a rare pathological condition with generic symptoms that may mimic many acute abdominal conditions.

EMBO J 2003,22(4):870–881.PubMedCrossRef 25. Henke JM, Bassler BL: Quorum sensing regulates type III secretion in Vibrio harveyi and Vibrio parahaemolyticus. J Bacteriol 2004,186(12):3794–3805.PubMedCrossRef 26. Garcia-Aljaro C, Muniesa M, Jofre J, Blanch AR: Prevalence

of the stx2 gene in coliform populations from aquatic environments. Appl Environ Microbiol 2004,70(6):3535–3540.PubMedCrossRef 27. Ochman H, Gerber AS, Hartl DL: Genetic applications of an inverse polymerase chain reaction. Genetics 1988, 120:621–623.PubMed 28. Milton DL, O’Toole R, Horstedt P, Wolf-Watz H: Flagellin A is essential for the virulence of Vibrio anguillarum. J Bacteriol 1996,178(5):1310–1319.PubMed 29. Denkin SM, Nelson DR: Induction of protease activity in Vibrio anguillarum AZD8055 manufacturer selleckchem by gastrointestinal mucus. Appl Environ Microbiol 1999,65(8):3555–3560.PubMed 30. Stepanovic S, Vukovic D, Hola V, Di Bonaventura G, Djukic S, Cirkovic I, Ruzicka F: Quantification of biofilm in microtiter plates: overview of testing conditions and practical recommendations for assessment of biofilm production by staphylococci. APMIS 2007,115(8):891–899.PubMedCrossRef 31. Schwyn B, Neilands JB: Universal chemical assay for the detection and determination of siderophores. Anal Biochem 1987,160(1):47–56.PubMedCrossRef

32. Miller VL, Mekalanos JJ: A novel suicide vector and its use in construction of insertion mutations: osmoregulation of outer membrane proteins and virulence determinants in Vibrio cholerae unless requires toxR. J Bacteriol 1988,170(6):2575–2583.PubMed 33. Morales VM, Backman A, Bagdasarian M: A series of wide-host-range low-copy-number vectors that allow direct screening for recombinants. Gene 1991,97(1):39–47.PubMedCrossRef 34. Rose RE: The nucleotide sequence of pACYC184. Nucleic Acids Res Microbiol 1988, 16:355.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions CGA participated in the design, acquisition of data and wrote the manuscript; SMR participated in the acquisition and analysis of

data; DLM has participated in the design of the study and has helped writing the manuscript; ARB participated in the design of the study and revision of the manuscript. All authors have read and approved the final version of the manuscript.”
“Background Salmonella is an enteric pathogen causing major public health problems throughout the world due to the consumption of contaminated food. Nontyphoidal Salmonella species, like Salmonella enterica serovar Typhimurium (STM), are the leading cause of hospitalization and death among the major foodborne pathogens [1]. Antibiotic resistance by Salmonella is dramatically increasing, so the development of an effective vaccine remains a global health priority [2, 3]. Creating a safe and immunogenic vaccine strain is the biggest challenge in developing an effective live-attenuated Salmonella vaccine [4].

PubMedCrossRef 27. Lee EY, Lee ZH, Song YW: CXCL10 and autoimmune diseases. Autoimmun Rev 2009,8(5):379–383.PubMedCrossRef 28. Liu M, Guo S, Hibbert JM, Jain V, Singh N, Wilson NO, Stiles JK: CXCL10/IP-10 in infectious diseases pathogenesis and potential therapeutic implications. Cytokine Growth Factor Rev 2011,22(3):121–130.PubMed 29. Ohno T, Okahashi N, Morisaki I, Amano A: Signaling pathways in osteoblast proinflammatory responses to infection by Porphyromonas gingivalis. Oral Microbiol Immunol

