scholarly journals Eyedrop Inoculation Causes Sublethal Leptospirosis in Mice

2017 ◽  
Vol 85 (4) ◽  
Author(s):  
Joseph Pierce Sullivan ◽  
Nisha Nair ◽  
Hari-Hara Potula ◽  
Maria Gomes-Solecki
Keyword(s):  
Periodic Acid ◽  
Interleukin 10 ◽  
Periodic Acid Schiff ◽  
Necrosis Factor Alpha ◽  
Content Type ◽  
Infectious Dose ◽  
Inflammatory Protein ◽  
Mucosal Surfaces ◽  
Infected Urine ◽  
Mononuclear Cell Infiltrates

ABSTRACT Leptospirosis is potentially a fatal zoonosis acquired by contact of skin and mucosal surfaces with soil and water contaminated with infected urine. We analyzed the outcome of infection of C3H/HeJ mice with Leptospira interrogans serovar Copenhageni using an enzootic mode of transmission, the conjunctival route. Infection led to weight loss and L. interrogans dissemination from blood to urine, and spirochetes were detected in blood and urine simultaneously. The infectious dose that led to consistent dissemination to kidney after conjunctival infection was ∼108 leptospires. Interestingly, a lower number of spirochetes appeared to colonize the kidney, given that we quantified ∼105 and ∼10 leptospires per μl of urine and per μg of kidney, respectively. Leptospira-specific IgM and IgG were detected at 15 days postinfection, and isotyping of the Ig subclass showed that the total IgG response switched from an IgG1 response to an IgG3 response after infection with L. interrogans. Histological periodic acid-Schiff D staining of infected kidney showed interstitial nephritis, mononuclear cell infiltrates, and reduced size of glomeruli. Quantification of proinflammatory immunomediators in kidney showed that keratinocyte-derived chemokine, macrophage inflammatory protein 2, RANTES, tumor necrosis factor alpha, gamma interferon, and interleukin-10 were upregulated in infected mice. We show that the kinetics of disease progression after infection via the ocular conjunctiva is delayed compared with infection via the standard intraperitoneal route. Differences may be related to the number of L. interrogans spirochetes that succeed in overcoming the natural defenses of the ocular conjunctiva and transit through tissue.

scholarly journals Global Effect of Interleukin-10 on the Transcriptional Profile Induced by Neisseria meningitidis in Human Monocytes

2012 ◽  
Vol 80 (11) ◽  
pp. 4046-4054 ◽  
Author(s):  
Unni Gopinathan ◽  
Reidun Øvstebø ◽  
Ole Kristoffer Olstad ◽  
Berit Brusletto ◽  
Hans Christian Dalsbotten Aass ◽  
...  
Keyword(s):  
Gene Expression ◽  
Septic Shock ◽  
Neisseria Meningitidis ◽  
Interleukin 10 ◽  
High Plasma ◽  
Human Monocytes ◽  
Necrosis Factor Alpha ◽  
Content Type ◽  
Inflammatory Protein ◽  
Meningococcal Septic Shock

ABSTRACTIn meningococcal septic shock, the dominant inducer of inflammation is lipopolysaccharide (LPS) in the outer membrane ofNeisseria meningitidis, while interleukin-10 (IL-10) is the principal anti-inflammatory cytokine. We have used microarrays and Ingenuity Pathway Analysis to study the global effects of IL-10 on gene expression induced byN. meningitidis, after exposure of human monocytes (n= 5) for 3 h toN. meningitidis(106cells/ml), recombinant human IL-10 (rhIL-10) (25 ng/ml), andN. meningitidiscombined with rhIL-10.N. meningitidisand IL-10 differentially expressed 3,579 and 648 genes, respectively. IL-10 downregulated 125 genes which were upregulated byN. meningitidis, including NLRP3, the key molecule of the NLRP3 inflammasome. IL-10 also upregulated 270 genes which were downregulated byN. meningitidis, including members of the leukocyte immunuglobulin-like receptor (LIR) family. Fifty-three genes revealed a synergistically increased expression whenN. meningitidisand IL-10 were combined. AIM2 (the principal molecule of the AIM2 inflammasome) was among these genes (fold change [FC], 18.3 versus 7.4 and 9.4 after stimulation byN. meningitidisand IL-10, respectively). We detected reduced concentrations (92% to 40%) of six cytokines (IL-1b, IL-6, IL-8, tumor necrosis factor alpha [TNF-α], macrophage inflammatory protein alpha [MIP-α], MIP-β) in the presence of IL-10, compared with concentrations with stimulation byN. meningitidisalone. Our data analysis of the effects of IL-10 on gene expression induced byN. meningitidissuggests that high plasma levels of IL-10 in meningococcal septic shock plasma may have a profound effect on a variety of functions and cellular processes in human monocytes, including cell-to-cell signaling, cellular movement, cellular development, antigen presentation, and cell death.

