Jay K Kolls

Washington University in St. Louis, San Luis, Missouri, United States

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Publications (377)2375.72 Total impact

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    ABSTRACT: Rationale Stress is associated with asthma morbidity in Puerto Ricans (PRs), who have reduced bronchodilator response (BDR). Objectives To examine whether stress and/or a gene regulating anxiety (ADCYAP1R1) is associated with BDR in PR/non-PR children with asthma. Methods Cross-sectional study of stress and BDR (percent change in FEV1 after BD) in 234 PRs ages 9-14 years with asthma. We assessed child stress using the Checklist of Children's Distress Symptoms (CCDS), and maternal stress using the perceived stress scale (PSS). Replication analyses were conducted in two cohorts. Polymorphisms in ADCYAP1R1 were genotyped in our study and six replication studies. Multivariable models of stress and BDR were adjusted for age, sex, income, environmental tobacco smoke and use of inhaled corticosteroids. Measurements and Main Results High child stress was associated with reduced BDR in three cohorts. PR children who were highly stressed (upper quartile, CCDS) and whose mothers had high stress (upper quartile, PSS) had a BDR that was 10.2% (95% CI= 6.1% to 14.2%) lower than children who had neither high stress nor a highly stressed mother. A polymorphism in ADCYAP1R1 (rs34548976) was associated with reduced BDR. This SNP is associated with reduced expression of the gene for the β2-adrenergic receptor (ADRB2) in CD4+ lymphocytes of subjects with asthma, and affects brain connectivity of the amygdala and the insula (a biomarker of anxiety). Conclusions High child stress and an ADCYAP1R1 SNP are associated with reduced BDR in children with asthma. This is likely due to down-regulation of ADRB2 in highly stressed children.
    American Journal of Respiratory and Critical Care Medicine 04/2015; DOI:10.1164/rccm.201501-0037OC · 11.99 Impact Factor
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    ABSTRACT: Acute ethanol intoxication suppresses the host immune responses against Streptococcus pneumoniae. As IL-17 is a critical cytokine in host defense against extracellular pathogens including S. pneumoniae, we hypothesized that ethanol impairs mucosal immunity against this pathogen by disrupting IL-17 production or IL-17R signaling. A chronic ethanol feeding model in SIV-infected Rhesus macaques and acute ethanol in a murine model were used. Transcriptome analysis of bronchial brushes in the non-human primate model showed downregulation of the expression of IL-17 regulated chemokines in ethanol fed animals, a finding also replicated in the murine model. Surprisingly, recombinant CXCL1 and CXCL5 but not IL-17 or IL-23 + IL1β rescued bacterial burden in the ethanol group to control levels. Taken together, this study suggests that ethanol impairs IL-17 mediated chemokine production in the lung. Thus, exogenous luminal restoration of IL-17 related chemokines, CXCL1 and CXCL5, improves host defenses against S. pneumoniae. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Infection and Immunity 03/2015; 83(5). DOI:10.1128/IAI.02869-14 · 4.16 Impact Factor
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    ABSTRACT: Anti-CD20 antibody therapy has been a useful medication to manage non-Hodgkin's lymphoma as well as autoimmune diseases characterized by auto-antibody generation. CD20 is expressed on most developmental stages of B-lymphocytes, thus CD20 depletion leads to B-lymphocyte deficiency. As the drug became more widely used, there was an increase in case reports of patients developing Pneumocystis pneumonia. The role of anti-CD20 and Pneumocystis jirovecii infection is under debate due to the fact that most patients are under a regimen of multiple immunosuppressive medications. To address the specific role of CD20 depletion on host immunity against Pneumocystis, we examined a murine anti-CD20 depleting antibody. We demonstrate that anti-CD20 alone is permissive for Pneumocystis infection and anti-CD20 impaired type 2 immunity, such as IL-4, IL-5, and IL-13, by whole lung cells to Pneumocystis murina. We also demonstrate that CD4+ T-cells from mice treated with anti-CD20 during Pneumocystis infection are incapable of mounting a protective immune response when transferred into Rag1-/- mice. Thus CD20+ cells are critical for generating protective CD4+ T-cell immune responses against this organism. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Infection and Immunity 03/2015; 83(5). DOI:10.1128/IAI.03099-14 · 4.16 Impact Factor
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    ABSTRACT: Infection with influenza virus has been a significant cause of morbidity and mortality for more than a hundred years. Severe disease and increased mortality often results from bacterial super-infection of patients with influenza virus infection. Preceding influenza infection alters the host's innate and adaptive immune responses, allowing increased susceptibility to secondary bacterial pneumonia. Recent advances in the field have helped to define how influenza alters the immune response to bacteria through the dysregulation of phagocytes, antimicrobial peptides, and lymphocytes. Viral-induced interferons play a key role in altering the phenotype of the immune response. Potential genetic modifiers of disease will help to define additional immunologic mechanisms that predispose to viral, bacterial super-infection with the overarching goal of developing effective therapeutic strategies to prevent and treat disease. Copyright © 2015. Published by Elsevier Ltd.