2008,23(2):96–104.PubMedCrossRef 30. Proost P, Vynckier AK, Mahieu F, Put W, Grillet B, Struyf S, Wuyts A, Opdenakker G, Van Damme J: Microbial Toll-like receptor ligands differentially regulate CXCL10/IP-10 expression in fibroblasts and mononuclear leukocytes in synergy with IFN-gamma selleck inhibitor and provide a mechanism for enhanced synovial chemokine levels in septic arthritis. Eur J Immunol 2003,33(11):3146–3153.PubMedCrossRef 31. Kortlever RM, Higgins PJ, Bernards R: Plasminogen activator inhibitor-1 is a critical downstream target of p53 in the induction of replicative senescence. Nat Cell Biol 2006,8(8):877–884.PubMedCrossRef Palbociclib Competing interests The authors declare

that they have no competing interests. Authors’ contributions HK, EP and TB designed the study. EP wrote the manuscript with HK and TB. EP and HK performed the experiments. All authors read and approved the final manuscript.”
“Background Various species of genera like Clostridium, Escherichia, Listeria, Salmonella, Shigella, Staphylococcus and Vibrio[1,

2] are known to cause food spoilage. In addition, different drug resistant strains of Escherichia and Salmonella belonging to family Enterobacteriaceae are reported to cause food-borne illness [3–6]. Increasing multidrug-resistance in bacteria resulted in a greater need to find alternative antimicrobial substances that can be used for various applications including clinical as well as preservation of food and dairy products. Therefore, research on antimicrobial peptides L-NAME HCl including antimicrobial biosurfactants as a new class of drugs has increased in the recent past as they exhibit both narrow and broad spectrum inhibition activities against Gram-positive and Gram-negative bacteria or fungi. Although members of the Enterobacteriaceae family are known to produce bacteriocins such as enterocins by Enterobacter sp. [7], serracin by Serratia sp. [8] bacteriocin by Citrobacter sp. [9] and microcins by Escherichia sp. [10], they are not reported to produce any antimicrobial biosurfactants. The different types of biosurfactants with antimicrobial activity include lipopeptides, glycolipids, phospholipids and lipopolysaccharides [11].

Both nematodes have a direct life cycle, and infection occurs by ingestion of free-living infective third-stage

larvae (L3); T. retortaeformis colonizes the small intestine, and G. strigosum inhabits the stomach. In the host, nematodes develop into adults and reproduce sexually, and eggs are shed through the rabbit faeces; the prepatent period is about 11 days for T. retortaeformis and 42 days for G. strigosum (23–26). For our laboratory infections, third-stage infective larvae of T. retortaeformis were kindly provided by Dr Dominique Kerboeuf (INRA, France), while G. strigosum larvae were extracted by culturing faeces from rabbits initially infected with adult parasites collected from our free-living population of rabbits in Tayside, Scotland (10). The laboratory experiments were designed as primary monospecific infections of rabbits with 5500 T. retortaeformis

Pritelivir purchase or 650 G. strigosum third-stage larvae (L3). The infection doses (force of infection) were estimated following Cattadori et al. (27) and based on the intensity of adult nematodes in a free-living rabbit population monitored from 1977 to 2003. Outbred, 60-day-old New Zealand White male rabbits, free of helminths and other parasites or pathogens (Harlan, Hillcrest, UK), were housed in individual cages with food and water ad libitum and a 12-h light cycle. Following a 1-week acclimation period, the individuals were orally challenged by gavage with a mineral water solution (5 mL) of L3 nematodes or mineral water for the controls. PD98059 in vivo Groups of six individuals (four infected

and two controls, eight infected and four controls at day 60) were euthanized with Euthatal™ (Merial, Harlow, UK), and post-mortem analysis carried out at days 4, 7, 14, 30, 45, 60, 75, 90 and 120 post-infection (DPI); for G. strigosum, the first two sampling points (day 4 and 7) were not collected. These points were chosen to quantify the immune response at time intervals Orotidine 5′-phosphate decarboxylase that correspond to the different developmental stages of these helminths, L3, L4, immature and adults (25,26) but also to closely follow changes in the immune response during the infection period. For T. retortaeformis single infection, the small intestine (SI) was divided into four equal sections, SI-1 to SI-4 from the duodenum to the ileum. Each section was further divided into four equal segments; segments 1 and 3 were stored in PBS (pH 7·4), for nematode counts, and segments 2 and 4 were processed. To quantify mucosal cytokine expression, five pieces of tissue (5 × 5 cm) were collected from segment 2 and stored in RNAlater (Sigma, St Louis, MO, USA) at −80°C. We selected the mucosa tissue because we were interested in a cytokine response at the site of infection and how this was related to nematode abundance. Here, we focus on SI-1, where most of the parasites were found.