Enterogenous cyst in the cervical spinal canal

1988 ◽  
Vol 68 (2) ◽  
pp. 292-296 ◽  
Author(s):  
Kouichi Miyagi ◽  
Jiro Mukawa ◽  
Susumu Mekaru ◽  
Yasunari Ishikawa ◽  
Toshihiko Kinjo ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Immunohistochemical Staining ◽  
Periodic Acid ◽  
Enterogenous Cyst ◽  
Resonance Imaging ◽  
Periodic Acid Schiff ◽  
Content Type ◽  
Low Intensity ◽  
Old Japanese ◽  
Fine Print

✓ The case of an 11-year-old Japanese girl with an intradural and extramedullary enterogenous cyst is presented. A mass giving a low-intensity signal in comparison with the spinal cord was demonstrated on magnetic resonance imaging. Histologically, the diagnosis was confirmed on specimens stained with periodic acid-Schiff, alcian blue, mucicarmine, and immunohistochemical staining of carcinoembryonic antigen, and by electron microscopy.

scholarly journals The Host Antimicrobial Protein Calgranulin C Participates in the Control ofCampylobacter jejuniGrowth via Zinc Sequestration

2018 ◽  
Vol 86 (6) ◽  
Author(s):  
Janette M. Shank ◽  
Brittni R. Kelley ◽  
Joseph W. Jackson ◽  
Jessica L. Tweedie ◽  
Dana Franklin ◽  
...  
Keyword(s):  
Campylobacter Jejuni ◽  
Serum Levels ◽  
Interleukin 10 ◽  
Poultry Meat ◽  
Antimicrobial Protein ◽  
Dependent Manner ◽  
Necrosis Factor Alpha ◽  
Content Type ◽  
Full Resolution ◽  
Factor Alpha

ABSTRACTCampylobacter jejuniis a leading cause of bacterially derived gastroenteritis worldwide.Campylobacteris most commonly acquired through the consumption of undercooked poultry meat or through drinking contaminated water. Following ingestion,Campylobacteradheres to the intestinal epithelium and mucus layer, causing toxin-mediated inflammation and inhibition of fluid reabsorption. Currently, the human response to infection is relatively unknown, and animal hosts that model these responses are rare. As such, we examined patient fecal samples for the accumulation of the neutrophil protein calgranulin C during infection withCampylobacter jejuni. In response to infection, calgranulin C was significantly increased in the feces of humans. To determine whether calgranulin C accumulation occurs in an animal model, we examined disease in ferrets. Ferrets were effectively infected byC. jejuni, with peak fecal loads observed at day 3 postinfection and full resolution by day 12. Serum levels of interleukin-10 (IL-10) and tumor necrosis factor alpha (TNF-α) significantly increased in response to infection, which resulted in leukocyte trafficking to the colon. As a result, calgranulin C increased in the feces of ferrets at the time whenC. jejuniloads decreased. Further, the addition of purified calgranulin C toC. jejunicultures was found to inhibit growth in a zinc-dependent manner. These results suggest that upon infection withC. jejuni, leukocytes trafficked to the intestine release calgranulin C as a mechanism for inhibitingC. jejunigrowth.