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    ABSTRACT: Background Influenza is a common respiratory virus and Staphylococcus aureus frequently causes secondary pneumonia during influenza infection, leading to increased morbidity and mortality. Influenza has been found to attenuate subsequent Type 17 immunity, enhancing susceptibility to secondary bacterial infections. IL-27 is known to inhibit Type 17 immunity, suggesting a potential critical role for IL-27 in viral and bacterial co-infection.MethodsA murine model of influenza and Staphylococcus aureus infection was used to mimic human viral, bacterial co-infection. C57BL/6 wild-type, IL-27 receptor ¿ knock-out, and IL-10 knock-out mice were infected with Influenza H1N1 (A/PR/8/34) or vehicle for 6 days followed by challenge with Staphylococcus aureus or vehicle for 24 hours. Lung inflammation, bacterial burden, gene expression, and cytokine production were determined.ResultsIL-27 receptor ¿ knock-out mice challenged with influenza A had increased morbidity compared to controls, but no change in viral burden. IL-27 receptor ¿ knock-out mice infected with influenza displayed significantly decreased IL-10 production compared to wild-type. IL-27 receptor ¿ knock-out mice co-infected with influenza and S. aureus had improved bacterial clearance compared to wild-type controls. Importantly, there were significantly increased Type 17 responses and decreased IL-10 production in IL-27 receptor ¿ knock-out mice. Dual infected IL-10¿/¿ mice had significantly less bacterial burden compared to dual infected WT mice.Conclusions These data reveal that IL-27 regulates enhanced susceptibility to S. aureus pneumonia following influenza infection, potentially through the induction of IL-10 and suppression of IL-17.
    Respiratory Research 02/2015; 16(1):10. DOI:10.1186/s12931-015-0168-8 · 3.13 Impact Factor
  • Florencia McAllister, Jay K. Kolls
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    ABSTRACT: T-helper type 17 cytokines have been implicated in epithelial cancer progression at mucosal sites. In this issue of the European Journal of Immunology, Nardinocchi, et al. [Eur. J. Immunol. 2015. 45: XXXX-XXXX] show that the Th17 cytokines IL-17 and IL-22 can both signal to non-melanoma skin cancer cells, inducing both cellular proliferation and enhanced migration of human basal-cell carcinoma (BCC) and squamous cell carcinoma (SCC) cell lines in vitro. These cytokines were also shown to exacerbate tumor growth in mice injected with the SCC line, CAL27. Thus, IL-17 and IL-22 may be key factors in skin cancer progression and may provide novel prognostic markers in non-melanoma skin cancer.This article is protected by copyright. All rights reserved
    European Journal of Immunology 02/2015; 45(3). DOI:10.1002/eji.201545456 · 4.52 Impact Factor
  • John F Alcorn, Jay K Kolls
  • Jay K Kolls, Gyongyi Szabo
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    ABSTRACT: Hepatitis C virus (HCV) is a leading cause of chronic liver disease, and efforts to develop therapeutic vaccine strategies have been limited by immune escape due to HCV variants that are resistant to current vaccines or HCV variants that rapidly acquire new resistance-conferring mutations. Recently, the crystal structure of the viral envelope protein E2 region was resolved as well as how E2 docks to the host CD81 protein; therefore, antibodies that block this interaction should prevent viral entry into host cells. In this issue of the JCI, Bailey and colleagues show that immune escape of HCV can occur by naturally occurring polymorphisms in E2 that are distinct from those at mapped sites of antibody binding. These data reveal alternative mechanisms of resistance that need to be considered in both natural viral escape as well as in rationale vaccine design against HCV.