[7] The klotho knockout mouse is now an established animal model of ageing, allowing further study of well-accepted processes that occur with ageing, such as arteriosclerosis, arterial calcification Opaganib and osteoporosis, and other less well-studied processes such as angiogenesis.[7, 11, 12] The klotho gene encodes a 1012 amino acid long single-pass transmembrane protein,[7] commonly referred

to as α-klotho, to differentiate it from two subsequently discovered members of the klotho family; β-klotho and γ-klotho. All three are single-pass transmembrane proteins of different lengths, which not only share a substantial degree of homology, but function as obligate co-receptors to endocrine FGF.[13] Within the extensive superfamily of FGF, only the FGF19 subfamily consisting of FGF19, FGF21 and FGF23 are endocrine FGF while the other FGF function as paracrine/autocrine factors.[13, 14] FGF receptors (FGFR) are detected ubiquitously while klotho expression is limited to certain tissues, thereby determining tissue specificity for the endocrine action of their respective FGF.[15] α-klotho is an obligate co-receptor for physiological FGF23

signalling and appears essential for FGF23-mediated phosphate regulation Epigenetics Compound Library in animal models.[15-17] It is now also evident that klotho proteins play a role in a range of other metabolic processes.[7, 8, 15, 18-20] β-klotho, that augments FGF19 and FGF21 signalling, is found in liver, gall bladder, pancreas, colon and adipose tissue and participates in bile acid metabolic pathways.[19, 20] γ-klotho is coupled to FGF19 and is found in the eye, adipose and kidney and its function remains cryptic.[13] The remainder of this review focuses on α-klotho and will henceforth be referred to as klotho. Klotho exists in two forms – membrane-bound klotho (mKl) and soluble klotho (sKl). mKl is variably expressed in different tissues including parathyroid, brain, heart and testis with low-level expression Thymidylate synthase also detected in the aorta.[7, 21] Klotho is most abundantly described in the kidney with earlier reports focused on distal convoluted tubule expression,[7] though more recently

proximal tubule expression of mKl has been reported.[22] sKl, on the other hand, is produced in two ways. The first is a result of ectodomain cleavage of mKl (∼130 kDa) although factors regulating ectodomain shedding remain poorly characterized. A number of proteases have been implicated, most notably a disintegrin and metalloproteinase (ADAM) 10/17, which is also expressed in the distal convoluted tubule. The second is a product of alternative splicing leading to a shorter form of sKl (∼70 kDa). Proteomic analysis of various extracellular fluids suggests that the longer form of sKl, generated by cleavage is the major circulating species in humans.[23-25] The actions of mKl and sKl differ, with mKl predominantly supporting FGF23 in regulating phosphate.

Women are most commonly infected by HIV-1 through heterosexual contact and immune mechanisms at or within the female GT would be expected to provide a crucial first barrier to transmission. As Ab that neutralize the countless HIV-1 variants remain elusive, many of the vaccines currently in clinical trials focus on the induction of HIV-1-specific CD8+ T cells. Such response cannot prevent the initial infection, but if present at the port of entry, might rapidly eliminate infected cells and thus thwart or potentially prevent spread of the virus. We showed in mice that a homologous prime-boost regimen using AdC vectors expressing

Gag Tamoxifen nmr induces transgene product-specific CD8+ T cells that could be isolated from the GT 13. This previous article used intracellular cytokine staining Barasertib clinical trial assays, which may not be optimal for the study of the GT-derived lymphocytes. Here, we extended these studies

testing different routes of immunization, more efficacious heterologous prime-boost regimens, and assessed migratory patterns of such cells. It is known that nasal immunization is able to induce immune responses not only in the respiratory tract but also at the GT 23. Results reported here show that CD8+ T cells, which home to the female GT, can be induced by i.n. immunization but this response is not sustained. In addition, vaginal booster immunization, as would be experienced in human vaccine recipients against HIV-1, causes only a slight local increase in i.n.-induced antigen-specific CD8+ T cells and fails to increase responses systemically. Last but not least, i.n. immunization may be problematic for some vectors Montelukast Sodium as this route allows access of the vaccine into the central nervous system. In brief, i.vag. immunization, as reported by others 24, induces only very low levels of antigen-specific