scholarly journals Ability of Hydroxypropyl Chitosan Nail Lacquer To Protect against Dermatophyte Nail Infection

2014 ◽  
Vol 59 (4) ◽  
pp. 1844-1848 ◽  
Author(s):  
M. A. Ghannoum ◽  
L. Long ◽  
N. Isham ◽  
A. Bulgheroni ◽  
M. Setaro ◽  
...  
Keyword(s):  
Untreated Control ◽  
Periodic Acid ◽  
Control Sample ◽  
Trichophyton Mentagrophytes ◽  
Periodic Acid Schiff ◽  
Sample Mean ◽  
Content Type ◽  
Model Following ◽  
Nail Lacquer ◽  
Nail Infection

ABSTRACTThe development of a topical agent that would strengthen the nail, improve the natural barrier, and provide better drug penetration to the nail bed is needed. In this study, we examined the effects of a hydroxypropyl chitosan (HPCH)-based nail solution using a bovine hoof model. Following application of the nail solution, changes in the hardness of the hoof samples were measured using the Vickers method. Tensile and flexural strengths were tested by stretching or punching the samples, respectively. The ultrastructure was examined using scanning electron microscopy (SEM), and samples stained with periodic acid-Schiff (PAS) stain were used to determine the fungal penetration depth. The comparators included 40% urea and 70% isopropyl alcohol solutions. The HPCH nail solution increased hoof sample hardness in comparison to the untreated control sample (mean, 22.3 versus 19.4 Vickers pyramid number [HV]). Similarly, the HPCH solution increased the tensile strength (mean, 33.07 versus 28.42 MPa) and flexural strength (mean, 183.79 versus 181.20 MPa) compared to the untreated control. In contrast, the comparators had adverse effects on hardness and strength. SEM showed that the HPCH solution reduced the area of sample crumbling following abrasion compared to the untreated control (7,418 versus 17,843 pixels), and the PAS-stained images showed that the HPCH solution reduced penetration of the dermatophyte hyphae (e.g., penetration byTrichophyton mentagrophyteswas <25 μm at day 9 versus 275 μm in the untreated control). Unlike chemicals normally used in cosmetic treatments, repeated application of the HPCH nail solution may help prevent the establishment of new or recurring fungal nail infection.

scholarly journals The Secreted Protein Rv1860 of Mycobacterium tuberculosis Stimulates Human Polyfunctional CD8+T Cells

2016 ◽  
Vol 23 (4) ◽  
pp. 282-293 ◽  
Author(s):  
Vijaya Satchidanandam ◽  
Naveen Kumar ◽  
Sunetra Biswas ◽  
Rajiv S. Jumani ◽  
Chandni Jain ◽  
...  
Keyword(s):  
T Cells ◽  
Mycobacterium Tuberculosis ◽  
T Cell ◽  
Mononuclear Cells ◽  
Interleukin 10 ◽  
T Cell Response ◽  
Peripheral Blood Mononuclear ◽  
Necrosis Factor Alpha ◽  
Content Type ◽  
Latent Tb Infection

ABSTRACTWe previously reported that Rv1860 protein fromMycobacterium tuberculosisstimulated CD4+and CD8+T cells secreting gamma interferon (IFN-γ) in healthy purified protein derivative (PPD)-positive individuals and protected guinea pigs immunized with a DNA vaccine and a recombinant poxvirus expressing Rv1860 from a challenge with virulentM. tuberculosis. We now show Rv1860-specific polyfunctional T (PFT) cell responses in the blood of healthy latentlyM. tuberculosis-infected individuals dominated by CD8+T cells, using a panel of 32 overlapping peptides spanning the length of Rv1860. Multiple subsets of CD8+PFT cells were significantly more numerous in healthy latently infected volunteers (HV) than in tuberculosis (TB) patients (PAT). The responses of peripheral blood mononuclear cells (PBMC) from PAT to the peptides of Rv1860 were dominated by tumor necrosis factor alpha (TNF-α) and interleukin-10 (IL-10) secretions, the former coming predominantly from non-T cell sources. Notably, the pattern of the T cell response to Rv1860 was distinctly different from those of the widely studiedM. tuberculosisantigens ESAT-6, CFP-10, Ag85A, and Ag85B, which elicited CD4+T cell-dominated responses as previously reported in other cohorts. We further identified a peptide spanning amino acids 21 to 39 of the Rv1860 protein with the potential to distinguish latent TB infection from disease due to its ability to stimulate differential cytokine signatures in HV and PAT. We suggest that a TB vaccine carrying these and other CD8+T-cell-stimulating antigens has the potential to prevent progression of latentM. tuberculosisinfection to TB disease.