    Journal of Clinical Investigation 12/2014; 125(1):1-2. DOI:10.1172/JCI79424 · 13.77 Impact Factor
  • Jay K Kolls
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    ABSTRACT: The HIV epidemic has clearly demonstrated the critical role CD4(+) T cells play in preventing opportunistic infections in the lung. The types of CD4(+) effector T-cell populations in the lung have significantly expanded over the last 8-10 years with the discovery of helper T type 17 cells, and this review summarizes the field and discusses how these effector cells may be exploited to augment mucosal immunity in the lung.
    12/2014; 11(Supplement 5):S284-S286. DOI:10.1513/AnnalsATS.201403-109AW
  • Taylor Eddens, Jay K Kolls
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    ABSTRACT: Pneumocystis jirovecii is a common opportunistic infection in the HIV-positive population and is re-emerging as a growing clinical concern in the HIV-negative immunosuppressed population. Newer targeted immunosuppressive therapies and the discovery of rare genetic mutations have furthered our understanding of the immunity required to clear Pneumocystis infection. The immune system can also mount a pathologic response against Pneumocystis following removal of immunosuppression and result in severe damage to the host lung. The current review will examine the most recent epidemiologic studies about the incidence of Pneumocystis in the HIV-positive and HIV-negative populations in the developing and developed world and will detail methods of diagnosis for Pneumocystis pneumonia. Finally, this review aims to summarize the known mediators of immunity to Pneumocystis and detail the pathologic immune response leading to Pneumocystis-related immune reconstitution inflammatory syndrome.
    Seminars in Immunopathology 11/2014; 37(2). DOI:10.1007/s00281-014-0459-z · 6.48 Impact Factor
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    ABSTRACT: The ability of Candida albicans to cause disease is associated with its capacity to undergo morphological transition between yeast and filamentous forms, but the role of morphology in colonisation and dissemination from the gastrointestinal (GI) tract remains poorly defined. To explore this, we made use of wild type and morphological mutants of C. albicans in an established model of GI tract colonization, induced following antibiotic-treatment of mice. Our data reveal that GI tract colonization favours the yeast form of C. albicans, that there is constitutive low level systemic dissemination in colonized mice that occurs irrespective of fungal morphology, and that colonization is not controlled by Th17 immunity in otherwise immunocompetent animals. These data provide new insights into the mechanisms of pathogenesis and commensalism of C. albicans, and have implications for our understanding of human disease.
    Cellular Microbiology 10/2014; DOI:10.1111/cmi.12388 · 4.82 Impact Factor
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    ABSTRACT: IL-22 is a Th17/Th22 cytokine that is increased in asthma. However, recent animal studies showed controversial findings in the effects of IL-22 in allergic asthma. To determine the role of IL-22 in ovalbumin-induced allergic inflammation we generated inducible lung-specific IL-22 transgenic mice. Transgenic IL-22 expression and signaling activity in the lung were determined. Ovalbumin (OVA)-induced pulmonary inflammation, immune responses, and airway hyperresponsiveness (AHR) were examined and compared between IL-22 transgenic mice and wild type controls. Following doxycycline (Dox) induction, IL-22 protein was readily detected in the large (CC10 promoter) and small (SPC promoter) airway epithelial cells. IL-22 signaling was evidenced by phosphorylated STAT3. After OVA sensitization and challenge, compared to wild type littermates, IL-22 transgenic mice showed decreased eosinophils in the bronchoalveolar lavage (BAL), and in lung tissue, decreased mucus metaplasia in the airways, and reduced AHR. Among the cytokines and chemokines examined, IL-13 levels were reduced in the BAL fluid as well as in lymphocytes from local draining lymph nodes of IL-22 transgenic mice. No effect was seen on the levels of serum total or OVA-specific IgE or IgG. These findings indicate that IL-22 has immune modulatory effects on pulmonary inflammatory responses in allergen-induced asthma.