CD8+ T cells, which combined with logistic problems in humans should discourage further pursuit of this route of immunization for Ad vectors. Results are more promising after i.m. immunization, which not only elicits antigen-specific CD8+ T cells in systemic tissues but also high and sustained responses within the GT, as also reported recently by another group 25. A second immunization given i.m. causes a robust booster effect within the GT of i.m.-primed mice, and Gag-specific CD8+ T cells remain detectable for at least 1 year. i.m. immunization is thus overall superior at inducing genital CD8+ T cell responses by AdC vectors compared with i.n. immunization, and offers the added benefit of also eliciting potent systemic CD8+ T-cell responses, which may serve as a second layer of defense in case the virus breaks through the mucosal barrier. These findings are in agreement with a study in mice showing that i.p. infection with lymphocytic choriomeningitis virus is superior to i.n. infection for the induction of CD8+ T-cell responses in the vaginal mucosa 26.

The ELISA technique required relatively large amounts of tissue extracts, and one mouse could therefore be used only for the measurements of the two actual cytokines

as the oral mucosa, ear skin or lymph nodes cannot be dispersed in too large volume of extraction buffer to display measurable amounts of the cytokines. Counting of lymph node cells.  In a separate set of experiments (n = 2), submandibular and auricular (2 + 2) and axillary (4) lymph nodes were excised and kept in PBS. The lymph nodes were then squeezed through a nylon mesh (NYHC 150–80; Tidbecks, Ljungsarp, Sweden) to acquire single cell suspensions. The volume was adjusted to 10 ml before counting in a Bürker haemocytometer. Total cell counts for the combined submandibular/auricular and axillary lymph selleck inhibitor nodes MG132 were estimated. Calculations.  The oral mucosa and ear skin IL-2 and IFN-γ content was estimated per mg wet weight tissue. The total content of respective cytokine in quadruple regional (submandibular and auricular) and distant (axillary) lymph nodes was calculated. The tissue levels of IL-2 and IFN-γ differed in individual mice and not least between the different experimental series. However, the peaks of cytokine appearance/disappearance were consistently sharp but could vary from 4 to 24 h after hapten exposure in individual mice. The figures shown (Figs. 1–3)

are representatives of single experimental series, as assembling Nintedanib (BIBF 1120) the results from the three different experimental series into one curve causes considerable obscuring of the real biological response. Mice with normal oral mucosa or ear skin showed very low levels of IL-2. One exposure of the hapten to the oral mucosa or the ear skin (sensitization) resulted in increased levels of IL-2 locally,

(maximum 24-fold increase for the oral mucosa, and maximum 27-fold increase for ear skin, both n = 3) peaking 4–6 h after exposure and thereafter quickly subsiding. At 24 h, the IL-2 levels were back to baseline. After a second hapten exposure (elicitation), a similar peak of IL-2 occurred (maximum 39-fold increase for oral mucosa and 35-fold for the ear skin, both n = 3). The levels of IL-2 after elicitation were normalized by 12–24 h regardless whether oral mucosa or ear skin was examined. One exposure to the hapten resulted in only minor variations in the levels of IFN-γ in both ear skin and buccal mucosa. Increased levels of IFN-γ were found mainly after the second hapten exposure where a rapid increase in this cytokine was demonstrated. The peaks of IFN-γ were found between 8 and 24 h after re-exposure to the hapten (maximum 14-fold increase for oral mucosa and 8-fold for ear skin, n = 3) in tissue sensitized a week earlier. The levels of IFN-γ after elicitation were normalized by 24–48 h regardless whether oral mucosa or ear skin was examined.