scholarly journals Underestimated Amoebic Appendicitis among HIV-1-Infected Individuals in Japan

2016 ◽  
Vol 55 (1) ◽  
pp. 313-320 ◽  
Author(s):  
Taiichiro Kobayashi ◽  
Koji Watanabe ◽  
Hideaki Yano ◽  
Yukinori Murata ◽  
Toru Igari ◽  
...  
Keyword(s):  
Acute Appendicitis ◽  
Clinical Features ◽  
Periodic Acid ◽  
Periodic Acid Schiff ◽  
Content Type ◽  
Formalin Fixed Paraffin ◽  
Formalin Fixed Paraffin Embedded ◽  
Life Threatening ◽  
Pas Staining ◽  
Hiv 1

ABSTRACT Entamoeba histolytica is not a common causative agent of acute appendicitis. However, amoebic appendicitis can sometimes be severe and life threatening, mainly due to a lack of awareness. Also, its frequency, clinical features, and pathogenesis remain unclear. The study subjects were HIV-1-infected individuals who presented with acute appendicitis and later underwent appendectomy at our hospital between 1996 and 2014. Formalin-fixed paraffin-embedded preserved appendix specimens were reexamined by periodic acid-Schiff (PAS) staining and PCR to identify undiagnosed amoebic appendicitis. Appendectomies were performed in 57 patients with acute appendicitis. The seroprevalence of E. histolytica was 33% (14/43) from the available stored sera. Based on the medical records, only 3 cases were clinically diagnosed as amoebic appendicitis, including 2 diagnosed at the time of appendectomy and 1 case diagnosed by rereview of the appendix after the development of postoperative complications. Retrospective analyses using PAS staining and PCR identified 3 and 3 more cases, respectively. Thus, E. histolytica infection was confirmed in 9 cases (15.8%) in the present study. Apart from a significantly higher leukocyte count in E. histolytica -positive patients than in negative patients (median, 13,760 versus 10,385 cells/μl, respectively, P = 0.02), there were no other differences in the clinical features of the PCR-positive and -negative groups. In conclusion, E. histolytica infection was confirmed in 9 (15.8%) of the appendicitis cases. However, only 3, including one diagnosed after intestinal perforation, were diagnosed before the present analyses. These results strongly suggest there is frequently a failure to detect trophozoites in routine examination, resulting in an underestimation of the incidence of amoebic appendicitis.

scholarly journals AscarisLarval Infection and Lung Invasion Directly Induce Severe Allergic Airway Disease in Mice

2018 ◽  
Vol 86 (12) ◽  
Author(s):  
Jill E. Weatherhead ◽  
Paul Porter ◽  
Amy Coffey ◽  
Dana Haydel ◽  
Leroy Versteeg ◽  
...  
Keyword(s):  
Airway Remodeling ◽  
Periodic Acid ◽  
Airway Disease ◽  
Allergic Airway Disease ◽  
Interleukin 4 ◽  
Lung Pathology ◽  
Periodic Acid Schiff ◽  
Content Type ◽  
Larval Migration