    PLoS ONE 09/2014; 9(9):e107454. DOI:10.1371/journal.pone.0107454 · 3.53 Impact Factor
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    ABSTRACT: Mammalian hosts are colonized with commensal microbes in various mucosal and epithelial tissues, including the intestinal tract. In mice, the presence of segmented filamentous bacteria (SFB) promotes Th17 differentiation and the development of autoimmune disease. Here, we demonstrate that the IL-23 pathway dynamically regulates the abundance of SFB as well as mucosal barrier function in the adult animal. Genetic or pharmacological inactivation of the pathway selectively perturbs the abundance of a small group of commensals, including SFB, and results in an impaired mucosal barrier. Defective barrier function leads to systemic dissemination of microbial products, provoking induction of the IL-23 pathway with dual consequences: IL-23 drives IL-22 production to reinforce mucosal barrier function and elicit antimicrobial activities, and it also drives the differentiation of Th17 cells in an attempt to combat escaped microbes in the lamina propria and in distal tissues. Thus, barrier defects generate a systemic environment that facilitates Th17 development.
    Proceedings of the National Academy of Sciences 09/2014; 111(38). DOI:10.1073/pnas.1323852111 · 9.81 Impact Factor
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    ABSTRACT: Lipocalin-2 (LCN2) was originally isolated from neutrophils and termed neutrophil gelatinase-associated lipocalin (NGAL). However, the functions of LCN2 and the cell types that are primarily responsible for LCN2 production remain unclear. To address these issues, hepatocyte-specific Lcn2 knockout (Lcn2Hep-/-) mice were generated and subjected to bacterial infection (with Klesbsiella pneumoniae or Escherichia coli) or partial hepatectomy (PHx). Studies of Lcn2Hep-/- mice revealed that hepatocytes contributed to 25% of the low basal serum level of LCN2 protein (˜62 ng/ml) but were responsible for more than 90% of the highly elevated serum LCN2 protein level (˜6,000 ng/ml) post-infection and more than 60% post-PHx (˜700 ng/ml). Interestingly, both Lcn2Hep-/- and global Lcn2 knockout (Lcn2-/-) mice demonstrated comparable increases in susceptibility to infection with K. pneumoniae or E. coli. These mice also had increased enteric bacterial translocation from the gut to the mesenteric lymph nodes and exhibited reduced liver regeneration after PHx. Treatment with IL-6 stimulated hepatocytes to produce LCN2 in vitro and in vivo. Hepatocyte-specific ablation of the IL-6 receptor or Stat3, a major downstream effector of IL-6, markedly abrogated LCN2 elevation in vivo. Furthermore, chromatin immunoprecipitation (ChIP) assay revealed that STAT3 was recruited to the promoter region of the Lcn2 gene upon STAT3 activation by IL-6. In conclusion, hepatocytes are the major cell type responsible for LCN2 production after bacterial infection or PHx, and this response is dependent on IL-6 activation of the STAT3 signaling pathway. Thus, hepatocyte-derived LCN2 plays an important role in inhibiting bacterial infection and promoting liver regeneration. (Hepatology 2014;)
    Hepatology 09/2014; 61(2). DOI:10.1002/hep.27447 · 11.19 Impact Factor
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    ABSTRACT: The epithelium plays an active role in the response to inhaled pathogens in part by responding to signals from the immune system. Epithelial responses may include changes in chemokine expression, increased mucin production and antimicrobial peptide secretion, and changes in ion transport. We previously demonstrated that interleukin-17A (IL-17A), which is critical for lung host defense against extracellular bacteria, significantly raised airway surface pH in vitro, a finding that is common to a number of inflammatory diseases. Using microarray analysis of normal human bronchial epithelial (HBE) cells treated with IL-17A, we identified the electroneutral chloride-bicarbonate exchanger Pendrin (SLC26A4) as a potential mediator of this effect. These data were verified by real-time, quantitative PCR that demonstrated a time-dependent increase in Pendrin mRNA expression in HBE cells treated with IL-17A up to 48 h. Using immunoblotting and immunofluorescence, we confirmed that Pendrin protein expression is increased in IL-17 treated HBE cells and that it is primarily localized to the mucosal surface of the cells. Functional studies using live-cell fluorescence to measure intracellular pH demonstrated that IL-17A induced chloride-bicarbonate exchange in HBE cells that was not present in the absence of IL-17A. Furthermore, HBE cells treated with short interfering RNA against Pendrin showed substantially reduced chloride-bicarbonate exchange. These data suggest that Pendrin is part of IL-17A-dependent epithelial changes and that Pendrin may therefore be a therapeutic target in IL-17A-dependent lung disease.
    PLoS ONE 08/2014; 9(8):e103263. DOI:10.1371/journal.pone.0103263 · 3.53 Impact Factor
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    ABSTRACT: The lungs are a major target for infection and a key battleground in the fight against the development of antimicrobial drug-resistant pathogens. Ventilator-associated pneumonia (VAP) is associated with mortality rates of 24-50%. The optimal duration of antibiotic therapy against VAP is unknown, but prolonged courses are associated with the emergence of bacterial resistance. De-escalation strategies in which treatment is discontinued based on signs of clinical resolution, fixed durations of therapy (generally 7-8 d), or serum procalcitonin responses have been shown to decrease antibiotic consumption. Outcomes are comparable to longer treatment courses, with the possible exception of VAP due to nonfermenting, gram-negative bacilli such as Pseudomonas aeruginosa. Staphylococcus aureus is a leading cause of VAP and other infections. Outcomes after S. aureus infection are shaped by the interplay between environmental, bacterial, and host genetic factors. It is increasingly clear that mechanisms of pathogenesis vary in different types of S. aureus infections. Genome-scale studies of S. aureus strains, host responses, and host genetics are redefining our understanding of the pathogenic mechanisms underlying VAP. Genome-sequencing technologies are also revolutionizing our understanding of the molecular epidemiology, evolution, and transmission of influenza. Deep sequencing using next-generation technology platforms is defining the remarkable genetic diversity of influenza strains within infected hosts. Investigators have demonstrated that antiviral drug-resistant influenza may be present prior to the initiation of treatment. Moreover, drug-resistant minor variant influenza strains can be transmitted from person to person in the absence of selection pressure. Studies of lung infections and the causative pathogens will remain at the cutting edge of clinical and basic medical research.
    08/2014; 11(Supplement 4):S193-S200. DOI:10.1513/AnnalsATS.201402-069PL
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    ABSTRACT: Recent findings demonstrate that inhaled cigarette smoke, the predominant lung carcinogen, elicits a T helper 17 (Th17) inflammatory phenotype. Interleukin-17A (IL-17), the hallmark cytokine of Th17 inflammation, displays pro- and anti-tumorigenic properties in a manner that varies according to tumor type and assay system. To investigate the role of IL-17 in lung tumor growth, we used an autochthonous tumor model (K-ras(LA1) mice) with lung delivery of a recombinant adenovirus that expresses IL-17A. Virus-mediated expression of IL-17A in K-Ras(LA1) mice at 8-10 weeks of age doubled lung tumor growth in three weeks relative to littermates that received a green fluorescent protein-expressing control adenovirus. IL-17 induced matrix metalloproteinase-9 (MMP-9) expression in vivo and in vitro. In accord with this finding, selective and specific inhibitors of MMP-9 repressed the increased motility and invasiveness IL-17-treated lung tumor cells in culture. Knockdown or mutation of p53 promoted the motility of murine lung tumor cells and abrogated the pro-migratory role of IL-17. Co-expression of siRNA-resistant wild-type, but not mutant, human p53 rescued both IL-17-mediated migration and MMP-9 mRNA induction in p53 knockdown lung tumor cells. IL-17 increased MMP-9 mRNA stability by reducing interaction with the mRNA destabilizing serine/arginine-rich splicing factor 1 (SRSF1). Taken together, our results indicate that IL-17 stimulates lung tumor growth and regulates MMP-9 mRNA levels in a p53- and SRSF1-dependent manner.