ABSTRACTAscaris lumbricoides(roundworm) is the most common helminth infection globally and a cause of lifelong morbidity that may include allergic airway disease, an asthma phenotype. We hypothesize thatAscarislarval migration through the lungs leads to persistent airway hyperresponsiveness (AHR) and type 2 inflammatory lung pathology despite resolution of infection that resembles allergic airway disease. Mice were infected withAscarisby oral gavage. Lung AHR was measured by plethysmography and histopathology with hematoxylin and eosin (H&E) and periodic acid-Schiff (PAS) stains, and cytokine concentrations were measured by using Luminex Magpix.Ascaris-infected mice were compared to controls or mice with allergic airway disease induced by ovalbumin (OVA) sensitization and challenge (OVA/OVA).Ascaris-infected mice developed profound AHR starting at day 8 postinfection (p.i.), peaking at day 12 p.i. and persisting through day 21 p.i., despite resolution of infection, which was significantly increased compared to controls and OVA/OVA mice.Ascaris-infected mice had a robust type 2 cytokine response in both the bronchoalveolar lavage (BAL) fluid and lung tissue, similar to that of the OVA/OVA mice, including interleukin-4 (IL-4) (P < 0.01 andP< 0.01, respectively), IL-5 (P < 0.001 andP < 0.001), and IL-13 (P < 0.001 andP < 0.01), compared to controls. By histopathology,Ascaris-infected mice demonstrated early airway remodeling similar to, but more profound than, that in OVA/OVA mice. We found thatAscarislarval migration causes significant pulmonary damage, including AHR and type 2 inflammatory lung pathology that resembles an extreme form of allergic airway disease. Our findings indicate that ascariasis may be an important cause of allergic airway disease in regions of endemicity.

scholarly journals Toll-Like Receptor 2 Agonist Pam3CSK4 Alleviates the Pathology of Leptospirosis in Hamster

2016 ◽  
Vol 84 (12) ◽  
pp. 3350-3357 ◽  
Author(s):  
Wenlong Zhang ◽  
Naisheng Zhang ◽  
Xufeng Xie ◽  
Jian Guo ◽  
Xuemin Jin ◽  
...  
Keyword(s):  
Tissue Injury ◽  
Interleukin 10 ◽  
Peritoneal Macrophages ◽  
High Ratio ◽  
Toll Like Receptor ◽  
Wild Type ◽  
Necrosis Factor Alpha ◽  
Content Type ◽  
Target Organs ◽  
Toll Like Receptor 2

Leptospirosis, caused by pathogenic spirochetes, is a zoonotic disease of global importance. The detailed pathogenesis of leptospirosis is still unclear, which limits the ideal treatment of leptospirosis. In this study, we analyzed the expression of Toll-like receptor 2 (TLR2) and TLR4 in target organs of both resistant mice and susceptible hamsters after Leptospira interrogans serovar Autumnalis infection. TLR2 but not TLR4 transcripts in mouse organs contrasted with delayed induction and overexpression in hamster organs. Coinjection of leptospires and the TLR2 agonist Pam3CSK4 into hamsters improved their survival rate, alleviated tissue injury, and decreased the abundance of leptospires in target organs. The production of interleukin-10 (IL-10) from tissues was enhanced in hamsters of the group coinjected with leptospires and Pam3CSK4 compared with the leptospira-injected group. Similarly, IL-10 levels in TLR2-deficient mice were lower than those in wild-type mice. A high ratio of IL-10/tumor necrosis factor alpha (TNF-α) levels was found in both infected wild-type mice and hamsters coinjected with leptospires and Pam3CSK4. Moreover, TLR2-dependent IL-10 expression was detected in peritoneal macrophages after leptospira infection. Our data demonstrate that coinjection of leptospires and Pam3CSK4 alleviates the pathology of leptospirosis in hamsters; this effect may result from the enhanced expression of TLR2-dependent IL-10.

scholarly journals Sequential Plasmodium chabaudi and Plasmodium berghei Infections Provide a Novel Model of Severe Malarial Anemia

2012 ◽  
Vol 80 (9) ◽  
pp. 2997-3007 ◽  
Author(s):  
Juliana V. Harris ◽  
Tiffany M. Bohr ◽  
Catherine Stracener ◽  
Mary E. Landmesser ◽  
Vladimir Torres ◽  
...  
Keyword(s):  
Ex Vivo ◽  
Interleukin 10 ◽  
Red Cells ◽  
Second Phase ◽  
Necrosis Factor Alpha ◽  
Content Type ◽  
Severe Malarial Anemia ◽  
Antibody Levels ◽  
Malarial Anemia