    AJP Lung Cellular and Molecular Physiology 07/2014; 307(6). DOI:10.1152/ajplung.00125.2014 · 4.04 Impact Factor
  • Jeremy P McAleer, Jay K Kolls
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    ABSTRACT: Respiratory infections and diseases are among the leading causes of death worldwide, and effective treatments probably require manipulating the inflammatory response to pathogenic microbes or allergens. Here, we review mechanisms controlling the production and functions of interleukin-17 (IL-17) and IL-22, cytokines that direct several aspects of lung immunity. Innate lymphocytes (γδ T cells, natural killer cells, innate lymphoid cells) are the major source of IL-17 and IL-22 during acute infections, while CD4(+) T-helper 17 (Th17) cells contribute to vaccine-induced immunity. The characterization of dendritic cell (DC) subsets has revealed their central roles in T-cell activation. CD11b(+) DCs stimulated with bacteria or fungi secrete IL-1β and IL-23, potent inducers of IL-17 and IL-22. On the other hand, recognition of viruses by plasmacytoid DCs inhibits IL-1β and IL-23 release, increasing susceptibility to bacterial superinfections. IL-17 and IL-22 primarily act on the lung epithelium, inducing antimicrobial proteins and neutrophil chemoattractants. Recent studies found that stimulation of macrophages and DCs with IL-17 also contributes to antibacterial immunity, while IL-22 promotes epithelial proliferation and repair following injury. Chronic diseases such as asthma and chronic obstructive pulmonary disease have been associated with IL-17 and IL-22 responses directed against innocuous antigens. Future studies will evaluate the therapeutic efficacy of targeting the IL-17/IL-22 pathway in pulmonary inflammation.
    Immunological Reviews 07/2014; 260(1):129-44. DOI:10.1111/imr.12183 · 12.91 Impact Factor
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    ABSTRACT: The Th17 cytokines IL-17A, IL-17F, and IL-22 are critical for the lung immune response to a variety of bacterial pathogens including Klebsiella pneumoniae (KP). Th2 cytokine expression in the airways is a characteristic feature of asthma and allergic airway inflammation. The Th2 cytokines IL-4 and IL-13 diminish ex vivo and in vivo IL-17A expression by Th17 cells. To determine the effect of IL-4 and IL-13 on IL-17-dependent lung immune responses to acute bacterial infection, we developed a combined model in which allergic airway inflammation and lung IL-4 and IL-13 expression were induced by ovalbumin sensitization and challenge prior to acute lung infection with KP. We hypothesized that pre-existing allergic airway inflammation decreases lung IL-17A expression and airway neutrophil recruitment in response to acute KP infection and thereby increases lung KP burden. As hypothesized, we found that allergic airway inflammation decreased KP-induced airway neutrophils and lung IL-17A, IL-17F, and IL-22 expression. Despite the marked reduction in post-infection airway neutrophilia and lung expression of Th17 cytokines, allergic airway inflammation significantly decreased lung KP burden and post-infection mortality. We showed that decreased lung KP burden was independent of IL-4, IL-5, and IL-17A, and partially-dependent on IL-13 and STAT6. Additionally, we demonstrated that decreased lung KP burden associated with allergic airway inflammation was both neutrophil and CCL8-dependent. These findings suggest a novel role for CCL8 in lung antibacterial immunity against KP and suggest new methods of orchestrating lung antibacterial immunity.
    Infection and immunity 06/2014; 82(9). DOI:10.1128/IAI.00035-14 · 4.16 Impact Factor
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    ABSTRACT: Many human cancers are dramatically accelerated by chronic inflammation. However, the specific cellular and molecular elements mediating this effect remain largely unknown. Using a murine model of pancreatic intraepithelial neoplasia (PanIN), we found that Kras(G12D) induces expression of functional IL-17 receptors on PanIN epithelial cells and also stimulates infiltration of the pancreatic stroma by IL-17-producing immune cells. Both effects are augmented by associated chronic pancreatitis, resulting in functional in vivo changes in PanIN epithelial gene expression. Forced IL-17 overexpression dramatically accelerates PanIN initiation and progression, while inhibition of IL-17 signaling using genetic or pharmacologic techniques effectively prevents PanIN formation. Together, these studies suggest that a hematopoietic-to-epithelial IL-17 signaling axis is a potent and requisite driver of PanIN formation.
    Cancer cell 05/2014; 25(5):621-37. DOI:10.1016/j.ccr.2014.03.014 · 23.89 Impact Factor

Publication Stats

18k Citations
2,375.72 Total Impact Points


  • 2014
    • Washington University in St. Louis
      • Department of Molecular Microbiology
      San Luis, Missouri, United States
  • 2012–2014
    • UPMC
      Pittsburgh, Pennsylvania, United States
    • Stratford University
      Стратфорд, Connecticut, United States
    • University of Lyon
      Lyons, Rhône-Alpes, France
  • 2004–2014
    • University of Pittsburgh
      • • Department of Pediatrics
      • • Division of Pediatric Pathology at Children's Hospital of Pittsburgh of UPMC
      • • Division of Pediatric Allergy and Immunology
      Pittsburgh, Pennsylvania, United States
    • Childrens Hospital of Pittsburgh
      • • Department of Pediatrics
      • • Division of Pulmonary Medicine, Allergy and Immunology
      Pittsburgh, Pennsylvania, United States
  • 1993–2013
    • Louisiana State University Health Sciences Center New Orleans
      • • Department of Genetics
      • • Section of Pulmonary/Critical Care Medicine
      • • Department of Medicine
      • • Section of Hematology / Oncology
      New Orleans, Louisiana, United States
  • 2009–2012
    • The Children's Hospital of Philadelphia
      • • Division of Neonatology
      • • Department of Pediatrics
      Philadelphia, PA, United States
    • University of Freiburg
      Freiburg, Baden-Württemberg, Germany
  • 2011
    • University of Alabama at Birmingham
      Birmingham, Alabama, United States
    • Texas Tech University Health Sciences Center
      • Paul L. Foster School of Medicine
      Lubbock, TX, United States
  • 2010
    • University of Texas at San Antonio
      • Department of Biology
      San Antonio, TX, United States
  • 2006
    • Thomas Jefferson University
      • Department of Pathology, Anatomy & Cell Biology
      Filadelfia, Pennsylvania, United States
  • 2005
    • Hospital of the University of Pennsylvania
      • Department of Pediatrics
      Filadelfia, Pennsylvania, United States
    • Vanderbilt University
      • Department of Medicine
      Nashville, MI, United States
  • 2002
    • Humboldt-Universität zu Berlin
      Berlín, Berlin, Germany
  • 2001–2002
    • Louisiana State University Health Sciences Center Shreveport
      • • School of Medicine
      • • Section of Critical Care
      Shreveport, Louisiana, United States
  • 1995–2002
    • Louisiana State University
      Baton Rouge, Louisiana, United States
    • State University of New York Downstate Medical Center
      • Department of Medicine
      Brooklyn, New York, United States
  • 1993–2000
    • Tulane University
      • Department of Physiology
      New Orleans, LA, United States
  • 1993–1997
    • LSU Medical Center
      • Department of Medicine
      United States
  • 1994
    • Howard Hughes Medical Institute
      Ashburn, Virginia, United States
    • Oakland University
      • Department of Chemistry
      Rochester, Michigan, United States