ABSTRACTLack of an adequate animal model ofPlasmodium falciparumsevere malarial anemia (SMA) has hampered the understanding of this highly lethal condition. We developed a model of SMA by infecting C57BL/6 mice withP. chabaudifollowed after recovery byP. bergheiinfection.P. chabaudi/P. berghei-infected mice had an initial 9- to 10-day phase of relatively low parasitemia and severe anemia, followed by a second phase of hyperparasitemia, more profound anemia, reticulocytosis, and death 14 to 21 days after infection.P. chabaudi/P. berghei-infected animals had more intense splenic hematopoiesis, higher interleukin-10 (IL-10)/tumor necrosis factor alpha and IL-12/gamma interferon (IFN-γ) ratios, and higher antibody levels againstP. bergheiandP. chabaudiantigens thanP. berghei-infected orP. chabaudi-recovered animals. Early treatment with chloroquine or artesunate did not prevent the anemia, suggesting that the bulk of red cell destruction was not due to the parasite. Red cells fromP. chabaudi/P. berghei-infected animals had increased surface IgG and C3 by flow cytometry. However, C3−/−mice still developed anemia. Tracking of red cells labeledex vivoandin vivoand analysis of frozen tissue sections by immunofluorescence microscopy showed that red cells fromP. chabaudi/P. berghei-infected animals were removed at an accelerated rate in the liver by erythrophagocytosis. This model is practical and reproducible, and its similarities withP. falciparumSMA in humans makes it an appealing system with which to study the pathogenesis of this condition and explore potential immunomodulatory interventions.

scholarly journals Leishmania amazonensis Amastigotes Trigger Neutrophil Activation but Resist Neutrophil Microbicidal Mechanisms

2013 ◽  
Vol 81 (11) ◽  
pp. 3966-3974 ◽  
Author(s):  
Eric D. Carlsen ◽  
Christie Hay ◽  
Calvin A. Henard ◽  
Vsevolod Popov ◽  
Nisha Jain Garg ◽  
...  
Keyword(s):  
Late Phase ◽  
Axenic Culture ◽  
Parasite Burden ◽  
Interleukin 10 ◽  
Neutrophil Activation ◽  
Neutrophil Recruitment ◽  
Necrosis Factor Alpha ◽  
Content Type ◽  
Activated Neutrophils ◽  
The Impact

ABSTRACTNeutrophils are the first cells to infiltrate to the site ofLeishmaniapromastigote infection, and these cells help to reduce parasite burden shortly after infection is initiated. Several clinical reports indicate that neutrophil recruitment is sustained over the course of leishmaniasis, and amastigote-laden neutrophils have been isolated from chronically infected patients and experimentally infected animals. The goal of this study was to compare how thioglycolate-elicited murine neutrophils respond toL. amazonensismetacyclic promastigotes and amastigotes derived from axenic cultures or from the lesions of infected mice. Neutrophils efficiently internalized both amastigote and promastigote forms of the parasite, and phagocytosis was enhanced in lipopolysaccharide (LPS)-activated neutrophils or when parasites were opsonized in serum from infected mice. Parasite uptake resulted in neutrophil activation, oxidative burst, and accelerated neutrophil death. While promastigotes triggered the release of tumor necrosis factor alpha (TNF-α), uptake of amastigotes preferentially resulted in the secretion of interleukin-10 (IL-10) from neutrophils. Finally, the majority of promastigotes were killed by neutrophils, while axenic culture- and lesion-derived amastigotes were highly resistant to neutrophil microbicidal mechanisms. This study indicates that neutrophils exhibit distinct responses to promastigote and amastigote infection. Our findings have important implications for determining the impact of sustained neutrophil recruitment and amastigote-neutrophil interactions during the late phase of cutaneous leishmaniasis.

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